Quipazine Increases Renin Release by a Peripheral Hemodynamic Mechanism
| Autor: | John F. Doane, Martin H. Zink, Alan F. Sved, Pablo E. Pergola, Richard H. Alper |
|---|---|
| Rok vydání: | 1990 |
| Předmět: |
Male
Agonist medicine.medical_specialty medicine.drug_class Blood Pressure Propranolol Plasma renin activity Renal Circulation chemistry.chemical_compound Heart Rate Internal medicine Renin Renin–angiotensin system medicine Prazosin Animals Drug Interactions Xylamidine Injections Intraventricular Pharmacology business.industry Angiotensin II Quipazine Hemodynamics Antagonist Rats Inbred Strains Rats Endocrinology chemistry Vasoconstriction Injections Intravenous Quinolines Serotonin Antagonists Cardiology and Cardiovascular Medicine business circulatory and respiratory physiology medicine.drug |
| Zdroj: | Journal of Cardiovascular Pharmacology. 15:1-9 |
| ISSN: | 0160-2446 |
| DOI: | 10.1097/00005344-199001000-00001 |
| Popis: | Summary Systemically administered serotonin (5-HT) agonists have been suggested to act centrally to increase plasma renin activity (PRA) and arterial pressure (AP) To test this hypothesis, hemodynamic responses were determined in conscious male rats after intracerebroventricular (i.c.v.) or intravenous (i.v.) administration of the di rect 5-HT agonist quipazine. When administered i.v. quipazine increased AP and PRA, and decreased rena blood flow (RBF); doses of quipazine i.c.v. that increasec AP to a similar degree failed to increase PRA. The in crease in PRA elicited by i.v. quipazine was not blockec by propranolol, suggesting non-neural mechanisms. The increase in AP and decrease in RBF elicited by i.v. quipazine were not eliminated by prazosin, enalapril, or V1-vasopressin antagonist administered alone or in combination. LY 53857, a 5-HT2 antagonist that enters the central nervous system (CNS), blocked all responses to i.v. quipazine. In contrast, the peripheral 5-HT2 antagonist xylamidine blocked the renin and RBF responses, but only attenuated the pressor response to quipazine. These data suggest that quipazine can act in the CNS to increase AP, but when administered systemically quipazine also activates vascular 5-HT2 receptors to increase AP further and to decrease RBF. The increase in PRA caused by i.v. quipazine is secondary to renal hemodynamics and is unrelated to CNS actions of this drug. |
| Databáze: | OpenAIRE |
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