Effects of a kinin antagonist on mean blood pressure

Luis F. Carbonell, Oscar A. Carretero, Paolo Madeddu, A. Guillermo Scicli

Research output: Contribution to journalArticle

Abstract

Administration of high doses of a kinin antagonist produces an increase in blood pressure. Thus, endogenous klnins may be involved in the regulation of blood pressure. Kinins can induce the release of vasoactive substances such as catecholamines, renin, vasopressin, histamine, and prostaglandins. To determine whether the blood pressure changes induced by high doses of kinin antagonist are due to agonistic activity mediated by these vasoactive substances, we studied the effect on blood pressure of a kinin antagonist (DArg0-Hyp3-Thi5,8-DPtie7-bradyklnln) administered to control, nephrectomized, and adrenalectomized rats, and to rats treated with vasopressin V1-receptor antagonist, ganglionic and α and β-adrenergic receptor blockers (either separately or combined), H1- and H2-receptor blockers, and indomethacin, a prostaglandin synthesis inhibitor. Blood pressure changes were monitored on awake, restrained rats. In the control rat, the kinin antagonist injected as a bolus (4 mg/kg) into the ascending aorta produced a transient biphasic blood pressure response, first a pressor effect (ΔBP=7 ± 1 mm Hg; p <0.05), then a depressor effect (ΔBP=-20 ± 6 mm Hg; p <0.05). The pressor response to the kinin antagonist was not affected by any of the treatments; however, the depressor effect of the kinin antagonist appeared to be caused by the release of vasodilator prostanoids from the kidney, since it was not observed in the nephrectomized rats or in those treated with indomethacin. The pressor effect induced by the kinin antagonist suggests that kinins may contribute to the regulation of blood pressure.

Original languageEnglish
Pages (from-to)I-84-I-88
JournalHypertension
Volume11
Issue number2
Publication statusPublished - 1988

Fingerprint

Kinins
Blood Pressure
Indomethacin
Prostaglandins
Prostaglandin Antagonists
Histamine H1 Receptors
Vasopressin Receptors
Histamine H2 Receptors
Adrenergic Antagonists
Vasopressins
Vasodilator Agents
Renin
Adrenergic Receptors
Histamine
Catecholamines
Aorta
Kidney

Keywords

  • Blood pressure regulation
  • Bradykinin
  • Depressor
  • Kinin antagonist
  • Pressor

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Carbonell, L. F., Carretero, O. A., Madeddu, P., & Scicli, A. G. (1988). Effects of a kinin antagonist on mean blood pressure. Hypertension, 11(2), I-84-I-88.

Effects of a kinin antagonist on mean blood pressure. / Carbonell, Luis F.; Carretero, Oscar A.; Madeddu, Paolo; Scicli, A. Guillermo.

In: Hypertension, Vol. 11, No. 2, 1988, p. I-84-I-88.

Research output: Contribution to journalArticle

Carbonell, LF, Carretero, OA, Madeddu, P & Scicli, AG 1988, 'Effects of a kinin antagonist on mean blood pressure', Hypertension, vol. 11, no. 2, pp. I-84-I-88.
Carbonell LF, Carretero OA, Madeddu P, Scicli AG. Effects of a kinin antagonist on mean blood pressure. Hypertension. 1988;11(2):I-84-I-88.
Carbonell, Luis F. ; Carretero, Oscar A. ; Madeddu, Paolo ; Scicli, A. Guillermo. / Effects of a kinin antagonist on mean blood pressure. In: Hypertension. 1988 ; Vol. 11, No. 2. pp. I-84-I-88.
@article{9eefe08d914540448316f1a1640932fe,
title = "Effects of a kinin antagonist on mean blood pressure",
abstract = "Administration of high doses of a kinin antagonist produces an increase in blood pressure. Thus, endogenous klnins may be involved in the regulation of blood pressure. Kinins can induce the release of vasoactive substances such as catecholamines, renin, vasopressin, histamine, and prostaglandins. To determine whether the blood pressure changes induced by high doses of kinin antagonist are due to agonistic activity mediated by these vasoactive substances, we studied the effect on blood pressure of a kinin antagonist (DArg0-Hyp3-Thi5,8-DPtie7-bradyklnln) administered to control, nephrectomized, and adrenalectomized rats, and to rats treated with vasopressin V1-receptor antagonist, ganglionic and α and β-adrenergic receptor blockers (either separately or combined), H1- and H2-receptor blockers, and indomethacin, a prostaglandin synthesis inhibitor. Blood pressure changes were monitored on awake, restrained rats. In the control rat, the kinin antagonist injected as a bolus (4 mg/kg) into the ascending aorta produced a transient biphasic blood pressure response, first a pressor effect (ΔBP=7 ± 1 mm Hg; p <0.05), then a depressor effect (ΔBP=-20 ± 6 mm Hg; p <0.05). The pressor response to the kinin antagonist was not affected by any of the treatments; however, the depressor effect of the kinin antagonist appeared to be caused by the release of vasodilator prostanoids from the kidney, since it was not observed in the nephrectomized rats or in those treated with indomethacin. The pressor effect induced by the kinin antagonist suggests that kinins may contribute to the regulation of blood pressure.",
keywords = "Blood pressure regulation, Bradykinin, Depressor, Kinin antagonist, Pressor",
author = "Carbonell, {Luis F.} and Carretero, {Oscar A.} and Paolo Madeddu and Scicli, {A. Guillermo}",
year = "1988",
language = "English",
volume = "11",
pages = "I--84--I--88",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Effects of a kinin antagonist on mean blood pressure

