The Role of the Baroreceptor Reflex in the Cardiovascular Effects of Propranolol in the Conscious Spontaneously Hypertensive Rat

1979 ◽  
Vol 56 (2) ◽  
pp. 163-167 ◽  
Author(s):  
H. A. J. Struyker-Boudier ◽  
J. F. Smits ◽  
H. Van Essen

1. The role of baroreceptors in the cardiovascular mechanism of action of dl-propranolol has been studied by comparing the acute effects of subcutaneous injection of 1 and 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) of this drug in conscious baroreceptor-denervated spontaneously hypertensive (SH) rats with those in sham-operated control SH rats. 2. At 5 mg/kg (16·5 × 10−6 mol/kg) propranolol caused a small, but significant, increase in blood pressure in sham-operated SH rats, whereas both after 1 and 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) immediate hypotension was observed in baroreceptor-denervated animals. 3. Heart rate dropped rapidly after injection of 1 or 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) propranolol both in the baroreceptor-denervated and sham-operated SH rats. Bradycardia was significantly larger in the baroreceptor-denervated animals after an injection of 5 mg/kg (16·5 × 10−6 mol/kg). 4. It is concluded that the lack of an early hypotensive effect of propranolol in intact animals is caused by an increased baroreceptor reflex activity as a consequence of the fall in cardiac output.

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.


2002 ◽  
Vol 10 (3) ◽  
pp. 199-210 ◽  
Author(s):  
Adamu Alemayehu ◽  
Laura Breen ◽  
Drahomira Krenova ◽  
Morton P. Printz

Evidence exists implying multiple blood pressure quantitative trait loci (QTL) on rat chromosome 2. To examine this possibility, four congenic strains and nine substrains were developed with varying size chromosome segments introgressed from the spontaneously hypertensive rat (SHR/lj) and normotensive Wistar-Kyoto rat (WKY/lj) onto the reciprocal genetic background. Cardiovascular phenotyping was conducted with telemetry over extended periods during standard salt (0.7%) and high-salt (8%) diets. Our results are consistent with at least three independent pressor QTL: transfer of SHR/lj alleles to WKY/lj reveals pressor QTL within D2Rat21-D2Rat27 and D2Mgh10-D2Rat62, whereas transfer of WKY/lj D2Rat161-D2Mit8 to SHR/lj reveals a depressor locus. Our results also suggest a depressor QTL in SHR/lj located within D2Rat161-D2Mgh10. Introgressed WKY/lj segments also reveal a heart rate QTL within D2Rat40-D2Rat50 which abolished salt-induced bradycardia, dependent upon adjoining SHR/lj alleles. This study confirms the presence of multiple blood pressure QTL on chromosome 2. Taken together with our other studies, we conclude that rat chromosome 2 is rich in alleles for cardiovascular and behavioral traits and for coordinated coupling between behavior and cardiovascular responses.


2012 ◽  
Vol 2 (1) ◽  
pp. 4 ◽  
Author(s):  
Elisabeth Ruiz Padial ◽  
Nieves Torres López ◽  
Javier Luna Bujaldón ◽  
Isabel Espadas Villanueva ◽  
Gustavo Reyes del Paso

The present study evaluates the cardiovascular effects of reflexology in a healthy sample. Forty-one participants were randomly assigned to one of three experimental groups: reflexology (n=15), non-professional foot massage (n=14), and a waiting time control group (n=12). Dependent variables were systolic, diastolic and mean blood pressure, inter-beat interval, heart rate variability and baroreceptor reflex sensitivity measured pre- and post- interventions. The study was performed during three 40-min sessions separated by weekly intervals. Results show that the three manipulations produce similar increases in inter-beat interval, heart rate variability and baroreceptor reflex sensitivity. Reflexology specifically produces an increase in blood pressure, which increases gradually over the three sessions. The parallel increase in heart rate variability and baroreceptor reflex sensitivity together with the increase in blood pressure suggest that reflexology is associated with a co-activation of both sympathetic and parasympathetic branches of the Autonomic Nervous System. These changes could be helpful in optimizing homeostatic activity, promoting the healing process and increasing the human organism’s capacity to respond adaptively to internal and external challenges. Finally, the observed physiological changes in the waiting-time control group shows the relevance of habituation processes and suggests the need for addition of waiting-time control groups in future studies.


1981 ◽  
Vol 240 (3) ◽  
pp. H421-H429 ◽  
Author(s):  
G. Baccelli ◽  
R. Albertini ◽  
A. Del Bo ◽  
G. Mancia ◽  
A. Zanchetti

To evaluate whether sinoaortic afferents contribute to the hemodynamic pattern of fighting, cardiovascular changes associated with fighting were studied in cats before and after sinoaortic denervation. Sinoaortic denervation exaggerates the decrease in heart rate, cardiac output, and arterial pressure during immobile confrontation (hissing, staring but no movement). During nonsupportive fighting (fighting with forelimbs while lying on one side) and supportive fighting ( fighting while standing on four feet) sinoaortic denervation reduces the increase in heart rate and cardiac output, minimizes the mesenteric vasoconstriction, induces a fall in arterial blood pressure, but does not affect iliac vasoconstriction or vasodilatation. The hemodynamic pattern of fighting is similarly changed by temporary inactivation of carotid sinus baroreflexes by common carotid occlusion as by chronic section of sinoaortic nerves. It is concluded that sinoaortic reflexes play an important role in the cardiovascular patterns accompanying natural fighting. They favor cardiac action and allow a marked visceral vasoconstriction to occur, thus minimizing or preventing a fall in blood pressure during emotional behavior.


