Electrophysiological differentiation of alpha-receptors on arteriolar smooth muscle

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Abstract
The effects of clonidine (a prototype of an .alpha.2-agonist) and phenylephrine (a prototype of an .alpha.1-agonist) on intracellularly recorded electrical activity and vessel size of feline submucosal arterioles were compared. Phenylephrine constricts the vessels and causes a depolarization and the initiation of oscillations of the membrane potential. These oscillations occasionally give rise to spike potentials. In contrast, clonidine produces no significant depolarization of the resting potential in spite of the simultaneous initiation of contraction. Neurally induced depolarizations (excitatory junction potentials) are not blocked and are sometimes augmented by the nonselective .alpha.-blocker phentolamine even though the depolarization induced by norepinephrine is blocked by phentolamine. Excitatory junction potentials are antagonized by the .alpha.1-blocker prazosin. The contraction caused by clonidine is blocked to a greater degree by yohimbine (a relatively selective .alpha.2-blocker) than by prazosin. The contraction caused by phenylephrine is blocked to a greater degree by prazosin than by yohimbine. These data indicate that phenylephrine and clonidine act by different mechanisms and, taken together with previous studies, suggest that .alpha.1- and .alpha.2-stimulation utilize different excitation-contraction coupling mechanisms.