Atrial natriuretic factor inhibits adrenergic and purinergic neurotransmission in the rabbit isolated vas deferens

This study tests the hypothesis that atrial natriuretic factor (ANF) acts to inhibit neurotransmission in the rabbit vas deferens. The vas deferens is a unique model of autonomic neurotransmission in that it is composed of primarily nonvascular smooth muscle and has both a purinergic or twitch contraction and an adrenergic or phasic contraction associated with its response to electrical stimulation. In this study ANF was found to inhibit both adrenergic and purinergic neurotransmission in the rabbit vas deferens. ANF inhibited both the electrically induced phasic contraction and electrically induced norepinephrine release in a concentration-dependent manner over the ANF concentration range of 10^-10 to 10^-7 M. ANF at a concentration of 10^-7 M had no effect on norepinephrine-induced or ATP-induced contractions. Therefore, the neuromodulatory effect of ANF in the rabbit vas deferens appears to be prejunctional, on the release of the neurotransmitters norepinephrine and ATP from the nerve terminal and not postjunctional on the smooth muscle. Neither the alpha-2 antagonist rauwolscine nor the cyclooxygenase inhibitor indomethacin had any effect on the inhibitory effect of ANF on electrically induced twitch or phasic contractions. Additionally, ANF did not affect vasa deferentia prostaglandin E production. Therefore, the inhibitory neuromodulatory ANF effect is not mediated via alpha-2 adrenergic receptors or prostaglandin E production. The observed inhibitory neuromodulatory effects in this study may be involved in the hypotensive effects of ANF including natriuresis, diuresis and vasodilation.