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Baroreceptor Dysfunction Induced by Nitric Oxide Synthase Inhibition in Humans Lukas E

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Baroreceptor Dysfunction Induced by Nitric Oxide Synthase Inhibition in Humans Lukas E View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Journal of the American College of Cardiology Vol. 36, No. 1, 2000 © 2000 by the American College of Cardiology ISSN 0735-1097/00/$20.00 Published by Elsevier Science Inc. PII S0735-1097(00)00674-4 Cardiac Physiology Baroreceptor Dysfunction Induced by Nitric Oxide Synthase Inhibition in Humans Lukas E. Spieker, MD, Roberto Corti, MD, Christian Binggeli, MD, Thomas F. Lu¨scher, MD, FACC, FRCP, FESC, Georg Noll, MD, FESC Zurich, Switzerland OBJECTIVES We sought to investigate baroreceptor regulation of sympathetic nerve activity and hemody- namics after inhibition of nitric oxide (NO) synthesis. BACKGROUND Both the sympathetic nervous system and endothelium-derived substances play essential roles in cardiovascular homeostasis and diseases. Little is known about their interactions. METHODS In healthy volunteers, we recorded muscle sympathetic nerve activity (MSA) with microneu- rography and central hemodynamics measured at different levels of central venous pressure induced by lower body negative pressure. G RESULTS After administration of the NO synthase inhibitor N -monomethyl-L-arginine (L-NMMA, 1 mg/kg/min), systolic blood pressure increased by 24 mm Hg (p ϭ 0.01) and diastolic blood pressure by 12 mm Hg (p ϭ 0.009), while stroke volume index (measured by thermodilution) fell from 53 to 38 mL/min/m2 (p Ͻ 0.002). Administration of L-NMMA prevented the compensatory increase of heart rate, but not MSA, to orthostatic stress. The altered response of heart rate was not due to higher blood pressure, because heart rate responses were not altered during infusion of the alpha-1-adrenoceptor agonist phenylephrine (titrated to an equal increase of systolic blood pressure). In the presence of equal systolic blood pressure and central venous pressure, we found no difference in MSA during phenylephrine and L-NMMA infusion. CONCLUSIONS This study demonstrates a highly specific alteration of baroreceptor regulation of heart rate but not muscle sympathetic activity after inhibition of NO synthesis in healthy volunteers. This suggests an important role of NO in reflex-mediated heart rate regulation in humans. (J Am Coll Cardiol 2000;36:213–8) © 2000 by the American College of Cardiology The vascular endothelium synthesizes and releases nitric abnormal baroreflex contributes to sympathetic activation, oxide (NO) and plays a fundamental role in the basal and which is an unfavorable prognostic factor (15–19). Alter- dynamic regulation of the circulation (1–4). Apart from the ations in endothelial function, with a resulting imbalance of tone of peripheral resistance vessels, NO also regulates endothelium-derived relaxing and contracting factors, may myocardial contractility and is synthesized in neuronal cells affect baroreceptor function because endothelial factors may (5–8). However, little is known about the interactions of act on baroreceptor nerve endings in the vessel wall. Various NO and other cardiovascular regulating systems, especially endogenous substances (e.g., NO, endothelin-1, prostacy- with the sympathetic nervous system. These interactions are clin, norepinephrine) have been shown to influence barore- of particular interest in congestive heart failure, arterial ceptor function in animals (12,20–24). It is not clear if these hypertension, atherosclerosis and septic shock, where sym- mediators also affect human baroreceptor function. pathetic nerves innervating and constricting blood vessels The aim of our study was to investigate the effects of NO act as important counterpart of the endothelium-derived synthase inhibition and alpha-1-adrenergic stimulation on vasodilator NO (5,9–11). baroreceptor-mediated regulation of sympathetic nerve ac- Sympathetic activity is mainly regulated by baroreceptors tivity, heart rate and hemodynamics in healthy humans. located in the cardiopulmonary and carotid vessel walls, which centrally inhibit sympathetic outflow. These stretch- METHODS activated mechanoreceptors not only regulate short-term changes of blood pressure but also react to chronic elevation Subjects. Nine healthy normotensive volunteers (118 Ϯ of blood pressure by resetting sensitivity to a lower level 2/65 Ϯ 2 mm Hg, seven men and two women) with a mean (12,13). In hypertension, altered baroreflex-mediated regu- age of 26 years (range 21 to 35 years) participated in this study. lation of muscle sympathetic nerve activity (MSA) has been Right heart catheterization was performed in seven subjects described (14). Similarly, in congestive heart failure, an (five men and two women), of whom three (one man and two women) were simultaneously studied by microneurography. From the Department of Cardiology, University Hospital, Zu¨rich, Switzerland. Microneurographic measurements of sympathetic activity and This study was supported by the Swiss National Foundation (Nos. 32-42560.94 and noninvasive hemodynamic measurements were additionally 32-5106997) and the Italian Society of Hypertension. Manuscript received August 5, 1999; revised manuscript received December 30, performed in two male volunteers (without right heart cathe- 1999, accepted February 28, 2000. terization). Each volunteer gave written, informed consent. 