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?
| Autor: | T. L. Grant, R. J. Marshall, John C. McGrath, Nicholas Flavahan, J. W. O'Brien |
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| Rok vydání: | 1985 |
| Předmět: |
Male
Xylazine Agonist medicine.medical_specialty Time Factors Alkalosis Vascular smooth muscle Nifedipine medicine.drug_class Pressoreceptors Pharmacology Phenylephrine chemistry.chemical_compound Internal medicine medicine Animals Teprotide Receptor biology Rats Inbred Strains Angiotensin-converting enzyme General Medicine Carbon Dioxide medicine.disease Rats Oxygen Endocrinology chemistry Ethanolamines Vasoconstriction ACE inhibitor biology.protein Adrenergic alpha-Agonists Oligopeptides medicine.drug |
| Zdroj: | Clinical Science. 68:99s-104s |
| ISSN: | 0144-9664 |
| DOI: | 10.1042/cs068s099 |
| Popis: | 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. 3. The results are discussed in relation to the modulation of adrenergic responses by physiological factors and drugs which disturb them. |
| Databáze: | OpenAIRE |
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