Sympathetic vasoconstriction sensitive to alpha 2-adrenergic receptor blockade. No evidence for preferential innervation of alpha 1-adrenergic receptors in the canine femoral bed.

Abstract

SUMMARY In the canine femoral bed, we studied the involvement of vascular o 2 -adrenergic receptors in vasoconstriction by stimulating the sympathetic nerve during different degrees of activation of metabolic counter-regulation (constant pressure and constant flow perfusion). In chloraloseanesthetized, despinalized dogs under /3-blockade (2 mg/kg nadolol) and under a constant femoral perfusion pressure, cumulative doses of rauwolscine (0.03, 0.3, and 3.0 mg/kg i.v., n = 8) or of prazosin (0.012, 0.12, and 1.2 mg/kg i.v., n = 8) caused dose-dependent shifts to the right of the doseresponse curve of intraarterial norepinephrine (NE) infusions. These cumulative doses also caused attenuations of the vasoconstriction initiated by lumbar sympathetic stimulation (0.1, 0.3, 1.0, and 3.0 Hz). Sham treatment (n = 8) had no such results. In experiments with constant flow perfusion (n = 6 for each antagonist), rauwolscine shifted the NE dose-response curve significantly more compared to the experiments with constant pressure perfusion, while prazosin was similarly effective under both conditions. Under constant flow perfusion, both antagonists dose-dependently attenuated the vasoconstrictions caused by sympathetic stimulation. While prazosin and sham treatment did not modify the overflow of NE from the femoral bed during stimulation, this overflow was augmented by rauwolscine during stimulation at 3 Hz, which indicated presynaptic modulation of NE release. Under both experimental conditions, no significant difference could be observed in the attenuation of lowfrequency sympathetic vasoconstriction by the two antagonists, when dosages were compared on the basis of their action against infused NE. It is concluded that both a rauwolscine-sensitive component and a prazosin-sensitive component are involved in the competition between sympathetic vasoconstriction and metabolic dilation. The vascular a-adrenergic receptors activated by these two components have a similar postsynaptic localization relative to the nerve endings. (Hypertension 6: 915-925, 1984) KEY WORDS • prazosin • rauwolscine • constant flow perfusion • constant pressure perfusion • intrasynaptic a-adrenergic receptors T HERE is general agreement that more than one type of postsynaptic vascular a-adrenergic receptor exists in laboratory mammalian species'-2 and in humans. 3 " 3 Norepinephrine (NE) induces vasoconstriction by activation of both a,-and a 2 -adrenergic receptors, which have been classified according to the effects of selective pharmacological agonists and antagonists.6 Recently, it has been shown that a 2 -meFrom the Institut fur Angewandte Physiologie

Contribution of α2‐adrenoceptors and Y1 neuropeptide Y receptors to the blunting of sympathetic vasoconstriction induced by systemic hypoxia in the rat

“…Our finding that the depressive effect of yohimbine on the increase in FVR evoked by continuous stimulation at 2 Hz failed to reach statistical significance, may reflect the opposing influences of pre‐ and postsynaptic α 2 ‐adrenoceptor stimulation on this response. However, our findings on the effect of yohimbine on increases in FVR evoked by bursts add to the evidence that stimulation of postjunctional α 2 ‐adrenoceptors contributes to sympathetically evoked increases in muscle vascular resistance in humans (Bolli et al 1983; Jie et al 1984; Taddei et al 1988), cats and dogs (Gardiner & Peters, 1982; Elsner et al 1984).…”

Lack of involvement of α‐adrenoceptors in sympathetic neural vasoconstriction in the hindquarters of the rabbit

“…The vascular responses to sympathetic nerve stimulation are generally considered to result from the activation of a-adrenoceptors by noradrenaline (e.g. Langer et al, 1981;McGrath et al, 1982;Elsner et al, 1984;Alabaster & Davey, 1984). However, data from electrophysiological studies in isolated tissues suggest that the receptor activated by the sympathetic transmitter is not an a-adrenoceptor (Holman & Surprenant, 1979;1980;Surprenant, 1980;Hirst & Neild, 1980;Itoh et al, 1983;Hirst et al, 1985).…”