Why Is Plasma Renin Activity Lower in Populations of African Origin?

Total Page:16

File Type:pdf, Size:1020Kb

Why Is Plasma Renin Activity Lower in Populations of African Origin? Journal of Human Hypertension (2001) 15, 17–25 2001 Macmillan Publishers Ltd All rights reserved 0950-9240/01 $15.00 www.nature.com/jhh REVIEW ARTICLE Why is plasma renin activity lower in populations of African origin? GA Sagnella Blood Pressure Unit, St George’s Hospital Medical School, Cranmer Terrace, London SW17 ORE, UK Plasma renin activity is significantly lower in black the molecular level suggests that the lower PRA may people compared with whites independent of age and arise from gene variation in the renal epithelial sodium blood pressure status. The lower PRA appears to be due channel. The functional significance of the lower PRA in to a reduction in the rate of secretion of renin but the relation to the different pattern of cardiovascular and exact mechanistic events underlying such differences in renal disease between blacks and whites remains renin release between blacks and whites are still not unclear. Moreover, direct investigations of pre-treat- fully understood. Nevertheless, given the paramount ment renin status in hypertensive blacks in relation to importance of the renin-angiotensin system in the con- blood pressure response have demonstrated that the trol of sodium balance, a most likely explanation is that pre-treatment PRA is not a good index of subsequent the lower renin is a consequence of differences in renal blood pressure response to pharmacological treatment. sodium handling between blacks and whites. The lower Nevertheless, the blood pressure reduction to short PRA does not reflect differences in dietary sodium term sodium restriction is greater in blacks compared intake but the evidence available suggests that the low with whites and, in the black subjects, the greater PRA could be part of the corrective mechanisms reduction in blood pressure to sodium restriction designed to maintain sodium balance in the presence appears to be related, at least in part, to the decreased of an increased tendency for sodium retention in black responsiveness of the renin-angiotensin system. people. While it is possible that several factors may con- Journal of Human Hypertension (2001) 15, 17–25 tribute to the reduced PRA, more recent investigation at Keywords: African origin; plasma renin activity; sodium; renal; genetics Introduction variability in candidate genes likely to influence renin release and activity especially because of early The possibility of differences in the renin-angioten- suggestions that genetic factors may have a strong sin-system between people of African origin (blacks) influence on PRA and urinary aldosterone.2,3 and Caucasians (whites) has been recognised since Indeed, the potential importance of polymorphic the late 1960s. In one of the first studies using a variation at the gene level is highlighted by the newly developed quantitative assay for the measure- identification of polymorphic variants in the angio- ment of plasma renin activity (PRA), Helmer and tensin-converting enzyme (ACE) gene known to 1 Judson reported a much higher frequency of low account for more than 50% of the variability in PRA in black hypertensives (52%) compared with plasma ACE activity4 and in genetic variants of the white hypertensives (31%). renin substrate gene (angiotensinogen) associated The main purpose of this review is to assess the with increased expression of angiotensionogen.5 differences in PRA between blacks and whites, to explore some of the reasons for the low PRA in blacks and, in particular, to examine to what extent Comparison of PRA between blacks and the available evidence supports the widely held whites view that it is a direct result of a greater extracellular Following the early work,1 numerous other investi- fluid volume due to increased renal sodium gators measured PRA in blacks and confirmed the retention. Moreover, in view of recent advances in presence of lower PRA in blacks compared with molecular biology, particular emphasis will also be whites. Some of these studies spanning a period of given to the potential importance of genetic nearly 25 years are summarised in Table 1. As can be seen, on average PRA in blacks is about 50% to that in whites and the differences are similar for Correspondence: GA Sagnella, Blood Pressure Unit, St George’s 15,16 Hospital Medical School, Cranmer Terrace, London SW17 ORE, men and women, however it is also relevant to UK note the wide variability indicating that the PRA in Received 22 June 2000; accepted 17 July 2000 a substantial proportion of blacks is likely to be in Why is PRA lower in populations of African origin? GA Sagnella 18 Table 1 Comparison of PRA in blacks and whites Author Blacks Whites % Levy SB et al (1977)6 