Search citation statements
Paper Sections
Citation Types
Year Published
Publication Types
Relationship
Authors
Journals
The present study examined the time course of changes in baroreceptor reflex function by means of sigmoidal curvefitting analysis in conscious, unrestrained renovascular one-kidney, one clip (1K1C) rats at 1,3,7,15, 30, and 60 days after renal artery clipping. The reflex heart rate responses were elicited by alternate intravenous bolus injections of phenylephrine (change, +5 to +50 mm Hg) and sodium nitroprusside (change, -5 to -50 mm Hg). Atropine methylnitrate and atenolol were given to evaluate the responses mediated by the cardiac sympathetic or vagal component, respectively. The average baroreceptor reflex gain (sensitivity) decreased progressively (day 1, 3.35±0.3 beats per minute [bpm] per millimeter of mercury), reaching a maximal attenuation in the 30-day 1K1C group (1.83±0.5 bpm/mm Hg) compared with sham rats (approximately 4.60 bpm/mm Hg).The data showed a decreased vagal activity contributing to the attenuation of the baroreceptor gain only in the 30-day 1K1C group. In contrast, the cardiac sympathetic component of the baroreceptor reflex was significantly decreased in all 1K1C groups (from 2.10±0.4 to 0.50±0.2 bpm/mm Hg) compared with the respective sham groups (from 3.80±0.3 to 3.10±0.4 bpm/mm Hg). These results suggest that a reduced contribution of the sympathetic component to the baroreceptor heart rate reflex may be the main cause of the progressive attenuation of the baroreceptor reflex sensitivity observed in conscious 1K1C hypertensive rats. Key Words • hypertension, renovascular • pressoreceptors • blood pressure • heart rate T he moment-to-moment regulation of the function of the heart and blood vessels is achieved through reflex action that detects and corrects changes in arterial pressure. It is now widely acknowledged that the baroreceptor heart rate (HR) reflex activity is diminished in animals with experimentally induced hypertension 1 -4 and in patients with essential hypertension. 57 In hypertensive animals, studies using renovascular models 489 have contributed to the understanding of the baroreceptor reflex function in hypertensive diseases. 12 In a previous study, 13 it was observed that renovascular hypertension is accompanied by an exaggerated cardiac sympathetic tone and a transitory reduction of vagal tone. However, to our knowledge there are no long-term studies analyzing the changes in baroreceptor reflex function during the different phases of one-kidney, one clip (1K1C) hypertension in conscious rats and the relative contribution of the sympathetic and vagal components to the baroreceptor reflex gain.Several methods have been used to assess the baroreceptor HR reflex in normotensive and hypertensive animals and humans. However, the relation between arterial pressure and HR is described satisfactorily by a sigmoidal logistic function 1415 rather than a linear function, as has been commonly assumed. Head and McCarty,16 using the method of sigmoidal-fitting baroreceptor curve analysis, showed for the first time in conscious rats that the average gain can be estima...
The present study examined the time course of changes in baroreceptor reflex function by means of sigmoidal curvefitting analysis in conscious, unrestrained renovascular one-kidney, one clip (1K1C) rats at 1,3,7,15, 30, and 60 days after renal artery clipping. The reflex heart rate responses were elicited by alternate intravenous bolus injections of phenylephrine (change, +5 to +50 mm Hg) and sodium nitroprusside (change, -5 to -50 mm Hg). Atropine methylnitrate and atenolol were given to evaluate the responses mediated by the cardiac sympathetic or vagal component, respectively. The average baroreceptor reflex gain (sensitivity) decreased progressively (day 1, 3.35±0.3 beats per minute [bpm] per millimeter of mercury), reaching a maximal attenuation in the 30-day 1K1C group (1.83±0.5 bpm/mm Hg) compared with sham rats (approximately 4.60 bpm/mm Hg).The data showed a decreased vagal activity contributing to the attenuation of the baroreceptor gain only in the 30-day 1K1C group. In contrast, the cardiac sympathetic component of the baroreceptor reflex was significantly decreased in all 1K1C groups (from 2.10±0.4 to 0.50±0.2 bpm/mm Hg) compared with the respective sham groups (from 3.80±0.3 to 3.10±0.4 bpm/mm Hg). These results suggest that a reduced contribution of the sympathetic component to the baroreceptor heart rate reflex may be the main cause of the progressive attenuation of the baroreceptor reflex sensitivity observed in conscious 1K1C hypertensive rats. Key Words • hypertension, renovascular • pressoreceptors • blood pressure • heart rate T he moment-to-moment regulation of the function of the heart and blood vessels is achieved through reflex action that detects and corrects changes in arterial pressure. It is now widely acknowledged that the baroreceptor heart rate (HR) reflex activity is diminished in animals with experimentally induced hypertension 1 -4 and in patients with essential hypertension. 57 In hypertensive animals, studies using renovascular models 489 have contributed to the understanding of the baroreceptor reflex function in hypertensive diseases. 12 In a previous study, 13 it was observed that renovascular hypertension is accompanied by an exaggerated cardiac sympathetic tone and a transitory reduction of vagal tone. However, to our knowledge there are no long-term studies analyzing the changes in baroreceptor reflex function during the different phases of one-kidney, one clip (1K1C) hypertension in conscious rats and the relative contribution of the sympathetic and vagal components to the baroreceptor reflex gain.Several methods have been used to assess the baroreceptor HR reflex in normotensive and hypertensive animals and humans. However, the relation between arterial pressure and HR is described satisfactorily by a sigmoidal logistic function 1415 rather than a linear function, as has been commonly assumed. Head and McCarty,16 using the method of sigmoidal-fitting baroreceptor curve analysis, showed for the first time in conscious rats that the average gain can be estima...
This study examined the microcirculatory and renin-angiotensin system changes following the reversal of hypertension in reduced renal mass rats. Nine-week-old Sprague-Dawley reduced renal mass rats were placed on a low or high sodium diet for 4 or 8 weeks or a combination of 4 weeks of high sodium followed by 4 weeks of low sodium. Blood pressure was directly measured during the development of hypertension and its reversal. Plasma renin activity, angiotensin-converting enzyme activity, and angiotensin II concentrations were measured throughout the experiment. The cremaster and hindlimb muscles were removed, and microvascular density was determined by quantitative stereology. Four weeks of high sodium increased blood pressure (152+/-7 mm Hg) and reduced microvessel density (13.7%). Reduced renal mass hypertension was rapidly reversed after the rats were returned to a low sodium diet (124+/-7 mm Hg after 3 days), and microvascular density returned to control levels. After 4 weeks of high sodium, circulating plasma renin activity and angiotensin II fell by 94% and 82%, respectively. Plasma angiotensin-converting enzyme activity was increased after 2 weeks of high sodium but returned to control levels after 4 weeks of high sodium. This study demonstrates that microvascular density is reduced in reduced renal mass hypertensive rats following exposure to high sodium diet and this is associated with a fall in circulating plasma renin activity and angiotensin II levels. Microvascular density can return to normal levels after a reactivation of the circulating renin-angiotensin system. This study provides further evidence for the hypothesis that modulation of the renin-angiotensin system is important in the regulation of microvascular structure.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.