Atrial natriuretic peptide inhibits the purinergic and not the adrenergic component of electrically induced contractile responses in guinea pig vas deferens.

The effects of atrial natriuretic peptide (ANP) on the purinergic and adrenergic components of electrically induced contractile responses in the prostatic portion of the guinea pig vas deferens were studied. ANP (0.01-100 nM) was found to inhibit the two phases of the biphasic contractions induced by field electrical stimulation (300 pulses, 0.1 msec, 9 Hz). The effects of ANP at a concentration of 10 nM were examined further. ANP had no effect on l-phenylephrine-induced or exogenous ATP-induced contractions in the presence of tetrodotoxin, indicating a prejunctional rather than postjunctional modulatory effect of ANP. Neither yohimbine, nor indomethacin, nor naloxone influenced the inhibitory effect of ANP on either phase of the electrically induced contractions. However, the inhibitory effect of ANP on the first phase was verapamil-sensitive and nitrendipine-insensitive, whereas the effect on the second phase was sensitive to both verapamil and nitrendipine. Thus, at least two different calcium pools could be involved in the ANP inhibitory effect. The inhibitory effect of ANP on the purinergic component of the electrically induced contractile responses after prazosin remained the same, whereas after alpha,beta-methylene adenosine-5'-triphosphate there was no effect on ANP on the residual adrenergic component. Therefore, ANP exerted an inhibitory effect on the purinergic and not on the adrenergic component of the electrically induced mechanical responses in the guinea pig vas deferens via prejunctional mechanisms which do not depend on alpha-2 adrenoceptors, opiate receptors or the production of prostaglandins and depend on different calcium pools.