normotensives 0.80 ± 0.85(8) 1.60 ± 1.10(13) 50 essential hypertensives 0.70 ± 0.20(7) 2.80 ± 4.67(18) 25 Sever et al (1978)7 essential hypertensives 0.34 ± 0.56(23) 0.97 ± 1.10(77) 35 Mitas JA et al (1979)8 normotensives 0.76 ± 0.11(14) 1.58 ± 0.48(15) 48 essential hypertensives 0.95 ± 0.26(9) 1.23 ± 0.16(27) 77 Veterans (1987)9 essential hypertensives 0.69 ± 0.82(407) 1.35 ± 1.27(216) 51 Hohn AR et al (1983)10 children 2.40 ± 1.70(36) 4.76 ± 2.8(33) 50 children with family history of hypertension 1.98 ± 1.50(18) 4.62 ± 3.5(41) 43 James GD et al (1986)11 normotensives 2.10 ± 1.60(112) 2.80 ± 2.0(124) 75 He F et al (1998)12 essential hypertensives 0.48 ± 0.46(33) 1.08 ± 0.76(71) 44 He J et al (1999)13 population-based study 0.92 ± 1.36(110) 1.26 ± 1.35(183) 73 Kotchen et al (2000)14 essential hypertensives 1.10 ± 1.07(29) 1.80 ± 1.15(33) 61 Values are means ± s.d. (n); PRA activity (ng/ml/hr); supine and for subjects on their normal sodium intake. % (ratio of PRA in blacks/whites expressed as %). the range found in whites. Moreover, PRA distri- renin hypertension’ in blacks. However, ‘low renin butions are not normal, although there is no evi- hypertension’ is clearly an arbitrary definition and dence for a bimodal distribution in blacks. A lower the actual frequency in blacks has ranged widely plasma PRA has also been observed in some10,17 but depending on the cut-off value taken to delimit the not in every study18,19 of black children compared state of ‘low PRA’. Furthermore, suppressed PRA is with white children, however, it is apparent that the also present in both normotensive and hypertensive difference between black and white children blacks even when on a low salt diet6,12 and in becomes more pronounced with increasing age even response to loss of sodium as induced by admini- over an age range of 8–14 years.17 Interestingly, stration of diuretics.23,24 slightly lower PRA has also been reported in black The low PRA in blacks is also associated with a neonates.20 lower plasma angiotensin II independent of ACE While a lower PRA was originally defined in activity.12 Given the potent cardiovascular and renal relation to hypertension in blacks, lower PRA has effects of angiotensin II (Figure 1) this has led to also been found in normotensives6,8,9,11,13 suggesting that the lower PRA is not simply a consequence of the high blood pressure, at least in individuals with- out malignant hypertension and renal failure. That the lower PRA is a characteristic feature of blacks as a group is also supported by a lack of difference in PRA between normotensive and hypertensive blacks from rural African regions.21,22 A major criticism of some of the earlier studies was that they were limited by small numbers in clinic-based designs. However, lower PRA has also been found in popu- lation-based studies of blacks and whites in the absence of significant differences in blood pressure between the two groups.7,9,13 Nevertheless, in both whites and blacks, a weak but statistically signifi- cant inverse association between PRA and both sys- tolic and diastolic blood pressure has been reported even after adjusting for age and gender13 (−2.4 mm Hg/1.24 ng/ml/hr renin for systolic and −1.5 mm Hg/1.24 ng/ml/hr renin for diastolic blood pressure, respectively). The regression coefficients were slightly higher for the blacks and this could Figure 1 Systemic, renal and other effects of Angiotensin II (AT1 account for the apparently higher frequency of ‘low receptor). (See Taal and Brenner25 for further details). Journal of Human Hypertension Why is PRA lower in populations of African origin? GA Sagnella 19 speculations about the functional significance of the Renin-angiotensinogen reaction lower PRA in blacks in relation to the physiological role of renin in the control of sodium balance; to the In humans, the concentration of angiotensinogen in pathophysiological significance for cardiovascular/ the plasma is less than that required for full satu- renal disease and to the treatment of hypertension ration and therefore even small changes in plasma in blacks. levels can influence the amount of angiotensin I pro- duced.27 There is little information on the kinetics of the renin-angiotensinogen reaction in plasma from Possible reasons for lower PRA in black people, nor on the presence of endogenous blacks inhibitors of renin activity. But any effects are likely to be small as a lower PRA in blacks was also asso- The control of renin release into the circulation is ciated with a lower plasma concentration of renin.28 under the influence of many neural, haemodynamic A number of polymorphic variants have recently and hormonal factors.26 Renin release depends on been identified within the renin gene raising the both renal perfusion pressure and on tubular func- possibility that these variants might influence renin tion.
