ANG II receptor blockade and arterial baroreflex regulation of renal nerve activity in cardiac failure

G. F. DiBona, S. Y. Jones, Virginia Brooks

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148 Citations (Scopus)

Abstract

In cardiac failure, efferent renal sympathetic nerve activity (ERSNA) and the activity of the renin-angiotensin system are increased, and arterial baroreflex regulation of ERSNA is attenuated. We examined the effect of intravenous and intracerebroventricular angiotensin II AT1 receptor blockade with losartan on the arterial baroreflex regulation of ERSNA in conscious control (C) and congestive heart failure (CHF) rats. Intravenous losartan (10 mg/kg, 21.7 μmol/kg) decreased arterial pressure more in CHF than in C rats (-28 ± 3 vs. -20 ± 3 mmHg, P <0.05). After restoration of arterial pressure to the prelosartan value with methoxamine infusion, ERSNA was decreased more in CHF than in C rats (-23 ± 4 vs. -1 ± 2%, P <0.05). Maximal gain of arterial baroreflex control of ERSNA (G(max)) was lower in CHF compared with C rats (-1.94 ± 0.10 vs. -3.78 ± 0.21%/mmHg, P <0.05). Intravenous losartan increased G(max) in CHF (to -3.01 ± 0.14%/mmHg, P <0.05) but not in C rats (to -3.56 ± 0.19%/mmHg). Intracerebroventricular losartan (4.61 μg, 10 nmol) did not affect arterial pressure but decreased ERSNA more in CHF than in C rats (-13 ± 2 vs. -8 ± 3%, P <0.05). Like intravenous losartan, intracerebroventricular losartan increased G(max) in CHF (from -2.11 ± 0.18 to -3.21 ± 0.30%/mmHg, P <0.05) but not in C rats (from -3.98 ± 0.25 to -3.84 ± 0.22%/mmHg). These results suggest that increased activity of the renin-angiotensin system contributes to the increase in ERSNA and its abnormal arterial baroreflex regulation in cardiac failure.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume269
Issue number5 38-5
StatePublished - 1995
Externally publishedYes

Fingerprint

Baroreflex
heart failure
nerve tissue
Losartan
Heart Failure
kidneys
Kidney
receptors
rats
renin-angiotensin system
Arterial Pressure
Renin-Angiotensin System
Methoxamine
Angiotensin Type 1 Receptor
Angiotensin Receptors
angiotensin II

Keywords

  • losartan
  • renal sympathetic nerve activity

ASJC Scopus subject areas

  • Physiology
  • Agricultural and Biological Sciences(all)

Cite this

@article{6e1868ac05ae4b4995797a782fb092bf,
title = "ANG II receptor blockade and arterial baroreflex regulation of renal nerve activity in cardiac failure",
abstract = "In cardiac failure, efferent renal sympathetic nerve activity (ERSNA) and the activity of the renin-angiotensin system are increased, and arterial baroreflex regulation of ERSNA is attenuated. We examined the effect of intravenous and intracerebroventricular angiotensin II AT1 receptor blockade with losartan on the arterial baroreflex regulation of ERSNA in conscious control (C) and congestive heart failure (CHF) rats. Intravenous losartan (10 mg/kg, 21.7 μmol/kg) decreased arterial pressure more in CHF than in C rats (-28 ± 3 vs. -20 ± 3 mmHg, P <0.05). After restoration of arterial pressure to the prelosartan value with methoxamine infusion, ERSNA was decreased more in CHF than in C rats (-23 ± 4 vs. -1 ± 2{\%}, P <0.05). Maximal gain of arterial baroreflex control of ERSNA (G(max)) was lower in CHF compared with C rats (-1.94 ± 0.10 vs. -3.78 ± 0.21{\%}/mmHg, P <0.05). Intravenous losartan increased G(max) in CHF (to -3.01 ± 0.14{\%}/mmHg, P <0.05) but not in C rats (to -3.56 ± 0.19{\%}/mmHg). Intracerebroventricular losartan (4.61 μg, 10 nmol) did not affect arterial pressure but decreased ERSNA more in CHF than in C rats (-13 ± 2 vs. -8 ± 3{\%}, P <0.05). Like intravenous losartan, intracerebroventricular losartan increased G(max) in CHF (from -2.11 ± 0.18 to -3.21 ± 0.30{\%}/mmHg, P <0.05) but not in C rats (from -3.98 ± 0.25 to -3.84 ± 0.22{\%}/mmHg). These results suggest that increased activity of the renin-angiotensin system contributes to the increase in ERSNA and its abnormal arterial baroreflex regulation in cardiac failure.",
keywords = "losartan, renal sympathetic nerve activity",
author = "DiBona, {G. F.} and Jones, {S. Y.} and Virginia Brooks",
year = "1995",
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journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
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AU - Jones, S. Y.

