Ninhibin: a sperm factor attenuates the atrial natriuretic factor mediated inhibition of adenylate cyclase: possible involvement of inhibitory guanine nucleotide regulatory protein.

The effect of ninhibin, a sperm factor extracted from bovine sperm, was studied on adenylate cyclase from rat aorta. Ninhibin treatment of the membranes activated adenylate cyclase in a concentration dependent manner. The maximal activation (approximately equal to 4-fold) was obtained at 2micrograms ninhibin and at 10 min of treatment at 37 degrees C. On the other hand, in untreated control membranes, ninhibin at 2 micrograms could stimulate adenylate cyclase by about 50-60% only. In addition, ninhibin potentiated the guanine nucleotide-, isoproterenol- and forskolin (FSK)-stimulated adenylate cyclase activities and also attenuated the GTP gamma s and atrial natriuretic factor (ANF)-mediated inhibition of enzyme activities. Furthermore the inhibition of isoproterenol- and FSK-stimulated adenylate cyclase activities by ANF was also abolished by ninhibin. These data indicate that ninhibin which has been suggested to inactivate or inhibit Ni-guanine nucleotide regulatory protein can also attenuate the ANF-receptor mediated inhibition of adenylate cyclase in rat aorta suggesting an involvement of Ni-guanine nucleotide regulatory protein in the coupling of ANF receptors to adenylate cyclase.