Recommended publications
  • Cardiovascular System 9
    Chapter Cardiovascular System 9 Learning Outcomes On completion of this chapter, you will be able to: 1. State the description and primary functions of the organs/structures of the car- diovascular system. 2. Explain the circulation of blood through the chambers of the heart. 3. Identify and locate the commonly used sites for taking a pulse. 4. Explain blood pressure. 5. Recognize terminology included in the ICD-10-CM. 6. Analyze, build, spell, and pronounce medical words. 7. Comprehend the drugs highlighted in this chapter. 8. Describe diagnostic and laboratory tests related to the cardiovascular system. 9. Identify and define selected abbreviations. 10. Apply your acquired knowledge of medical terms by successfully completing the Practical Application exercise. 255 Anatomy and Physiology The cardiovascular (CV) system, also called the circulatory system, circulates blood to all parts of the body by the action of the heart. This process provides the body’s cells with oxygen and nutritive ele- ments and removes waste materials and carbon dioxide. The heart, a muscular pump, is the central organ of the system. It beats approximately 100,000 times each day, pumping roughly 8,000 liters of blood, enough to fill about 8,500 quart-sized milk cartons. Arteries, veins, and capillaries comprise the network of vessels that transport blood (fluid consisting of blood cells and plasma) throughout the body. Blood flows through the heart, to the lungs, back to the heart, and on to the various body parts. Table 9.1 provides an at-a-glance look at the cardiovascular system. Figure 9.1 shows a schematic overview of the cardiovascular system.
    [Show full text]
  • Aldosterone and Parathyroid Hormone: Evidence for a Clinically Relevant Relationship
    Journal of Endocrinology and Thyroid Research ISSN: 2573-2188 Review Article J Endocrinol Thyroid Res Volume 4 Issue 3 - May 2019 Copyright © All rights are reserved by Vismay Naik DOI: 10.19080/JETR.2019.04.555637 Aldosterone and Parathyroid Hormone: Evidence for a Clinically Relevant Relationship Vismay Naik* PG Diploma in Endocrinology and Diabetes, Ashirvad Heart and Diabetes Centre, India Submission: April 13, 2019; Published: May 06, 2019 *Corresponding author: Vismay Naik, MD, MRCP(UK), PG Diploma in Endocrinology and Diabetes, Ashirvad Heart and Diabetes Centre, India Introduction hyperparathyroidism due to increased renal and faecal calcium A ‘new endocrine axis’, involving the bi-directional relati- excretion. PTH is increased as a result of the MR (mineralocorticoid onship between the parathyroid hormone (PTH) and the renin– receptor) mediated calciuretic and magnesiuretic effects, with a angiotensin–aldosterone system (RAAS) has been established trend towards hypocalcemia, hypomagnesemia and the direct recently. Individually these have long been recognized, althou- effects of aldosterone on parathyroid cells via binding to the MR. gh it is only in recent times that we are realizing the interplay Moreover, the angiotensin II receptor is expressed by human between the two and the corresponding effects this has on the parathyroid tissue, and angiotensin may therefore directly physiological and pathological roles within the body. Other cal- stimulate PTH secretion [6]. ciotropic hormones such as Vitamin D are also impacting on this relationship [1]. This report aims to highlight the cyclic nature of RAAS and Vitamin D these relationships, through the physiological pathways, which Aldosterone acts through the mineralocorticoid receptor, will then lead into pathological disease in multiple areas such as which belongs to the same superfamily of nuclear receptors as heart failure, cardiovascular health and bone homeostasis.
    [Show full text]
  • Hypertension: Shall We Focus on Adipose Tissue?