AU - Carbonell, Luis F.

AU - Carretero, Oscar A.

AU - Madeddu, Paolo

AU - Scicli, A. Guillermo

PY - 1988

Y1 - 1988

N2 - Administration of high doses of a kinin antagonist produces an increase in blood pressure. Thus, endogenous klnins may be involved in the regulation of blood pressure. Kinins can induce the release of vasoactive substances such as catecholamines, renin, vasopressin, histamine, and prostaglandins. To determine whether the blood pressure changes induced by high doses of kinin antagonist are due to agonistic activity mediated by these vasoactive substances, we studied the effect on blood pressure of a kinin antagonist (DArg0-Hyp3-Thi5,8-DPtie7-bradyklnln) administered to control, nephrectomized, and adrenalectomized rats, and to rats treated with vasopressin V1-receptor antagonist, ganglionic and α and β-adrenergic receptor blockers (either separately or combined), H1- and H2-receptor blockers, and indomethacin, a prostaglandin synthesis inhibitor. Blood pressure changes were monitored on awake, restrained rats. In the control rat, the kinin antagonist injected as a bolus (4 mg/kg) into the ascending aorta produced a transient biphasic blood pressure response, first a pressor effect (ΔBP=7 ± 1 mm Hg; p <0.05), then a depressor effect (ΔBP=-20 ± 6 mm Hg; p <0.05). The pressor response to the kinin antagonist was not affected by any of the treatments; however, the depressor effect of the kinin antagonist appeared to be caused by the release of vasodilator prostanoids from the kidney, since it was not observed in the nephrectomized rats or in those treated with indomethacin. The pressor effect induced by the kinin antagonist suggests that kinins may contribute to the regulation of blood pressure.

AB - Administration of high doses of a kinin antagonist produces an increase in blood pressure. Thus, endogenous klnins may be involved in the regulation of blood pressure. Kinins can induce the release of vasoactive substances such as catecholamines, renin, vasopressin, histamine, and prostaglandins. To determine whether the blood pressure changes induced by high doses of kinin antagonist are due to agonistic activity mediated by these vasoactive substances, we studied the effect on blood pressure of a kinin antagonist (DArg0-Hyp3-Thi5,8-DPtie7-bradyklnln) administered to control, nephrectomized, and adrenalectomized rats, and to rats treated with vasopressin V1-receptor antagonist, ganglionic and α and β-adrenergic receptor blockers (either separately or combined), H1- and H2-receptor blockers, and indomethacin, a prostaglandin synthesis inhibitor. Blood pressure changes were monitored on awake, restrained rats. In the control rat, the kinin antagonist injected as a bolus (4 mg/kg) into the ascending aorta produced a transient biphasic blood pressure response, first a pressor effect (ΔBP=7 ± 1 mm Hg; p <0.05), then a depressor effect (ΔBP=-20 ± 6 mm Hg; p <0.05). The pressor response to the kinin antagonist was not affected by any of the treatments; however, the depressor effect of the kinin antagonist appeared to be caused by the release of vasodilator prostanoids from the kidney, since it was not observed in the nephrectomized rats or in those treated with indomethacin. The pressor effect induced by the kinin antagonist suggests that kinins may contribute to the regulation of blood pressure.

KW - Blood pressure regulation

KW - Bradykinin

KW - Depressor

KW - Kinin antagonist

KW - Pressor

UR - http://www.scopus.com/inward/record.url?scp=0023951512&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023951512&partnerID=8YFLogxK

M3 - Article

C2 - 3346068

AN - SCOPUS:0023951512

VL - 11

SP - I-84-I-88

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 2

ER -