Sodium chloride-induced partial inhibition in vivo of alpha 2-adrenoceptor agonist function

Details

Serval ID
serval:BIB_B5163A717E94
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Sodium chloride-induced partial inhibition in vivo of alpha 2-adrenoceptor agonist function
Journal
Journal of Hypertension
Author(s)
Kohlmann, O., Jr. , Gavras  I., Biollaz  J., Biollaz  B., Gavras  H.
ISSN
0263-6352 (Print)
Publication state
Published
Issued date
06/1985
Volume
3
Number
3
Pages
269-74
Notes
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Jun
Abstract
Recent research has demonstrated that sodium diminishes the affinity of alpha 2-adrenoceptors for agonists in vitro. Clonidine, a highly specific agonist for alpha 2-receptors, has a transient hypertensive effect when administered parenterally. We studied in conscious anephric Wistar rats the effect of equimolar saline or mannitol solutions on the hypertensive response to clonidine administered subcutaneously in doses of 10, 100 and 1000 micrograms/kg body weight. Prior saline infusion reduced the hypertensive response to the two higher doses of clonidine by 65 and 70%, and displaced the slope of the dose-response curve downwards, but mannitol had no such effect. Pre-treatment with the alpha 2-antagonist yohimbine abolished the differences in clonidine-induced pressor response between saline-treated, mannitol-treated and control rats. On the contrary, after pre-treatment with the alpha 1-antagonist prazosin, the pressor action of clonidine was significantly reduced in the saline-infused rats compared to the other two groups. Thus the saline-induced blunting of the pressor response elicited by clonidine could be negated by prior alpha 2- but not alpha 1-blockade, indicating that sodium interfered with the stimulation of post-synaptic vascular alpha 2-adrenoceptors. These findings indicate that loading with sodium chloride attenuates the alpha 2-adrenoceptor function in vivo. Based on this, we suggest that the mechanism by which sodium excess causes a rise in blood pressure involves modification of the alpha 2-adrenoceptors.
Keywords
Adrenergic alpha-Agonists/*pharmacology Animals Blood Pressure/*drug effects Clonidine/administration & dosage/*pharmacology Male Mannitol/pharmacology Nephrectomy Prazosin/pharmacology Rats Rats, Inbred Strains Receptors, Adrenergic, alpha/*drug effects Sodium Chloride/*pharmacology Yohimbine/pharmacology
Pubmed
Web of science
Create date
25/01/2008 10:41
Last modification date
20/08/2019 15:23
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