Inhibition of the baroreceptor heart rate reflex by angiotensin II in normal man

Mace, P. J. E.; Watson, R.; Skan, Wendy; Littler, W. A.

doi:10.1093/cvr/19.9.525

Cited by 37 publications

(18 citation statements)

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“…AT, receptors mediroduced by other vasoconstrictors ( 1,(3)(4)(5)(6)(7)(8). This modulaate many actions of Ang II, including vasoconstriction, but f the baroreflex control of heart rate has variously been there is little information concerning the physiological role of ited to a resetting of the cardiac baroreflex to a higher AT2 receptors.…”

Section: Resultsmentioning

confidence: 99%

“…However, Ang II also affects blood pressure indirectly by modulating the baroreceptor reflex control of heart rate (1, 2). As a result, the pressor response to the peptide is accompanied either by no decrease in heart rate, or a bradycardia that, for a given increase in blood pressure, is much smaller than that produced by other vasoconstrictors (1,(3)(4)(5)(6)(7)(8). This action of Ang II apparently serves to minimize the buffering action of the baroreceptor reflexes (9).…”

Section: Introductionmentioning

confidence: 99%

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Role of AT1 receptors in the resetting of the baroreflex control of heart rate by angiotensin II in the rabbit.

Wong¹,

Chou²,

Reid³

1993

J. Clin. Invest.

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Angiotensin II (Ang II) resets the baroreflex control of heart rate to a higher blood pressure. This action is apparently mediated via Ang II receptors in the area postrema, but it is not known if these are of the AT, or AT2 subtype. In the present study the effects of losartan, a selective AT, receptor antagonist, and PD 123319, a selective AT2 antagonist, on the cardiac baroreflex response to Ang II were investigated in conscious rabbits with chronically implanted arterial and venous catheters. Baroreflex curves were generated with intravenous infusions of phenylephrine and nitroprusside (2.6-25 $ug/kg per min) and analyzed using a four-parameter logistic model to yield their upper and lower plateaus, arterial pressure at the midpoint of the heart rate range (BP50), and slope coefficient.From these four parameters, the gain and range of the baroreflex were calculated. Background intravenous infusion of Ang II at 10 ng/kg per min increased mean arterial pressure by 17 mmHg but did not change heart rate. Ang II shifted the baroreflex curve to the right as indicated by an increase in BP5o from 70.9±2.0 to 89.3±2.7 mmHg (P < 0.05), but did not change baroreflex gain significantly. Ang II did not alter the upper plateau of the baroreflex, but decreased the lower plateau from 119.4±10.3 to 73.6±11.5 beats per minute (bpm) (P < 0.05), extending the heart rate range by 52.5 bpm. Pretreatment with losartan completely abolished the pressor and cardiac baroreflex responses to Ang II. In contrast, PD 123319 had no effect on these responses. Administration of losartan alone to block endogenous Ang II shifted the baroreflex curve to the left as indicated by a decrease in BP5o from 71.2±2.7 to 64.7±2.5 mmHg (P < 0.05). These results demonstrate that the resetting of the baroreflex control of heart rate by Ang II is mediated by AT1 receptors, and that basal levels of endogenous Ang II exert a tonic action on the cardiac baroreflex to increase the setpoint around which the baroreflex regulates heart rate. (J.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of AT1 receptors in the resetting of the baroreflex control of heart rate by angiotensin II in the rabbit.

Wong¹,

Chou²,

Reid³

1993

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…For example, obesity is associated with elevated activity of the renin-angiotensin-aldosterone system (15), and angiotensinogen is expressed more abundantly in abdominal visceral compared with subcutaneous fat (38). In addition, angiotensin II infusion reduces (27) and pharmacological reduction in angiotensin II concentrations improves cardiovagal baroreflex gain (28). Thus it is possible that elevated angiotensin II concentrations could contribute to the reduced cardiovagal baroreflex gain in individuals with elevated total body and abdominal visceral fat.…”

Section: Discussionmentioning

confidence: 99%

Reduced cardiovagal baroreflex gain in visceral obesity: implications for the metabolic syndrome

Beske¹,

Alvarez²,

Ballard³

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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The influence of excess total and abdominal adiposity on cardiovagal baroreflex gain remains unclear. We tested the hypotheses that cardiovagal baroreflex gain would be reduced in men with 1) higher [higher fat (HF), mass >20 kg, n = 11] compared with lower [lower fat (LF), mass <20 kg, n = 10] levels of total body and abdominal fat and 2) higher abdominal visceral fat (HAVF; n = 10) compared with total body weight- and subcutaneous fat-matched peers with lower abdominal visceral fat (LAVF; n = 7) levels. To accomplish this, we measured cardiovagal baroreflex gain (modified Oxford technique), body composition (dual energy X-ray absorptiometry), and abdominal visceral and subcutaneous fat (computed tomography) in sedentary men (age, 18–40 yr; body mass index, <34.9 kg/m2) across a wide range of adiposity. Cardiovagal baroreflex gain was significantly lower in HF compared with LF (14.3 ± 2.8 vs. 21.4 ± 2.8 ms/mmHg, respectively). In addition, cardiovagal baroreflex gain was lower in HAVF compared with LAVF (13.0 ± 2.0 vs. 21.4 ± 3.6 ms/mmHg, P< 0.05). Therefore, the results of the present study indicate that cardiovagal baroreflex gain is reduced in men with elevated total body and abdominal fat mass. The reduced cardiovagal baroreflex gain in these individuals appears to be linked to their higher level of abdominal visceral fat. Importantly, reduced cardiovagal baroreflex gain may contribute to the increased risk of cardiovascular disease observed in men with the metabolic syndrome.