    www.jasn.org EDITORIALS Hypertension: Shall We Focus associated with incident hypertension among women with- out diabetes. The authors prospectively studied 872 women on Adipose Tissue? without diabetes or hypertension from the Nurses’ Health Study. After a follow-up of 14 years, 361 (41.4%) women Simona Bo and Paolo Cavallo-Perin developed hypertension. Plasma resistin values were signif- Department of Internal Medicine, University of Turin, Turin, Italy icantly associated with incident hypertension: The highest resistin tertile conferred a 75% higher risk for hypertension J Am Soc Nephrol 21: 1067–1068, 2010. doi: 10.1681/ASN.2010050524 than the lowest (relative risk 1.75; 95% confidence interval 1.19 to 2.56). The relative risk did not substantially change after adjustment for multiple potential metabolic and nu- Adipose tissue is an active endocrine organ that produces sub- tritional confounding factors and for other adipokines. The stances having local and systemic actions on blood vessels, kid- risk was greater among older women. In a secondary analy- neys, and the heart. Leptin, adiponectin, resistin, angiotensin sis, inflammatory and endothelial biomarkers were mea- ␣ II, adipsin, TNF- , IGF-1, plasminogen-activator inhibitor 1, sured in a subset of women. Resistin levels were significantly and prostaglandins compose an incomplete list.1 associated with both groups of biomarkers. After further Resistin, an adipokine belonging to the cysteine-rich secre- adjustment for C-reactive protein, IL-6, soluble TNF recep- tory protein family, was described as an adipocyte-derived tor 2, intercellular adhesion molecule 1, vascular adhesion polypeptide that links obesity and insulin resistance in mice2; molecule 1, and E-selectin, resistin concentrations re- however, striking differences in the genomic organization and mained positively associated with an increased risk for inci- cellular source of resistin in rodents versus humans and the dent hypertension.
    [Show full text]
  • Blood and Lymph Vascular Systems
    BLOOD AND LYMPH VASCULAR SYSTEMS BLOOD TRANSFUSIONS Objectives Functions of vessels Layers in vascular walls Classification of vessels Components of vascular walls Control of blood flow in microvasculature Variation in microvasculature Blood barriers Lymphatic system Introduction Multicellular Organisms Need 3 Mechanisms --------------------------------------------------------------- 1. Distribute oxygen, nutrients, and hormones CARDIOVASCULAR SYSTEM 2. Collect waste 3. Transport waste to excretory organs CARDIOVASCULAR SYSTEM Cardiovascular System Component function Heart - Produce blood pressure (systole) Elastic arteries - Conduct blood and maintain pressure during diastole Muscular arteries - Distribute blood, maintain pressure Arterioles - Peripheral resistance and distribute blood Capillaries - Exchange nutrients and waste Venules - Collect blood from capillaries (Edema) Veins - Transmit blood to large veins Reservoir Larger veins - receive lymph and return blood to Heart, blood reservoir Cardiovascular System Heart produces blood pressure (systole) ARTERIOLES – PERIPHERAL RESISTANCE Vessels are structurally adapted to physical and metabolic requirements. Vessels are structurally adapted to physical and metabolic requirements. Cardiovascular System Elastic arteries- conduct blood and maintain pressure during diastole Cardiovascular System Muscular Arteries - distribute blood, maintain pressure Arterioles - peripheral resistance and distribute blood Capillaries - exchange nutrients and waste Venules - collect blood from capillaries
    [Show full text]
  • High and Non-Suppressible Plasma Renin Activity in a Patient with Aldosterone Producing Adenoma: Pathophysiologic and Diagnostic Implications
    Journal of Human Hypertension (1999) 13, 75–78 1999 Stockton Press. All rights reserved 0950-9240/99 $12.00 http://www.stockton-press.co.uk/jhh CASE REPORT High and non-suppressible plasma renin activity in a patient with aldosterone producing adenoma: pathophysiologic and diagnostic implications E Shyong Tai and PHK Eng Department of Endocrinology, Singapore General Hospital, Singapore We describe a case of primary aldosteronism due to an possible pathophysiological causes of a rise in PRA in aldosterone producing adenoma with high and non-sup- this clinical setting and suggest that underlying arteri- pressible plasma renin activity (PRA). She had sup- olar disease due to prolonged hypertension may be the pressed PRA at initial diagnosis. This rose above the cause of increased and non-suppressible PRA in pri- reference range for normal individuals over a period of mary aldosteronism. 7 years with untreated hypertension. We discuss the Keywords: primary aldosteronism; plasma renin activity; diagnosis Introduction Case report Primary aldosteronism is classically associated with Our patient was a 34-year-old woman who was hypertension, hypokalaemia and suppressed plasma found to have hypertension during the fifteenth renin activity (PRA). Most cases are due to an aldo- week of pregnancy. Plasma aldosterone was sterone producing adenoma (APA). We present a 2039 pmol/l, PRA Ͻ0.15 ␮g/l/h and a diagnosis of case of prolonged, untreated, primary aldosteronism primary aldosteronism was made. Following the due to an APA. She had suppressed PRA at the time delivery of her child, she defaulted follow-up and of diagnosis, which became elevated and non-sup- was not treated with any antihypertensives nor pot- pressible by intravenous salt loading.
