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LACK OF PRESYNAPTIC EFFECTS OF KETANSERIN ON CARDIAC NORADRENERGIC NERVE TERMINALS IN THE SHR
Author(s) -
SCALBERT E.,
RICHER C.,
GIUDICELLI J.F.
Publication year - 1988
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.1988.tb00641.x
Subject(s) - ketanserin , medicine , norepinephrine , endocrinology , heart rate , chemistry , stimulation , clonidine , aminophylline , tachycardia , bradycardia , propranolol , receptor , serotonin , 5 ht receptor , blood pressure , dopamine
Summary— The potential cardiac presynaptic effects of ketanserin (K) (0.01–3.00 mg/kg IV) were investigated in pithed SHR in 4 experimental conditions: ( a ) basal heart rate (HR); ( b ) HR increased by selective cardiac sympathetic stimulation (SS); ( c ) HR increased by aminophylline infusion; and ( d ) HR increased by SS and brought back to basal value by clonidine. Control groups were treated with saline. In the 4 types of experiments, K, starting from 0.3 mg/kg, induced almost identical and dose‐dependent decreases in HR (maximal reduction: 45 beats/(min at 3 mg/kg). Thus we conclude: (1) that K is devoid of any presynaptic facilitatory effect on norepinephrine release since it was unable to raise HR in experiment D; (2) that K is devoid of any presynaptic inhibitory effect on norepinephrine release since it lowered HR to the same extent in both experiments B (noradrenergic tachycardia) and (non‐noradrenergic tachycardia); and C (3) that the bradycardia which was induced by high doses of K (much above those required to block 5‐HT 2 and α 1 ‐adrenergic receptors) and which was of similar magnitude in the 4 experimental conditions is probably due to a direct, nonspecific depressant effect of K on the sinus node.