CENTRALLY MEDIATED CARDIOVASCULAR EFFECTS OF INTRACISTERNAL APPLICATION OF CARBACHOL IN ANESTHETIZED RATS

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The pressor response to the intracisternal (i.c.) injection of carbachol (1 μg) in anesthetized rats was analyzed. This response was significantly reduced by the intravenous (i.v.) injection of guanethidine (5 mg), hexamethonium (10 mg) or phentolamine (5 mg), and conversely, potentiated by i.v. desmethylimipramine (0.3 mg), while propranolol (0.5 mg) i.v. selectively inhibited the enlargement of pulse pressure and the tachycardia following i.c. carbachol (1 μg). On the other hand, the pressor response to i.c. carbachol (1 μg) was almost completely blocked by i.c. atropine (3 μg) or hexamethonium (500 μg), and significantly reduced by i.c. chlorpromazine (50 μg) but significantly potentiated by i.c. desmethylimipramine (30 μg). The pressor response to i.c. carbachol (1 μg) remained unchanged after sectioning of the bilateral cervical vagal nerves but disappeared after sectioning of the spinal cord (C<SUB>7</SUB>-C<SUB>8</SUB>). From the above result it is suggested that the pressor response to i.c. carbachol originates in the central muscarinic mechanism, is exerted through the central and peripheral adrenergic mechanisms, and that the sympathetic trunk is the main pathway.
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