    [Show full text]
  • Cardiovascular System Summary Notes the Cardiovascular System
    Cardiovascular System Summary Notes The cardiovascular system includes: The heart, a muscular pump The blood, a fluid connective tissue The blood vessels, arteries, veins and capillaries Blood flows away from the heart in arteries, to the capillaries and back to the heart in the veins There is a decrease in blood pressure as the blood travels away from the heart Arterial branches of the aorta supply oxygenated blood to all parts of the body Deoxygenated blood leaves the organs in veins Veins unite to form the vena cava which returns the blood to the heart Pulmonary System This is the route by which blood is circulated from the heart to the lungs and back to the heart again The pulmonary system is exceptional in that the pulmonary artery carries deoxygenated blood and the pulmonary vein carries oxygenated blood Hepatic Portal Vein There is another exception in the circulatory system – the hepatic portal vein Veins normally carry blood from an organ back to the heart The hepatic portal vein carries blood from the capillary bed of the intestine to the capillary bed of the liver As a result, the liver has three blood vessels associated with it Arteries and Veins The central cavity of a blood vessel is called the lumen The lumen is lined with a thin layer of cells called the endothelium The composition of the vessel wall surrounding the endothelium is different in arteries, veins and capillaries Arteries carry blood away from the heart Arteries have a thick middle layer of smooth muscle They have an inner and outer layer of elastic fibres Elastic
    [Show full text]
  • Aldosterone-Renin Ratio (Arr)
    RENIN -ALDOSTERONE PROFILING: ALDOSTERONE-RENIN RATIO (ARR) 1. Obtain a morning specimen for serum aldosterone (redtop tube) and plasma renin (lavender-top) tube from an upright patient sitting for a period of 15 min prior to (being seated for) blood drawing. Fasting is not required and no salt restriction is necessary. 2. Spironolactone. The ratio cannot be assessed in patients receiving spironlactone. If primary aldosteronism (PA) is suspected in a patient receiving this drug, treatment should be discontinued for 4-6 weeks (1). 3. Hypokalemia should be corrected before ARR is measured as a low K will lower aldosterone and can lead to a falsely negative ARR (1). 4. Preferred antihypertensives that have a minimal effect on the ARR are doxazozin (Cardura), prazosin (Minipress), verapramil slow release, or hydralazine, singly or in combination for one month before sampling (1). 5. False-positive ARR: Beta-blockers, clonidine, methyldopa, and NSAID’s lower levels of renin and can cause a falsely positive ARR (1). A minimum 3-day cessation prior to sampling is recommended (3). The renin direct assay is also lower in patients on oral contraceptives and hormone replacement therapy potentially causing the ARR to be falsely increased. Measurement of plasma renin activity is preferred in this situation, calculating the aldosterone/PRA ratio (positive if >20/1). 6. False-negative ARR: Diuretics cause false negatives by causing K loss lowering aldosterone and stimulating renin through volume loss. Angiotensin blockers (ARB’s), ACE inhibitors, and some calcium channel blockers raise renin and can cause false negatives (1). A minimum three-day cessation prior to sampling is recommended (3).
    [Show full text]
  • The Renin-Angiotensin System and the Heart: a Historical Review Heart: First Published As 10.1136/Hrt.76.3 Suppl 3.7 on 1 November 1996
    Heart (Supplement 3) 1996;76:7-12 7 The renin-angiotensin system and the heart: a historical review Heart: first published as 10.1136/hrt.76.3_Suppl_3.7 on 1 November 1996. Downloaded from Stephen J Cleland, John L Reid Early observations on a possible link effect but was in fact an enzyme. The names between the kidney and the "hypertensin""l and "angiotonin"12 were given cardiovascular system to the pressor substance formed from the renin In 1836 an English clinician Richard Bright substrate by the enzymatic action of renin. observed that patients dying with contracted Subsequently, it was agreed that the term kidneys often had a hard, full pulse and cardiac "angiotensin" would be used to describe this hypertrophy.' In 1889 Brown-Sequard, the substance. During this period the potential for "father" of endocrinology, showed that injec- pathological effects of renin was recognised. tions of extracts from guinea pig testicles were Winternitz described necrotising arteriolar able to produce systemic effects of vigour and lesions in animals which had undergone renal the perception of rejuvenation.2 On this back- artery ligation and also in nephrectomised ani- ground, in 1896 the Finnish physiologist mals which had been given kidney extracts.'3 Robert Tigerstedt and his student Per Finally, the relevance of renal control of blood Bergman began to explore the possibility that pressure in man was described by Young who, kidney extracts from rabbits may have some in 1936, cured a case of malignant hyperten- systemic effects on the cardiovascular system. sion by removing an ischaemic kidney.'4 In 1898 their classic paper was published showing that intravenous injection of these renal extracts exerted a pressor effect.
