TitleActivation of alpha 1-adrenoceptors increases [3H]inositol metabolism in rat vas deferens and caudal artery.
Publication TypeJournal Article
Year of Publication1985
AuthorsFox AW, Abel PW, Minneman KP
JournalEur J Pharmacol
Date Published1985 Oct 08
KeywordsAdrenergic alpha-Agonists, Adrenergic alpha-Antagonists, Animals, Arteries, In Vitro Techniques, Inositol, Inositol Phosphates, Male, Muscle, Smooth, Muscle, Smooth, Vascular, Rats, Rats, Inbred Strains, Receptors, Adrenergic, alpha, Vas Deferens

Rings of rat vas deferens and caudal artery were incubated with [3H]inositol in Krebs-Ringer bicarbonate buffer containing 10 mM lithium chloride, and the production of water-soluble [3H]inositol phosphates was monitored. Norepinephrine increased [3H]inositol phosphate accumulation 7-fold in rings from vas deferens and 3-fold in rings from caudal artery. Epinephrine, phenylephrine and methoxamine were as effective as norepinephrine, suggesting that these drugs are full agonists in causing this response. Prazosin, phentolamine and yohimbine completely blocked the stimulation by norepinephrine in both tissues with potencies typical of blockade of alpha 1-adrenoceptors. Despite a substantial receptor reserve for alpha 1-adrenoceptor mediated contractile responses, clonidine, p-amino-clonidine, phenylpropanolamine and ephedrine can only cause a partial contractile response in rat vas deferens. However, all of these partial agonists were either as effective or more effective in increasing [3H]inositol phosphate accumulation in rat vas deferens as they were in activating a contractile response. These data suggest that alpha 1-adrenoceptors increase phosphatidylinositol turnover in rat vas deferens and caudal artery, and that there may be a receptor reserve for alpha 1-adrenoceptor mediated increases in [3H]inositol phosphate accumulation in these smooth muscles.

Alternate JournalEur. J. Pharmacol.
PubMed ID2865157
Grant ListHL 29871 / HL / NHLBI NIH HHS / United States