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“…The absence of decrease in heart rate during Ang II infusion has been noticed in previous studies. 13,20 It is caused by a centrally mediated inhibitory effect of Ang II on the response to baroreflex activation and not to an Ang IImediated increase in sympathetic tone. 21,22 If this inhibitory effect on baroreflex activation had not occurred, the blood pressure dose-response curve to Ang II with the infusion rates applied would have been lower and likely comparable to that of norepinephrine.…”

Section: Van Der Linde Et Al Ldl Cholesterol and Ang II Sensitivitymentioning

confidence: 99%

Effect of Low-Density Lipoprotein Cholesterol on Angiotensin II Sensitivity

et al. 2006

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Abstract-Increased angiotensin II (Ang II) sensitivity predisposes to hypertension and plaque instability. Raised low-density lipoprotein cholesterol (LDL-c) may increase Ang II sensitivity, but evidence in humans for this effect of LDL-c is limited. In 28, healthy, nonsmoking subjects, aged 30Ϯ8 years, with familial hypercholesterolemia, we determined the difference in infusion rate of Ang II and norepinephrine required to increase systolic blood pressure by 20 mm Hg (Pd-20) after 4 weeks of placebo and fluvastatin 80 mg daily in a randomized, double-blind, placebocontrolled, crossover study. Before infusions were started, fasting blood samples were taken to measure lipids. After 4 weeks of placebo, the mean LDL-c concentration was 6.3Ϯ1.4 mmol/L. [2][3][4][5] Moreover, an AT 1 -receptor antagonist inhibited LDL oxidation and streak formation in hypercholesterolemic monkeys. 6 In vitro and animal data support the idea that raised LDL-c associates with increased AT 1 -receptor gene expression in vascular smooth muscle cells. 7,8 Evidence for a direct effect of raised LDL-c on the sensitivity to Ang II in humans is limited. In previous studies we analyzed older subjects with additional cardiovascular risk factors, like hypertension and the metabolic syndrome, that could explain the increased sensitivity to Ang II as well. 9 -11 Proof of a direct effect of LDL-c on Ang II sensitivity could have preventive implications. We hypothesized that raised LDL-c increases sensitivity to Ang II, and, conversely, lowering LDL-c levels should decrease this sensitivity.In the present randomized, double blind, placebo-controlled crossover study, the effect of fluvastatin on Ang II sensitivity was assessed in healthy, young subjects with familial hypercholesterolemia (FH). FH is a monogenetic disorder characterized by markedly raised LDL-c levels. Methods SubjectsWe used predefined criteria to recruit 30 healthy, young, nonsmoking FH subjects without signs of cardiovascular disease. The diagnosis FH was based on LDL-c above age-and sex-specific 95th percentiles during a cholesterol-lowering diet with triglycerides and HDL-cholesterol (HDL-c) within the normal limits and a molecular diagnosis or the presence of tendon xanthomas or hypercholesterolemia in Ն1 first-degree relative. 12 Exclusion criteria were secondary forms of hypercholesterolemia, hypertension, obesity, a history or signs of cardiovascular disease, smoking during the year before the trial, a history of alcohol or drug abuse, or noncompliance to treatment.To obtain normal reference values, we previously studied 10 untreated, healthy, normocholesterolemic volunteers (6 males) matched as group for age (28Ϯ11 years), blood pressure (123Ϯ10/75Ϯ10 mm Hg), and body mass (23.4Ϯ2.0 kg/m 2 ), who underwent an identical protocol as the subjects of the present study. 13 Their fasting values of LDL-c, high-density lipoprotein (HDL) cholesterol (HDL-c), triglycerides and glucose were, respectively, 2.2Ϯ0.7 mmol/L, 1.4Ϯ0.6 mmol/L, 0.9Ϯ 0.8 mmol/L, and 3.8Ϯ0.4 mmol/L. The study...

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Inhibition of the baroreceptor heart rate reflex by angiotensin II in normal man

Cited by 37 publications

References 0 publications

Role of AT1 receptors in the resetting of the baroreflex control of heart rate by angiotensin II in the rabbit.

Role of AT1 receptors in the resetting of the baroreflex control of heart rate by angiotensin II in the rabbit.

Reduced cardiovagal baroreflex gain in visceral obesity: implications for the metabolic syndrome

Effect of Low-Density Lipoprotein Cholesterol on Angiotensin II Sensitivity

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