    [Show full text]
  • SGLT2 Inhibition and Potential Renal Protection
    The knowns and unknowns of SGLT2 inhibition in CKD Paola Fioretto, MD Padua, Italy June 14, 2019 - Budapest, Hungary SGLT2 inhibition in CKD: Discussing the key questions and evidence Budapest, june 14 2019 The knowns and unknowns of SGLT2 inhibition in CKD Paola Fioretto Department of Medicine University of Padova, Italy 180 g of glucose filtered Glomerulus Proximal tubule Distal tubule Collecting duct each day S1 S2 Glucose filtration S3 SGLT2 SGLT1 90% 10% Glucose reabsorption Loop of Henle Up to ~ 90% of glucose ~ 10% of glucose Minimal is reabsorbed is reabsorbed glucose from the S1/S2 segments from the S3 segment excretion Possible mechanisms responsible for cardiovascular and renal protection with SGLT2 inhibition SGLT2 inhibition Glycosuria Natriuresis ↓Blood ↓Plasma Negative caloric balance ↑Uricosuria pressure ↑Tubuloglomerular volume feedback ↓Myocardial ↓HbA1c ↓ Afferent stretch ↓ ↓Plasma uric ↓Arterial ↓ arteriole acid stiffness ↑ constriction ↓Total body fat mass ↓Inflammation ↓Glucose toxicity ↓Epicardial fat ↓Intraglomerular hypertension ↓Ventricular ↓Hyperfiltration arrhythmias ↓Atherosclerosis Activation of ACE2 – Ang1/7 ↑Cardiac contractility ↓Inflammation No sympathetic nervous system activation ↓Fibrosis Cardiac and renal protection Heerspink HJ et al, Circulation 2016 Tonneijck et al, J Am Soc Nephrol 2017 Diabetic nephron Diabetic nephron with SGLT2 i Effects of SGLT2 i on afferent arteriole tone: in vivo studies with multiphoton microscope imaging techniques Kidokoro K et al, Circulation 2019 Effects of SGLT2 i
    [Show full text]
  • Plasma Renin Activity and Pro-B-Type Natriuretic Peptide Levels in Different Atrial Fibrillation Types
    Original Investigation Özgün Araşt›rma 317 Plasma renin activity and pro-B-type natriuretic peptide levels in different atrial fibrillation types Farklı atriyal fibrilasyon türlerinde plazma renin aktivitesi ve pro-B-tipi natriüretik peptit düzeyleri Abdullah Doğan, Ömer Gedikli1, Mehmet Özaydın, Gürkan Acar2 Department of Cardiology, Faculty of Medicine, Süleyman Demirel University, Isparta 1Department of Cardiology, Faculty of Medicine, Karadeniz Technical University, Trabzon 2Department of Cardiology, Faculty of Medicine, Sütçü Imam University, Kahramanmaraş, Turkey ABSTRACT Objective: Renin-angiotensin system may be activated during atrial fibrillation (AF). Our aim was to evaluate plasma renin activity (PRA) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels in patients with different AF types who had normal left ventricular (LV) systolic function. Methods: This cross-sectional study included 97 patients with recent (≤7 days), persistent (7 days to 12 months) and permanent AF (>12 months), and age- and sex-matched 30 controls with sinus rhythm. Plasma levels of PRA and NT-pro-BNP were measured and presented as median (25th-75th percentiles). Echocardiographic examination was performed in all population. Variance and logistic regression analyses were also used for multiple comparisons and independent predictors, respectively. Results: Median NT-proBNP levels were higher in overall patients with AF than in controls [114 (63-165) vs 50 (38-58) pg/ml, p<0.001), but PRA level was comparable in both groups. Similarly, NT-proBNP levels were also higher in all subtypes of AF compared with controls (p<0.05). In addition, there was a significant difference in NT-proBNP level among recent, persistent and permanent AF subtypes (p=0.001).
