ALPHA‐AGONIST MODIFIES BAROREFLEX VASOCONSTRICTION BY A POSTJUNCTIONAL MECHANISM IN DOGS

Abstract

1. We examined whether or not circulating alpha-agonist modified baroreflex vasoconstriction of the hindlimb, using anaesthetized dogs in which the limb was vascularly isolated and perfused with blood from a donor dog using a pulsatile pump. 2. The open-loop gain (G) of the baroreflex was estimated from changes in mean arterial pressure following mild quick haemorrhage from the aorta of the recipient dog. 3. The hindlimb perfusion pressure increased after haemorrhage due to neurogenic vasoconstriction. 4. An overall gain (Gh) of the baroreflex hindlimb vascular bed control system was estimated from the ratio of the increase in hindlimb perfusion pressure to the change in systemic arterial pressure of the recipient dog. 5. Administration of a relatively selective alpha 1-agonist with no prejunctional beta 2 stimulating action (phenylephrine) or a selective alpha 2-agonist (clonidine) to the donor dog increased its systemic arterial pressure and augmented Gh. 6. Since both drugs were administered to the donor dog and could not enter into the recipient dog, these drugs did not affect the recipient's sympathetic nervous system, including the central nervous system and afferent limb of the baroreflex system. Therefore, these drugs could modify baroreflex vasoconstriction of the hindlimb only at the junction of the efferent sympathetic nerve and the vascular smooth muscle. 7. It was concluded that postjunctional alpha-adrenoceptor stimulation augments neurogenic vasoconstriction.