In:
Canadian Journal of Physiology and Pharmacology, Canadian Science Publishing, Vol. 79, No. 6 ( 2001-06-01), p. 545-550
Abstract:
The purpose of this study was to assess the direct effect of progesterone on rabbit pulmonary arteries and to examine the mechanism of its action. Rings of pulmonary artery from male rabbits were suspended in organ baths containing Krebs solution, and isometric tension was measured. The response to progesterone was investigated in arterial rings contracted with noradrenaline (NA), KCl, and CaCl 2 . The effects of endothelium, nitric oxide(NO), prostaglandins, cyclic GMP(cGMP), and the adrenergic β-receptor on progesterone-induced relaxation were also assessed. Progesterone inhibited the vasocontractivity to NA, KCl, and CaCl 2 , and relaxed rabbit pulmonary artery. The relaxing response of progesterone in pulmonary artery was significantly reduced by removal of endothelium, inhibitors of nitric oxide synthase and guanylate cyclase, but not by prostaglandin synthase inhibitor and blockage of the adrenergic β-receptor. In Ca 2+ -free (0.1 mM EGTA) Krebs solution, progesterone inhibited NA-induced contraction that was intracellular Ca 2+ -dependent, but didn't affect the contraction of extracellular Ca 2+ -dependent component. Our results suggest that progesterone induces relaxation of isolated rabbit pulmonary arteries partially via NO and cGMP. Progesterone may also inhibit Ca 2+ influx through potential-dependent calcium channels (PDCs) and Ca 2+ release from intracellular stores.Key words: progesterone, pulmonary artery, Ca 2+ channel, endothelium.
Type of Medium:
Online Resource
ISSN:
0008-4212
,
1205-7541
Language:
English
Publisher:
Canadian Science Publishing
Publication Date:
2001
detail.hit.zdb_id:
2004356-9
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