Mechanisms of relaxation of rat aorta in response to progesterone and synthetic progestins
| Autor: | S Wagner, M Oettel, E Glusa, T Gräser |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Chlormadinone Acetate Endothelium Muscle Relaxation Vasodilator Agents Aorta Thoracic Vasodilation Muscle Smooth Vascular General Biochemistry Genetics and Molecular Biology Glibenclamide Phenylephrine Chlormadinone acetate chemistry.chemical_compound Hormone Antagonists Internal medicine medicine Animals Nandrolone Vasoconstrictor Agents Rats Wistar Fulvestrant Progesterone Estradiol Progesterone Congeners Voltage-dependent calcium channel business.industry Estrogen Antagonists Obstetrics and Gynecology Potassium channel Rats Endocrinology medicine.anatomical_structure Verapamil chemistry Endothelium Vascular Norethindrone business Muscle Contraction medicine.drug |
| Zdroj: | Maturitas. 28:181-191 |
| ISSN: | 0378-5122 |
| DOI: | 10.1016/s0378-5122(97)00057-1 |
| Popis: | To compare the acute effects of progesterone, chlormadinone acetate (CMA), norethisterone acetate (NETA) and dienogest (DNG) with those of 17 beta-estradiol (17 beta-E2) on the vascular reactivity of male rat thoracic aorta.Aortic rings with or without endothelium were placed in an organ bath for isometric tension recording. The integrity of the endothelium was assessed by the relaxant response of precontracted rings to acetylcholine (1 and 10 microM), which was diminished after mechanical removal of the endothelium. The concentrations of the steroid hormones were 0.01-10 microM.In vessels precontracted with phenylephrine (1 microM), CaCl2 (3 mM) or KCl (30 mM), progesterone, CMA and NETA (10 microM each) an endothelium-independent relaxation of 20-35% resulted, with a maximum response after 20-30 min, while DNG had a negligible effect in all experiments. The same concentration of 17 beta-E2 was twice as potent as the progestins. Indomethacin, the cyclooxygenase inhibitor and glibenclamide, an inhibitor of the ATP-sensitive potassium channels, did not affect the relaxant responses. The antagonists of progesterone receptors J 867 (1 microM) as well as of estrogen receptors ICI 182780 (1 microM) did not counteract the relaxation induced by progesterone and 17 beta-E2, respectively. Progesterone (10 microM) did not interfere with endothelium-dependent acetylcholine-induced relaxation of precontracted aortic rings. Pretreatment of the vessels with the hormones attenuated the maximal contractile response to phenylephrine. In the presence of verapamil (1 microM) or progesterone (10 microM) or 17 beta-E2 (1 and 10 microM) the concentration-response curves for calcium-induced contractions in K(+)-depolarized vessels were shifted to the right, with suppression of the maximum response.These studies suggest that in addition to 17 beta-E2 the progestins, progesterone, CMA and NETA caused a reduction of vascular tone, probably due to blockade of voltage-dependent and/or receptor-operated calcium channels. |
| Databáze: | OpenAIRE |
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