ANTAGONISM OF VASOCONSTRICTION BY MUSCLE-CONTRACTION DIFFERS WITH ALPHA-ADRENERGIC SUBTYPE

It has been suggested that muscle contraction causes prejunctional inhibition of transmitter release from sympathetic nerves. In accordance with this, we found that second-order (50 mum ID) arterioles of the cat sartorius muscle dilate 40-80% more with muscle contraction during 2-, 4-, or 8-Hz sympathetic nerve stimulation than during equivalent constriction produced by intravenous norepinephrine injection. However, when constriction was to the selective alpha1-agonist phenylephrine, the magnitude of dilation induced by muscle contraction was similar to that seen with sympathetic nerve stimulation, suggesting that prejunctional inhibition is not involved. Alternatively, different receptor subtypes may be activated by sympathetic nerve stimulation and exogenous norepinephrine. In support of this explanation, we found that approximately 50% of the vasoconstrictor effect of sympathetic nerve stimulation (8 Hz) was blocked by prazosin, an alpha1-adrenergic antagonist, but no further diminution of tone was seen with addition of yohimbine, an alpha2-adrenergic antagonist. In contrast, the vasoconstrictor response to exogenous norepinephrine was not affected by prazosin, while addition of yohimbine almost completely blocked the response. These findings suggest that muscle contraction selectively attenuates vasoconstriction mediated by junctional receptors in second-order arterioles.