Abstract
To determine whether the vasodilator, hydralazine (HYD), produces hyperpolarization of vascular muscle cells, we measured the effect of HYD on membrane potential and contractile responses to phenylephrine and K+. HYD (1 μM) caused a 4 mV hyperpolarization of phenylephrine-depolarized arteries (compared with controls without HYD), which could possibly account for up to three-fourths of the 39% decrease in tension measured. K+-contracted vessels were also 34% relaxed by 1 μM HYD without an effect on membrane potential. In addition, HYD further relaxed phenylephrine-stimulated vessels previously relaxed by D-600, suggesting that Ca++ channel blockade may not be an important mechanism of vasodilation for HYD. The evidence suggests that a nonmembrane action of HYD on arterial muscle probably multiplies the relaxant effect of membrane potential hyperpolarization. Both mechanisms would attenuate the effects of adrenergic stimulation.