214 Spieker et al. JACC Vol. 36, No. 1, 2000 NO and Baroreceptor Regulation July 2000:213–8 ilance Monitor Model VGS1; Baxter Healthcare Corporation, Abbreviations and Acronyms Irvine, California) with a Swan-Ganz catheter (Model 746H- LBNP ϭ lower body negative pressure 8F; Baxter Healthcare Corporation) inserted through a sheath G L-NMMA ϭ N -monomethyl-L-arginine introducer system (Cordis, Langenthal, Switzerland) in a ϭ MSA muscle sympathetic nerve activity cubital vein and propagated to the pulmonary artery under NO ϭ nitric oxide fluoroscopic guidance. Arterial blood pressure was measured noninvasively (relative changes: Finapres; Ohmeda, Sweden; absolute baseline values: Dinamap; Critikon, Tampa, Florida) This study was approved by the local ethical committee. and a one-lead electrocardiogram was recorded and digitized Smokers and offspring of hypertensive parents were excluded for computation of heart rate (29). (25). None of the subjects was taking any medications. Experimental protocol. After recording stable baseline val- Microneurographic measurements. Microneurography ues for 15 min, phenylephrine was administered intravenously was performed as described previously (25–27). Subjects through the distal lumen of the Swan-Ganz catheter (or a were studied in standardized fashion, that is, at 2 PM in a peripheral intravenous line in three volunteers) at two dosages quiet, temperature-controlled room, after micturition to (75 and 100 ␮g/min, each over 3 min at 0.75 and 1 ml/min). avoid any increase of sympathetic nerve activity through Cardiac output was measured by thermodilution after each bladder distension (10). Multifiber recordings of MSA were dose of the drugs. During the last dose, LBNP was performed. obtained from the peroneal nerve. A reference electrode was G After reestablishing baseline conditions, N -monomethyl-L- inserted subcutaneously 1 to 2 cm from the recording arginine (L-NMMA) (Clinalfa, La¨ufelfingen, Switzerland) electrode. Signals were amplified, filtered (700 to was administered in two doses (0.3 and 1 mg/kg/min, each for 2,000 Hz), integrated (time constant, 0.1 s) and digitized 3 min at 1 to 3 ml/min) and cardiac output was determined using an analog-digital board (MIO-16L; National Instru- after each dose. Lower body negative pressure was performed ments, Austin, TX) and a modified commercial software again. The drug infusion order was not alternated because of (LabView; National Instruments). Data recorded on a the long elimination half life of L-NMMA. computer (Macintosh Power PC 7100; Apple) were ana- Statistical analysis. Results are presented as means Ϯ lyzed offline (MatLab; MathWorks, Natick, Massachu- SEM. Differences between drugs were evaluated using setts). The results were expressed as bursts per minute and paired Student t tests with Bonferroni adjusted p values for cumulative sum of the amplitude in volts per minute. multiple comparisons. The effects of LBNP were evaluated Lower body negative pressure. Lower body negative pres- by repeated-measures analysis of variance (StatView 4.5; sure (LBNP) decreases central venous pressure by restricting Abacus Concepts, Berkeley, California) (30). Statistical venous return of blood from the lower extremities to the significance was accepted at p Ͻ 0.05. heart (28). We used an air-tight plexiglass chamber in which the subjects were enclosed up to the waist. Negative RESULTS pressure was applied with a commercial vacuum cleaner (15 and 30 mm Hg, each for 2 min), monitored with a Hemodynamic effects. Changes in hemodynamic param- manometer connected to the interior of the chamber. eters and sympathetic nerve activity after administration of Hemodynamic measurements. Cardiac output (average of drugs are shown in Table 1. L-NMMA and phenylephrine three measurements) was determined by thermodilution (Vig- caused dose-related increases in arterial blood pressure. Table 1. Hemodynamic and Sympathetic Nervous Effects of L-NMMA and Phenylephrine L-NMMA Phenylephrine (mg/kg/min) (␮g/min) Baseline 0.3 1.0 75 100 SBP 134 Ϯ 7 152 Ϯ 5 150 Ϯ 3* 155 Ϯ 7 153 Ϯ 8* DBP 73 Ϯ 487Ϯ 585Ϯ 5† 88 Ϯ 690Ϯ 5† SVR 1,114 Ϯ 124 1,413 Ϯ 145* 1,973 Ϯ 203‡ 1,602 Ϯ 205† 1,743 Ϯ 209† HR 67 Ϯ 470Ϯ 663Ϯ 657Ϯ 5‡ 52 Ϯ 3‡ CI 3.5 Ϯ 0.3 3.1 Ϯ 0.2* 2.3 Ϯ 0.2§ 2.7 Ϯ 0.3† 2.6 Ϯ 0.2† SVI 53 Ϯ 648Ϯ 638Ϯ 5† 51 Ϯ 851Ϯ 4 CVP 4 Ϯ 0.7 3.6 Ϯ 0.4 4.3 Ϯ 0.05 6.3 Ϯ 0.5* 9.5 Ϯ 0.6† B/min 23.1 Ϯ 3.5 14 Ϯ 4.5* 18.6 Ϯ 5.5 12.8 Ϯ 5.8 17.6 Ϯ 5.7 B/100 HB 35.6 Ϯ 5.8 21.3 Ϯ 7.6 32.8 Ϯ 10.8 21.7 Ϯ 9.4 33.8 Ϯ 10 ACS 100 53 Ϯ 27 67 Ϯ 21 26 Ϯ 16* 78 Ϯ 17 Values represent means Ϯ SEM (n ϭ 9 for noninvasive, n ϭ 7 for invasive hemodynamic, and n ϭ 5 for microneurographic measurements).
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