    [Show full text]
  • Effects of Moxonidine on the Sympathetic Nervous System
    Journal of Clinical and Basic Cardiology An Independent International Scientific Journal Journal of Clinical and Basic Cardiology 2004; 7 (1-4), 19-25 Effects of Moxonidine on the Sympathetic Nervous System, Blood Pressure, Plasma Renin Activity, Plasma Aldosterone, Leptin, and Metabolic Profile in Obese Hypertensive Patients Sanjuliani AF, Francischetti EA, Genelhu de Abreu V Ueleres Braga J Homepage: www.kup.at/jcbc Online Data Base Search for Authors and Keywords Indexed in Chemical Abstracts EMBASE/Excerpta Medica Krause & Pachernegg GmbH · VERLAG für MEDIZIN und WIRTSCHAFT · A-3003 Gablitz/Austria ORIGINAL PAPERS, CLINICAL CARDIOLOGY Moxonidine in Obese Hypertensive Patients J Clin Basic Cardiol 2004; 7: 19 Effects of Moxonidine on the Sympathetic Nervous System, Blood Pressure, Plasma Renin Activity, Plasma Aldosterone, Leptin, and Metabolic Profile in Obese Hypertensive Patients A. F. Sanjuliani, V. Genelhu de Abreu, J. Ueleres Braga, E. A. Francischetti Obesity accounts for around 70 % of the patients with primary hypertension. This association accentuates the risk of cardiovascular disease as it is frequently accompanied by the components of the metabolic syndrome. Clinical, epidemiological and experimental studies show an association between obesity-hypertension with insulin resistance and increased sympathetic nervous system activity. We conducted the present study to evaluate in forty obese hypertensives of both genders, aged 27 to 63 years old, the chronic effects of moxonidine – a selective imidazoline receptor agonist – on blood pressure, plasma catecholamines, leptin, renin-angiotensin aldosterone system and components of the metabolic syndrome. It was a randomized parallel open study, amlodipine was used as the control drug. Our results show that moxonidine and amlodipine significantly reduced blood pressure without affecting heart rate when measured by the oscillometric method and with twenty-four-hour blood pressure monitoring.
    [Show full text]
  • Blood Vessels and Circulation
    19 Blood Vessels and Circulation Lecture Presentation by Lori Garrett © 2018 Pearson Education, Inc. Section 1: Functional Anatomy of Blood Vessels Learning Outcomes 19.1 Distinguish between the pulmonary and systemic circuits, and identify afferent and efferent blood vessels. 19.2 Distinguish among the types of blood vessels on the basis of their structure and function. 19.3 Describe the structures of capillaries and their functions in the exchange of dissolved materials between blood and interstitial fluid. 19.4 Describe the venous system, and indicate the distribution of blood within the cardiovascular system. © 2018 Pearson Education, Inc. Module 19.1: The heart pumps blood, in sequence, through the arteries, capillaries, and veins of the pulmonary and systemic circuits Blood vessels . Blood vessels conduct blood between the heart and peripheral tissues . Arteries (carry blood away from the heart) • Also called efferent vessels . Veins (carry blood to the heart) • Also called afferent vessels . Capillaries (exchange substances between blood and tissues) • Interconnect smallest arteries and smallest veins © 2018 Pearson Education, Inc. Module 19.1: Blood vessels and circuits Two circuits 1. Pulmonary circuit • To and from gas exchange surfaces in the lungs 2. Systemic circuit • To and from rest of body © 2018 Pearson Education, Inc. Module 19.1: Blood vessels and circuits Circulation pathway through circuits 1. Right atrium (entry chamber) • Collects blood from systemic circuit • To right ventricle to pulmonary circuit 2. Pulmonary circuit • Pulmonary arteries to pulmonary capillaries to pulmonary veins © 2018 Pearson Education, Inc. Module 19.1: Blood vessels and circuits Circulation pathway through circuits (continued) 3. Left atrium • Receives blood from pulmonary circuit • To left ventricle to systemic circuit 4.
    [Show full text]