AU - Brooks, Virginia

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N2 - In cardiac failure, efferent renal sympathetic nerve activity (ERSNA) and the activity of the renin-angiotensin system are increased, and arterial baroreflex regulation of ERSNA is attenuated. We examined the effect of intravenous and intracerebroventricular angiotensin II AT1 receptor blockade with losartan on the arterial baroreflex regulation of ERSNA in conscious control (C) and congestive heart failure (CHF) rats. Intravenous losartan (10 mg/kg, 21.7 μmol/kg) decreased arterial pressure more in CHF than in C rats (-28 ± 3 vs. -20 ± 3 mmHg, P <0.05). After restoration of arterial pressure to the prelosartan value with methoxamine infusion, ERSNA was decreased more in CHF than in C rats (-23 ± 4 vs. -1 ± 2%, P <0.05). Maximal gain of arterial baroreflex control of ERSNA (G(max)) was lower in CHF compared with C rats (-1.94 ± 0.10 vs. -3.78 ± 0.21%/mmHg, P <0.05). Intravenous losartan increased G(max) in CHF (to -3.01 ± 0.14%/mmHg, P <0.05) but not in C rats (to -3.56 ± 0.19%/mmHg). Intracerebroventricular losartan (4.61 μg, 10 nmol) did not affect arterial pressure but decreased ERSNA more in CHF than in C rats (-13 ± 2 vs. -8 ± 3%, P <0.05). Like intravenous losartan, intracerebroventricular losartan increased G(max) in CHF (from -2.11 ± 0.18 to -3.21 ± 0.30%/mmHg, P <0.05) but not in C rats (from -3.98 ± 0.25 to -3.84 ± 0.22%/mmHg). These results suggest that increased activity of the renin-angiotensin system contributes to the increase in ERSNA and its abnormal arterial baroreflex regulation in cardiac failure.

AB - In cardiac failure, efferent renal sympathetic nerve activity (ERSNA) and the activity of the renin-angiotensin system are increased, and arterial baroreflex regulation of ERSNA is attenuated. We examined the effect of intravenous and intracerebroventricular angiotensin II AT1 receptor blockade with losartan on the arterial baroreflex regulation of ERSNA in conscious control (C) and congestive heart failure (CHF) rats. Intravenous losartan (10 mg/kg, 21.7 μmol/kg) decreased arterial pressure more in CHF than in C rats (-28 ± 3 vs. -20 ± 3 mmHg, P <0.05). After restoration of arterial pressure to the prelosartan value with methoxamine infusion, ERSNA was decreased more in CHF than in C rats (-23 ± 4 vs. -1 ± 2%, P <0.05). Maximal gain of arterial baroreflex control of ERSNA (G(max)) was lower in CHF compared with C rats (-1.94 ± 0.10 vs. -3.78 ± 0.21%/mmHg, P <0.05). Intravenous losartan increased G(max) in CHF (to -3.01 ± 0.14%/mmHg, P <0.05) but not in C rats (to -3.56 ± 0.19%/mmHg). Intracerebroventricular losartan (4.61 μg, 10 nmol) did not affect arterial pressure but decreased ERSNA more in CHF than in C rats (-13 ± 2 vs. -8 ± 3%, P <0.05). Like intravenous losartan, intracerebroventricular losartan increased G(max) in CHF (from -2.11 ± 0.18 to -3.21 ± 0.30%/mmHg, P <0.05) but not in C rats (from -3.98 ± 0.25 to -3.84 ± 0.22%/mmHg). These results suggest that increased activity of the renin-angiotensin system contributes to the increase in ERSNA and its abnormal arterial baroreflex regulation in cardiac failure.

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