Baroreflex control of heart rate in rats with heart failure after myocardial infarction: Effects of captopril

C. C. Deck, T. E. Raya, M. A. Gaballa, Steven Goldman

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Activation of the renin-angiotensin and sympathetic nervous systems in heart failure may result in altered baroreflex control of heart rate. To determine the specific effects of treatment with captopril on baroreceptor dysfunction in heart failure, baroreflex control of heart rate was measured in conscious rats with heart failure 6 weeks after ligation of the left coronary artery. Plasma norepinephrine was measured as a reflection of sympathetic nervous system activity. After bolus injections of phenylephrine (2-50 μg/kg) and nitroprusside (2-50 μg/kg), the arterial baroreflex was analyzed by fitting percentage of mean arterial pressure changes and heart rate changes to a logistic regression function. There were no differences in baroreflex function between normal and sham-operated rats. Plasma norepinephrine was increased (P < .05) in the heart-failure rats and did not change with captopril treatment. In untreated rats, heart failure increased (P < .05) the centering point by 900%, threshold by 243% and saturation by 89%, whereas decreasing (P < .05) the operational point by 73%. There was a decrease (P < .05) in the nitroprusside-related gain and an increase (P < .05) in phenylephrine-related gain, but the overall baroreflex gain was not changed. In heart-failure rats, captopril increased (P < .05) threshold, saturation and centering point and decreased (P < .05) operational point and nitroprusside- and phenylephrine-related gain abnormalities. The increase in operational point and decreases in threshold, saturation, centering point and phenylephrine-related gain were the results of a specific interactive effect of captopril in heart failure (P = .0033, .0176, .0509, .0217 and .0567, respectively). Thus, in rats with heart failure baroreflex control of heart rate was altered, without a change in overall baroreflex gain. Treatment with captopril improved baroreflex control of heart rate. The effects of captopril were independent of changes in plasma norepinephrine.

Original languageEnglish (US)
Pages (from-to)1424-1431
Number of pages8
JournalJournal of Pharmacology and Experimental Therapeutics
Volume263
Issue number3
StatePublished - 1992
Externally publishedYes

Fingerprint

Baroreflex
Captopril
Heart Failure
Heart Rate
Myocardial Infarction
Phenylephrine
Nitroprusside
Norepinephrine
Sympathetic Nervous System
Pressoreceptors
Angiotensins
Renin
Ligation
Coronary Vessels
Arterial Pressure
Therapeutics
Logistic Models
Injections

ASJC Scopus subject areas

  • Pharmacology

Cite this

Baroreflex control of heart rate in rats with heart failure after myocardial infarction : Effects of captopril. / Deck, C. C.; Raya, T. E.; Gaballa, M. A.; Goldman, Steven.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 263, No. 3, 1992, p. 1424-1431.

Research output: Contribution to journalArticle

@article{9866becab0e341ad8449202d8fd5d38d,
title = "Baroreflex control of heart rate in rats with heart failure after myocardial infarction: Effects of captopril",
abstract = "Activation of the renin-angiotensin and sympathetic nervous systems in heart failure may result in altered baroreflex control of heart rate. To determine the specific effects of treatment with captopril on baroreceptor dysfunction in heart failure, baroreflex control of heart rate was measured in conscious rats with heart failure 6 weeks after ligation of the left coronary artery. Plasma norepinephrine was measured as a reflection of sympathetic nervous system activity. After bolus injections of phenylephrine (2-50 μg/kg) and nitroprusside (2-50 μg/kg), the arterial baroreflex was analyzed by fitting percentage of mean arterial pressure changes and heart rate changes to a logistic regression function. There were no differences in baroreflex function between normal and sham-operated rats. Plasma norepinephrine was increased (P < .05) in the heart-failure rats and did not change with captopril treatment. In untreated rats, heart failure increased (P < .05) the centering point by 900{\%}, threshold by 243{\%} and saturation by 89{\%}, whereas decreasing (P < .05) the operational point by 73{\%}. There was a decrease (P < .05) in the nitroprusside-related gain and an increase (P < .05) in phenylephrine-related gain, but the overall baroreflex gain was not changed. In heart-failure rats, captopril increased (P < .05) threshold, saturation and centering point and decreased (P < .05) operational point and nitroprusside- and phenylephrine-related gain abnormalities. The increase in operational point and decreases in threshold, saturation, centering point and phenylephrine-related gain were the results of a specific interactive effect of captopril in heart failure (P = .0033, .0176, .0509, .0217 and .0567, respectively). Thus, in rats with heart failure baroreflex control of heart rate was altered, without a change in overall baroreflex gain. Treatment with captopril improved baroreflex control of heart rate. The effects of captopril were independent of changes in plasma norepinephrine.",
author = "Deck, {C. C.} and Raya, {T. E.} and Gaballa, {M. A.} and Steven Goldman",
year = "1992",
language = "English (US)",
volume = "263",
pages = "1424--1431",
journal = "Journal of Pharmacology and Experimental Therapeutics",
issn = "0022-3565",
publisher = "American Society for Pharmacology and Experimental Therapeutics",
number = "3",

}

TY - JOUR

T1 - Baroreflex control of heart rate in rats with heart failure after myocardial infarction

T2 - Effects of captopril

AU - Deck, C. C.