2015 ◽  
Vol 308 (8) ◽  
pp. E641-E649 ◽  
Author(s):  
Ali Asmar ◽  
Lene Simonsen ◽  
Meena Asmar ◽  
Sten Madsbad ◽  
Jens J. Holst ◽  
...  

The present experiments were performed to elucidate the acute effects of intravenous infusion of glucagon-like peptide (GLP)-1 on central and renal hemodynamics in healthy men. Seven healthy middle-aged men were examined on two different occasions in random order. During a 3-h infusion of either GLP-1 (1.5 pmol·kg−1·min−1) or saline, cardiac output was estimated noninvasively, and intraarterial blood pressure and heart rate were measured continuously. Renal plasma flow, glomerular filtration rate, and uptake/release of hormones and ions were measured by Fick's Principle after catheterization of a renal vein. Subjects remained supine during the experiments. During GLP-1 infusion, both systolic blood pressure and arterial pulse pressure increased by 5 ± 1 mmHg ( P = 0.015 and P = 0.002, respectively). Heart rate increased by 5 ± 1 beats/min ( P = 0.005), and cardiac output increased by 18% ( P = 0.016). Renal plasma flow and glomerular filtration rate as well as the clearance of Na+ and Li+ were not affected by GLP-1. However, plasma renin activity decreased ( P = 0.037), whereas plasma levels of atrial natriuretic peptide were unaffected. Renal extraction of intact GLP-1 was 43% ( P < 0.001), whereas 60% of the primary metabolite GLP-1 9-36amide was extracted ( P = 0.017). In humans, an acute intravenous administration of GLP-1 leads to increased cardiac output due to a simultaneous increase in stroke volume and heart rate, whereas no effect on renal hemodynamics could be demonstrated despite significant extraction of both the intact hormone and its primary metabolite.


1999 ◽  
Vol 277 (3) ◽  
pp. H1200-H1206 ◽  
Author(s):  
Zheng-Zheng Shan ◽  
Sheng-Ming Dai ◽  
Ding-Feng Su

The purpose of this study was to further illustrate the relationship between baroreceptor reflex sensitivity (BRS) and hypertensive end-organ damage (EOD) and to test the hypothesis that impairment of BRS aggravates EOD in hypertension. We studied baroreflex-mediated changes in heart rate [expressed as baroreceptor sensitivity to heart rate control (BRSHR)] and blood pressure [expressed as baroreceptor sensitivity to blood pressure control (BRSBP)] in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) that were used as controls, both at the age of 50–52 wk. Rats were also instrumented to record BP, HR, and BP variability (BPV) in the conscious, unrestrained state. In SHR compared with WKY, BP and BPV were significantly increased, whereas BRSHR and BRSBP were significantly decreased. SHR had remarkable EOD when compared with WKY (EOD score: 6.3 ± 2.5 vs. 2.9 ± 0.8, P < 0.01). Univariate regressive analysis demonstrated that EOD score was increased with BP and BPV and decreased with BRS. In multivariate analysis, EOD score was predicted by greater systolic BP and lower BRS and HR variability. These results indicate that BRS is negatively related to BPV and EOD score, and impaired BRS might be one of the major causes for hypertensive EOD.


1997 ◽  
Vol 273 (6) ◽  
pp. H2627-H2631 ◽  
Author(s):  
Acácio Salvador Véras-Silva ◽  
Katt Coelho Mattos ◽  
Nilo Sérgio Gava ◽  
Patricia Chakur Brum ◽  
Carlos Eduardo Negrão ◽  
...  

The decrease in cardiac sympathetic tone and heart rate after low-intensity exercise training may have hemodynamic consequences in spontaneously hypertensive rats (SHR). The effects of exercise training of low and high intensity on resting blood pressure, cardiac output, and total peripheral resistance were studied in sedentary ( n = 17), low- ( n = 17), and high-intensity exercise-trained ( n = 17) SHR. Exercise training was performed on a treadmill for 60 min, 5 times per week for 18 weeks, at 55% or 85% maximum oxygen uptake. Blood pressure was evaluated by a cannula inserted into the carotid artery, and cardiac output was evaluated by a microprobe placed around the ascending aorta. Low-intensity exercise-trained rats had a significantly lower mean blood pressure than sedentary and high-intensity exercise-trained rats (160 ± 4 vs. 175 ± 3 and 173 ± 2 mmHg, respectively). Cardiac index (20 ± 1 vs. 24 ± 1 and 24 ± 1 ml ⋅ min−1 ⋅ 100 g−1, respectively) and heart rate (332 ± 6 vs. 372 ± 14 and 345 ± 9 beats/min, respectively) were significantly lower in low-intensity exercise-trained rats than in sedentary and high-intensity exercise-trained rats. No significant difference was observed in stroke volume index and total peripheral resistance index in all groups studied. In conclusion, low-intensity, but not high-intensity, exercise training decreases heart rate and cardiac output and, consequently, attenuates hypertension in SHR.


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