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Deactivation of Carotid Body Chemoreceptors by Hyperoxia Decreases Blood Pressure in Hypertensive Patients

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Deactivation of Carotid Body Chemoreceptors by Hyperoxia Decreases Blood Pressure in Hypertensive Patients Hypertension Research (2014) 37, 858–862 & 2014 The Japanese Society of Hypertension All rights reserved 0916-9636/14 www.nature.com/hr ORIGINAL ARTICLE Deactivation of carotid body chemoreceptors by hyperoxia decreases blood pressure in hypertensive patients Maciej Sinski1, Jacek Lewandowski1, Jacek Przybylski2, Pawe" Zalewski3, Bartosz Symonides1, Piotr Abramczyk1 and Zbigniew Gaciong1 Previous studies have shown that hyperoxia-induced deactivation of carotid body chemoreceptors reduces sympathetic activity in hypertensive patients but it does not affect blood pressure. The maintenance of blood pressure can be explained by the direct, vasoconstrictive effect of hyperoxia, which offsets diminished sympathetic activity. This study compares the effect of acute hyperoxia on hemodynamic parameters between hypertensive and normotensive subjects. Twelve males with hypertension (age 39.4±2.4 years; body mass index 27.4±1.1 kg m À2) and 11 normotensive males (age 39.9±2.7 years; body mass index 25.4±0.7 kg m À2) received, via non-rebreathing mask ventilation, ambient air, followed by 100% oxygen for 20 min. The stroke volume, heart rate, cardiac output, blood pressure, total peripheral resistance, respiratory rate, baroreceptor control of heart rate and oxygen saturation were recorded continuously. Several 30 s periods were analyzed before, during and after inducing hyperoxia. At baseline, the hypertensive subject’s blood pressure was higher and their baroreflex control of heart rate was lower when compared with the normotensive control group. After the first 30 s of hyperoxia, systolic, diastolic and mean blood pressures, as well as the total peripheral resistance, decreased significantly in hypertensives but not in normotensives. After 20 min of 100% oxygen ventilation, systolic and mean blood pressures and total peripheral resistance was increased in hypertensive patients, and the cardiac output and stroke volume had decreased in both groups. The results of this study confirm that deactivation of carotid body chemoreceptors can acutely decrease blood pressure in humans. Hypertension Research (2014) 37, 858–862; doi:10.1038/hr.2014.91; published online 8 May 2014 Keywords: baroreflex; blood pressure; carotid body chemoreceptors; hyperoxia INTRODUCTION system and its increased activity in hypertensive patients is well Pharmacotherapy in hypertension aims to improve the control of documented. It may even be worth to consider what extent the blood pressure (BP) and reduce cardiovascular risk. However, only carotid body chemoreceptors have in the pathogenesis of primary 30% of hypertensive patients have good BP control, and 50% of hypertension.13–16 Animal model studies have already demonstrated those treated discontinue their therapy after 1 year.1–4 To improve that surgical chemoreceptor deactivation decreases BP and prevents BP control and reduce cardiovascular mortality, newer non- the development of hypertension.17 pharmacological methods of hypertension treatment have been Our previous study showed that the deactivation of carotid body introduced to target the autonomic nervous system. These include chemoreceptors, by inducing hyperoxia, reduces sympathetic activity kidney denervation and baroreceptor stimulation. The rationale for in hypertensive subjects but not in the normotensive individuals.18 both methods are based on the observed increased sympathetic However, we did not observe any significant changes in BP between activity in hypertensive patients.5–9 An increased basal sympathetic the two groups. Hyperoxia induces direct vasoconstriction and it is tone is not only an attribute of young and borderline hypertensives9,10 possible that this effect offsets the drop of BP related to chemoreceptor but it is also present in subjects with moderate and severe deactivation.18 The latency of direct vasoconstriction caused by hypertension.6,11–13 Furthermore, an elevated sympathetic drive hyperoxia is much longer than the latency of deactivating arterial correlates with BP values,6 which may postulate a direct causal chemoreceptors, and we have taken this into account while preparing relationship between the two.6,12 The carotid body chemoreceptors the methodology of our study (see below). It should be expected that contribute significantly to the activity of the autonomic nervous there will be a decrease in BP during the early stage of hyperoxia. 