AU - Raya, T. E.

AU - Gaballa, M. A.

AU - Goldman, Steven

PY - 1992

Y1 - 1992

N2 - Activation of the renin-angiotensin and sympathetic nervous systems in heart failure may result in altered baroreflex control of heart rate. To determine the specific effects of treatment with captopril on baroreceptor dysfunction in heart failure, baroreflex control of heart rate was measured in conscious rats with heart failure 6 weeks after ligation of the left coronary artery. Plasma norepinephrine was measured as a reflection of sympathetic nervous system activity. After bolus injections of phenylephrine (2-50 μg/kg) and nitroprusside (2-50 μg/kg), the arterial baroreflex was analyzed by fitting percentage of mean arterial pressure changes and heart rate changes to a logistic regression function. There were no differences in baroreflex function between normal and sham-operated rats. Plasma norepinephrine was increased (P < .05) in the heart-failure rats and did not change with captopril treatment. In untreated rats, heart failure increased (P < .05) the centering point by 900%, threshold by 243% and saturation by 89%, whereas decreasing (P < .05) the operational point by 73%. There was a decrease (P < .05) in the nitroprusside-related gain and an increase (P < .05) in phenylephrine-related gain, but the overall baroreflex gain was not changed. In heart-failure rats, captopril increased (P < .05) threshold, saturation and centering point and decreased (P < .05) operational point and nitroprusside- and phenylephrine-related gain abnormalities. The increase in operational point and decreases in threshold, saturation, centering point and phenylephrine-related gain were the results of a specific interactive effect of captopril in heart failure (P = .0033, .0176, .0509, .0217 and .0567, respectively). Thus, in rats with heart failure baroreflex control of heart rate was altered, without a change in overall baroreflex gain. Treatment with captopril improved baroreflex control of heart rate. The effects of captopril were independent of changes in plasma norepinephrine.

AB - Activation of the renin-angiotensin and sympathetic nervous systems in heart failure may result in altered baroreflex control of heart rate. To determine the specific effects of treatment with captopril on baroreceptor dysfunction in heart failure, baroreflex control of heart rate was measured in conscious rats with heart failure 6 weeks after ligation of the left coronary artery. Plasma norepinephrine was measured as a reflection of sympathetic nervous system activity. After bolus injections of phenylephrine (2-50 μg/kg) and nitroprusside (2-50 μg/kg), the arterial baroreflex was analyzed by fitting percentage of mean arterial pressure changes and heart rate changes to a logistic regression function. There were no differences in baroreflex function between normal and sham-operated rats. Plasma norepinephrine was increased (P < .05) in the heart-failure rats and did not change with captopril treatment. In untreated rats, heart failure increased (P < .05) the centering point by 900%, threshold by 243% and saturation by 89%, whereas decreasing (P < .05) the operational point by 73%. There was a decrease (P < .05) in the nitroprusside-related gain and an increase (P < .05) in phenylephrine-related gain, but the overall baroreflex gain was not changed. In heart-failure rats, captopril increased (P < .05) threshold, saturation and centering point and decreased (P < .05) operational point and nitroprusside- and phenylephrine-related gain abnormalities. The increase in operational point and decreases in threshold, saturation, centering point and phenylephrine-related gain were the results of a specific interactive effect of captopril in heart failure (P = .0033, .0176, .0509, .0217 and .0567, respectively). Thus, in rats with heart failure baroreflex control of heart rate was altered, without a change in overall baroreflex gain. Treatment with captopril improved baroreflex control of heart rate. The effects of captopril were independent of changes in plasma norepinephrine.

UR - http://www.scopus.com/inward/record.url?scp=0026998379&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026998379&partnerID=8YFLogxK

M3 - Article

C2 - 1469643

AN - SCOPUS:0026998379

VL - 263

SP - 1424

EP - 1431

JO - Journal of Pharmacology and Experimental Therapeutics

JF - Journal of Pharmacology and Experimental Therapeutics

SN - 0022-3565

IS - 3

ER -