1. Central interactions between dihydropyridines and cholinergic systems in the control of blood pressure in rat.
- Author
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Brisac AM, Huguet F, Champeroux P, Montastruc JL, Lucet B, Gerard P, Laurent S, Narcisse G, and Schmitt H
- Subjects
- Animals, Atropine Derivatives pharmacology, Cerebral Ventricles drug effects, Hemicholinium 3 pharmacology, Hexamethonium, Hexamethonium Compounds pharmacology, Hippocampus drug effects, In Vitro Techniques, Male, Potassium pharmacology, Rats, Rats, Inbred SHR, Rats, Inbred Strains, Reference Values, Species Specificity, 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester pharmacology, Acetylcholine metabolism, Blood Pressure drug effects, Cerebral Ventricles physiology, Dihydropyridines pharmacology, Hippocampus physiology, Nicardipine pharmacology
- Abstract
Intracerebroventricular (i.c.v.) injection of the 1,4-dihydropyridine (DHP) calcium channel agonist, Bay K8644 (30 micrograms/kg) increased mean blood pressure and the K+-evoked release of [3H]acetylcholine ([3H]ACh) from hippocampal slices in spontaneously hypertensive rats (SHR). The Bay K8644-induced hypertension was inhibited by a pretreatment with methylatropine (80 micrograms/kg i.c.v.). In SHR, nicardipine, a DHP calcium channel antagonist, reduced mean blood pressure when i.c.v. injected (10 micrograms/kg). The nicardipine-induced hypotension was reduced by a pretreatment with hemicholinium-3 (20 micrograms, i.c.v.). Nicardipine (1 microM) did not modify, in SHR, the K+-evoked release of [3H]ACh, but inhibited the Bay K8644-induced increase in the ACh release. In normotensive rats, neither Bay K8644 nor nicardipine modify blood pressure, when centrally injected, or the stimulated release of [3H]ACh from hippocampal slices. The participation of central DHP sites in the cholinergic transmission in genetic hypertension is discussed.
- Published
- 1987
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