1Department of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, Warsaw, Poland; 2Department of Biophysics and Physiology, Medical University of Warsaw, Warsaw, Poland and 3Department of Hygiene and Epidemiology, Faculty of Health Sciences Ludwik Rydygier Collegium Medicum in Bydgoszcz Nicolaus Copernicus University in Torun, Bydgoszcz, Poland Correspondence: Dr J Lewandowski, Department of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, Banacha 1a, 02-097 Warsaw, Poland. E-mail: [email protected] Received 29 December 2013; revised 8 March 2014; accepted 27 March 2014; published online 8 May 2014 Chemoreceptor deactivation decreases blood pressure MSinskiet al 859 The purpose of our study was to determine the acute effect of constant throughout the study at 10 l min À1. The subjects were blinded to the hyperoxia on BP and other hemodynamic parameters in hypertensive type and percentage of gas they were inspiring. Oxygen saturation (sat O2)and and normotensive subjects. end tidal CO2 and respiratory rate (RR) were monitored through the study (CapnoCheck Plus, Smith Medical International, Watford, Herts, UK). METHODS Subjects Assessment of hemodynamic responses Twelve patients with essential hypertension (age 39.4±2.3 years; body mass All measurements were performed with a task force monitor (CNSystems index 27.4±1.0) and 11 normotensive males (age 39.9±2.7 years; body mass Medizintechnik, Graz, Austria). The task force monitor application is an index 25.4±0.7) were invited for assessment in our laboratory. Six of the automated and computed beat-to-beat analyzer, providing heart rate (HR) patients with hypertension followed the antihypertensive regimens: two (electrocardiogram signal), oscillometric and noninvasive continuous BP patients were being treated with a combination of perindopril and indapamide, measurements (photoelectric vascular unloading method—systolic BP (SBP) two with a combination of perindopril and amlodipine and two with and diastolic BP (DBP)) and continuous measurement of cardiac output (CO), amlodipine only. The treatments were unaltered for at least 4 weeks before stroke volume (SV) and total peripheral resistance (TPR) based on impedance conducting our study. The remaining 6 patients with hypertension and the cardiography. The task force monitor facilitates continuous (beat-to-beat), 11 control subjects were not taking medications. All patients underwent reliable and reproducible measurements of hemodynamic parameters.19–22 routine diagnostic evaluation for hypertension in our department clinic. Baroreflex control of the HR was also calculated using the task force monitor Patients with grade 3 hypertension, secondary forms of hypertension, system and the sequence method with signals was derived from continuous BP including obstructive sleep apnea syndrome, diabetes and arrhythmias, were measurement and electrocardiogram tracing. Briefly, the sequence method excluded from the study. Other exclusion criteria included chronic obstructive detects sequences of SBP increases or decreases, accompanied by prolongation pulmonary disease, asthma, congenital cyanotic heart disease and active or shortening of electrocardiogram RR intervals, respectively. If three or more smoking. The Ethical Committee of the Medical University of Warsaw consecutive beats show an increase (or decrease) in SBP (X1 mm Hg per beat), accepted the study protocol. All participants provided informed consent. a BP ramp is detected. If the BP ramp is accompanied by an increase (or decrease) of X4 ms in the RR interval, a baroreceptor sequence is detected. In Study procedures our study, we used combined up and down sequence count. All subjects were studied at midday, in a quiet room, in supine position. The room temperature was kept constant at 20–21 1C. Subjects were instructed to Statistics have a light breakfast in the morning, and those on hypertensive therapy were During the session the subject’s hemodynamic parameters were continuously asked to take their routine morning medication. All patients underwent recorded. Each parameter was analyzed six times throughout the study, using baseline recordings (as defined below) for 10 min before the placement of a the average values over 30 s periods (P-1, P0, P1, P2, P3 and P4). The decision non-rebreathable mask. The subjects were then started on ventilating 21% to use 30 s periods was to ascertain early hemodynamic response to hyperoxia- oxygen for 10 min by mask, followed by 20 min of 100% oxygen ventilation to induced carotid body deactivation.23,24 A timeline representing the period of induce hyperoxia. This was followed by a 10-min recovery period of 21% analyses is presented in Figure 1. P-1 was recorded during the last 30 s of oxygen for 10 min. The flow rate through the non-rebreathable mask was normal room air breathing before mask ventilation. P0 was the baseline and it Start Baseline 30 s 90 s 20 min End P-1 P 0 P 1 P 2 P 3 P 4 10 min 21 % O2 10 min 21 % O2 mask 20 min 100 % O2 mask 10 min 21 % O2 mask Figure 1 Scheme of study periods and data acquisition. Table 1 Effect
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