Release of prostaglandin E responsible for tachyphylaxis to noradrenaline
Szuperska-Ocetkiewicz, A.
Folia Medica Cracoviensia 18(1): 43-56
1976
ISSN/ISBN: 0015-5616 PMID: 1261944 Document Number: 108803
Chick rectum (CR) washed with oxygenated venous cat blood reacts to prostaglandin and acetylcholine at concentrations of the order of 5-10 ng/ml. CR preincubated in solution containing atropine (1 .mu.g/ml) and indomethacin (5 .mu.g/ml) is selectively sensitive to the contractile action of PGE1 [prostaglandin E1] and PGE2 at concentrations of the order of 0.5-2 ng/ml. In contrast to other detector organs, CR does not relax in presence of noradrenaline at concentrations on the order of 5 ng/ml. During noradrenaline infusion (2 .mu.g/ml per min) in anesthetized cats, tachyphylaxis of pressor response appears, and CR washed with oxygenated blood from the right atrium contracts. The administration of 10 mg/kg indomethacin, PG biosynthesis inhibitor, prevents tachphylaxis to NA with regard to its pressor action, and the substance contracting CR disappears from the blood at the same time. Prolonged infusion of noradrenaline after administration of indomethacin does not contract CR, and tachyphylaxis to the pressor action of NA does not appear. Both phenomena can be reproduced by superimposing intra-arterial infesion of PGE2 (0.25 .mu.g/kg per min) on the noradrenaline infusion. .alpha.-Adrenergic blockade abolishes the pressor effect of noradrenaline and release of PGE into the blood under the influence of noradrenaline infusion, whereas .beta.-adrenergic blockade has no influence on both effects of noradrenaline. Intra-arterial infusion of noradrenaline in low doses into various areas of the vascular system also releases the substance contracting CR and tachyphylaxis.