Influence of blood gases, Ca2+-entry blockade and angiotensin converting enzyme inhibition on pressor responses to α-adrenoceptor agonists: Evidence in vivo for subtypes of response independent of receptor subtype?

J. W. O'Brien, Nicholas Flavahan, T. L. Grant, J. C. McGrath, R. J. Marshall

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Abstract

1. The pressor responses in the pithed rat to α-adrenoceptor agonists can be modified by alterations in arterial blood gas levels or by drugs which interfere with excitation-contraction coupling processes in the vascular smooth muscle, e.g. Ca2+-entry blockers or angiotensin converting enzyme (ACE) inhibitors. However, the extent of these influences depends on which agonist is used. 2. The pressor response to intravenous injection of α-adrenoceptor agonists consists of two phases: an initial rapid but transient response (phase I) is followed by a response of slower onset but longer duration (phase II). We have examined the effects of manipulation of arterial blood gases, a Ca2+-entry blocker, nifedipine, and an ACE inhibitor, teprotide, on the pressor responses to a series of α-adrenoceptor agonists. In each case, the effects showed selectivity for one or other of the two phases and the differences in susceptibility between agonists could be explained by the relative sizes of the two phases in their responses. In general, phase II was more susceptible to alkalosis, nifedipine and teprotide, so that drugs in which this component predominated were more susceptible to these factors. In contrast there was no direct correlation with the receptor subtypes activated by the agonists.

Original languageEnglish (US)
JournalClinical Science
Volume68
Issue numberSUPPL. 10
StatePublished - 1985
Externally publishedYes

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Teprotide
Peptidyl-Dipeptidase A
Adrenergic Receptors
Gases
Nifedipine
Angiotensin-Converting Enzyme Inhibitors
Excitation Contraction Coupling
Alkalosis
Vascular Smooth Muscle
Intravenous Injections
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{bd3fcda6b1e1454398f7abf47a818535,
title = "Influence of blood gases, Ca2+-entry blockade and angiotensin converting enzyme inhibition on pressor responses to α-adrenoceptor agonists: Evidence in vivo for subtypes of response independent of receptor subtype?",
abstract = "1. The pressor responses in the pithed rat to α-adrenoceptor agonists can be modified by alterations in arterial blood gas levels or by drugs which interfere with excitation-contraction coupling processes in the vascular smooth muscle, e.g. Ca2+-entry blockers or angiotensin converting enzyme (ACE) inhibitors. However, the extent of these influences depends on which agonist is used. 2. The pressor response to intravenous injection of α-adrenoceptor agonists consists of two phases: an initial rapid but transient response (phase I) is followed by a response of slower onset but longer duration (phase II). We have examined the effects of manipulation of arterial blood gases, a Ca2+-entry blocker, nifedipine, and an ACE inhibitor, teprotide, on the pressor responses to a series of α-adrenoceptor agonists. In each case, the effects showed selectivity for one or other of the two phases and the differences in susceptibility between agonists could be explained by the relative sizes of the two phases in their responses. In general, phase II was more susceptible to alkalosis, nifedipine and teprotide, so that drugs in which this component predominated were more susceptible to these factors. In contrast there was no direct correlation with the receptor subtypes activated by the agonists.",
author = "O'Brien, {J. W.} and Nicholas Flavahan and Grant, {T. L.} and McGrath, {J. C.} and Marshall, {R. J.}",
year = "1985",
language = "English (US)",
volume = "68",
journal = "Clinical Science",
issn = "0143-5221",
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TY - JOUR

T1 - Influence of blood gases, Ca2+-entry blockade and angiotensin converting enzyme inhibition on pressor responses to α-adrenoceptor agonists

T2 - Evidence in vivo for subtypes of response independent of receptor subtype?

AU - O'Brien, J. W.

AU - Flavahan, Nicholas

AU - Grant, T. L.

AU - McGrath, J. C.

AU - Marshall, R. J.

PY - 1985

Y1 - 1985

N2 - 1. The pressor responses in the pithed rat to α-adrenoceptor agonists can be modified by alterations in arterial blood gas levels or by drugs which interfere with excitation-contraction coupling processes in the vascular smooth muscle, e.g. Ca2+-entry blockers or angiotensin converting enzyme (ACE) inhibitors. However, the extent of these influences depends on which agonist is used. 2. The pressor response to intravenous injection of α-adrenoceptor agonists consists of two phases: an initial rapid but transient response (phase I) is followed by a response of slower onset but longer duration (phase II). We have examined the effects of manipulation of arterial blood gases, a Ca2+-entry blocker, nifedipine, and an ACE inhibitor, teprotide, on the pressor responses to a series of α-adrenoceptor agonists. In each case, the effects showed selectivity for one or other of the two phases and the differences in susceptibility between agonists could be explained by the relative sizes of the two phases in their responses. In general, phase II was more susceptible to alkalosis, nifedipine and teprotide, so that drugs in which this component predominated were more susceptible to these factors. In contrast there was no direct correlation with the receptor subtypes activated by the agonists.

AB - 1. The pressor responses in the pithed rat to α-adrenoceptor agonists can be modified by alterations in arterial blood gas levels or by drugs which interfere with excitation-contraction coupling processes in the vascular smooth muscle, e.g. Ca2+-entry blockers or angiotensin converting enzyme (ACE) inhibitors. However, the extent of these influences depends on which agonist is used. 2. The pressor response to intravenous injection of α-adrenoceptor agonists consists of two phases: an initial rapid but transient response (phase I) is followed by a response of slower onset but longer duration (phase II). We have examined the effects of manipulation of arterial blood gases, a Ca2+-entry blocker, nifedipine, and an ACE inhibitor, teprotide, on the pressor responses to a series of α-adrenoceptor agonists. In each case, the effects showed selectivity for one or other of the two phases and the differences in susceptibility between agonists could be explained by the relative sizes of the two phases in their responses. In general, phase II was more susceptible to alkalosis, nifedipine and teprotide, so that drugs in which this component predominated were more susceptible to these factors. In contrast there was no direct correlation with the receptor subtypes activated by the agonists.

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