Bradykinin in reflex cardiovascular responses to static muscular contraction

Charles L Stebbins, J. C. Longhurst

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3-4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000-30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500-750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 ± 3 to 39 ± 7 mmHg and 1,405 ± 362 to 2,285 ± 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 ± 4 to 9 ± 2 mmHg) and maximal dP/dt (1,284 ± 261 to 469 ± 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 ± 12 to 24 ± 11 mmHg, maximal dP/dt from 1,618 ± 652 to 957 ± 392 mmHg/s, and heart rate from 12 ± 2 to 7 ± 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.

Original languageEnglish (US)
Pages (from-to)271-279
Number of pages9
JournalJournal of Applied Physiology
Volume61
Issue number1
StatePublished - 1986

Fingerprint

Bradykinin
Muscle Contraction
Reflex
Arterial Pressure
Aprotinin
Carboxypeptidase B
Captopril
Hindlimb
Kallikreins
Spinal Nerve Roots
Peptidyl-Dipeptidase A
Electric Stimulation
Cats
Heart Rate
Hemodynamics
Pressure
Muscles
Injections
Enzymes

ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Bradykinin in reflex cardiovascular responses to static muscular contraction. / Stebbins, Charles L; Longhurst, J. C.

In: Journal of Applied Physiology, Vol. 61, No. 1, 1986, p. 271-279.

Research output: Contribution to journalArticle

Stebbins, Charles L ; Longhurst, J. C. / Bradykinin in reflex cardiovascular responses to static muscular contraction. In: Journal of Applied Physiology. 1986 ; Vol. 61, No. 1. pp. 271-279.
@article{e1a42b59bf3e47d58c98562e052ec8e3,
title = "Bradykinin in reflex cardiovascular responses to static muscular contraction",
abstract = "We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3-4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000-30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500-750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 ± 3 to 39 ± 7 mmHg and 1,405 ± 362 to 2,285 ± 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 ± 4 to 9 ± 2 mmHg) and maximal dP/dt (1,284 ± 261 to 469 ± 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 ± 12 to 24 ± 11 mmHg, maximal dP/dt from 1,618 ± 652 to 957 ± 392 mmHg/s, and heart rate from 12 ± 2 to 7 ± 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.",
author = "Stebbins, {Charles L} and Longhurst, {J. C.}",
year = "1986",
language = "English (US)",
volume = "61",
pages = "271--279",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "1",

}

TY - JOUR

T1 - Bradykinin in reflex cardiovascular responses to static muscular contraction

AU - Stebbins, Charles L

AU - Longhurst, J. C.

PY - 1986

Y1 - 1986

N2 - We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3-4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000-30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500-750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 ± 3 to 39 ± 7 mmHg and 1,405 ± 362 to 2,285 ± 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 ± 4 to 9 ± 2 mmHg) and maximal dP/dt (1,284 ± 261 to 469 ± 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 ± 12 to 24 ± 11 mmHg, maximal dP/dt from 1,618 ± 652 to 957 ± 392 mmHg/s, and heart rate from 12 ± 2 to 7 ± 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.

AB - We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3-4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000-30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500-750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 ± 3 to 39 ± 7 mmHg and 1,405 ± 362 to 2,285 ± 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 ± 4 to 9 ± 2 mmHg) and maximal dP/dt (1,284 ± 261 to 469 ± 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 ± 12 to 24 ± 11 mmHg, maximal dP/dt from 1,618 ± 652 to 957 ± 392 mmHg/s, and heart rate from 12 ± 2 to 7 ± 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.

UR - http://www.scopus.com/inward/record.url?scp=0022444249&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022444249&partnerID=8YFLogxK

M3 - Article

VL - 61

SP - 271

EP - 279

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 1

ER -