Abstract
Rings of rat vas deferens and caudal artery were incubated with ( super(3)H)inositol in Krebs-Ringer bicarbonate buffer containing lithium chloride, and the production of water-soluble ( super(3)H)inositol phosphates was monitored. Norepinephrine increased ( super(3)H)inositol phosphate accumulation 7-fold in both vas deferens and caudal artery. Epinephrine, phenylephrine and methoxamine were as effective as norepinephrine, suggesting that these drugs are full agonists in causing this respose. Prazosin, phentolamine and yohimbine completely blocked the stimulation by norepinephrine in both tissues. All the partial agonists were either as effective or more effective in increasing ( super(3)H)inositol phosphate accumulation in rat vas deferens as they were in activating a contractile response. The data suggest that alpha sub(1)-adrenoceptors increase phosphatidylinositol turnover in rat vas deferens and caudal artery, and that there may be a receptor reserve for alpha sub(1)-adrenoceptor mediated increases in ( super(3)H)inositol phosphate accumulation in these smooth muscles.