Urotensin I effects on intracellular content of cyclic AMP in the rat tail artery.
Rat tail artery strips were incubated in the presence of 4 x 10(-3) M theophylline and urotensin I (UI). At the concentrations of 1.50, 7.50 mU/ml but not of 0.75 mU/ml UI, the content of cAMP increased significantly. Cyclic AMP content and muscle tension were measured at 5--30 sec intervals during noradrenaline (NA)- and potassium chloride (KCl)-induced contractions and during subsequent urotensin I-induced relaxation. Cyclic AMP content declined initially after addition of NA but returned to baseline levels during the contraction. Significant dose-related increases in cAMP were noted upon addition of UI, prior to the onset of the relaxation response followed by a marked decrease during the relaxation response. An increase in cAMP was observed after initiation of the contractile response to KCl-contracted tissues, but no further increase in cAMP after addition of UI was detected. These findings suggest an involvement of cyclic AMP in the initial events leading to the relaxation response to urotensin I in the NA-contracted rat tail artery. Urotensin I-induced relaxation in KCl-contracted tissues appears to proceed by an alternative mechanism which does not require increased levels of cAMP.
D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000378:metabolism; D000242:Cyclic AMP / Q000378:metabolism*; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology; D010455:Peptides / Q000494:pharmacology*; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D013997:Time Factors; D014579:Urotensins / Q000494:pharmacology*
D010455:Peptides; D014579:Urotensins; D011189:Potassium Chloride; D000242:Cyclic AMP; D009638:Norepinephrine