Mechanism by Which Serotonin, Norepinephrine and Reserpine Cause Central Vasomotor Inhibition

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Abstract
Several vasoconstrictor drugs and reserpine administered into a cerebral lateral ventricle inhibited the reflex pressor response to occlusion of the common carotid arteries in both anesthetized and unanesthetized dogs. This effect was opposed by central administration of the vasodilator drugs, nitroprusside and histamine. Serotonin, norepinephrine and their precursors, 5-hydroxytryptophan and 3,4-dihydroxyphenylalanine, and reserpine caused lowering of arterial pressure and slowing of heart rate as well as inhibition of the carotid occlusion response; angiotensin and vasopressin did not. The central inhibitory effect of norepinephrine was opposed by phentolamine; that of 5-hydroxytryptophan was not affected by lysergic acid diethylamide or its brom derivative. Cooling of cerebrospinal fluid, which presumably caused local vasoconstriction, also caused inhibition of the carotid occlusion response, hypotension and bradycardia, and these effects were counteracted by central injection of vasodilator drugs. Warming of cerebrospinal fluid, presumably associated with local vasodilation, opposed the central inhibitory effect of vasoconstrictor drugs and of reserpine. In view of the consistently opposite effects of vasoconstrictor and vasodilator drugs and procedures on central vasomotor sympathetic activity, it is tentatively concluded that these effects depend on change in local blood flow. The acute cardiovascular effects of reserpine of central origin are probably due to local decrease of tissue perfusion caused by serotonin, norepinephrine or other vasoconstrictor agent released from a bound to an active form.

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