Intracerebroventricular (i.c.v.) injection of bradykinin (0.1-10 micrograms) or angiotensin II (0.01-10 micrograms) in conscious, freely moving rats evoked dose-related increases in arterial pressure. The pressor response to bradykinin (BK) was accompanied by an increase in heart rate while angiotensin II (ANG II) decreased heart rate. Pretreatment with hemicholinium-3 to deplete brain acetylcholine levels produced a choline-reversible blockade of the cardiovascular response to BK. In contrast, the pressor response to ANG II was only weakly inhibited by hemicholinium-3 and the bradycardia was unaffected. Central pretreatment with the nicotinic antagonist, hexamethonium (50 micrograms) was more effective than the muscarinic antagonist atropine (20 micrograms) at blocking the cardiovascular responses to i.c.v. injection of BK. Both blocking agents produced a weaker inhibitory effect on the pressor response to ANG II although no anticholinergic pretreatment significantly inhibited the fall in heart rate. These results are consistent with the possibility of a peptidergic-cholinergic interaction in the central cardiovascular actions of BK and perhaps for a component of the pressor response to ANG II.
Role of cholinergic neurons in the cardiovascular responses evoked by central injection of bradykinin or angiotensin II in conscious rats
SERRA, MARIANGELA
1985-01-01
Abstract
Intracerebroventricular (i.c.v.) injection of bradykinin (0.1-10 micrograms) or angiotensin II (0.01-10 micrograms) in conscious, freely moving rats evoked dose-related increases in arterial pressure. The pressor response to bradykinin (BK) was accompanied by an increase in heart rate while angiotensin II (ANG II) decreased heart rate. Pretreatment with hemicholinium-3 to deplete brain acetylcholine levels produced a choline-reversible blockade of the cardiovascular response to BK. In contrast, the pressor response to ANG II was only weakly inhibited by hemicholinium-3 and the bradycardia was unaffected. Central pretreatment with the nicotinic antagonist, hexamethonium (50 micrograms) was more effective than the muscarinic antagonist atropine (20 micrograms) at blocking the cardiovascular responses to i.c.v. injection of BK. Both blocking agents produced a weaker inhibitory effect on the pressor response to ANG II although no anticholinergic pretreatment significantly inhibited the fall in heart rate. These results are consistent with the possibility of a peptidergic-cholinergic interaction in the central cardiovascular actions of BK and perhaps for a component of the pressor response to ANG II.
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