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The Effect of17 beta-Estradiol on Rat alpa 1D Adrenergic Receptor Density and Vascular Smooth Muscle Contractility.

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The incidence of hypertension in menopausal and post menopausal women related to plasma estrogen level and sympathetic nervous activity. Estrogenmay have a specific effect to modulate adrenergic vasoconstriction by modulating adrenergic receptors. Blood vessels contractility is regulated mainly by the sympathetic nervous system, in aorta mediated particularly by α1D adrenergic receptor. We hypothesize that 17ß estradiol decreases vascular smooth muscle contractility by decreasing α1D adrenergic receptor density. To prove the above mechanism in the present study we performed several interrelated assays, i.e biossays, i.e bioassay using isolated organ and protein blotting. An isolated rat aorticring without endothelium (2-3 month, 150-200 garm) was incubated in 17ß-estradiol (10 pangkat-5 M, and 10 pangkat-3 M0 for two hours prior to stimulation using phenylephrine as α1D adrenergic receptor agonist was measured as the subsequent change on aortic contractility using bioassay, and the change of α1D adrenergic receptor agonist was measured as the subsequent change on aortic contraction significantly as a response to stimulation of phenylephrine (=0.000). It is demonstrated as the higher level of 17ß-estradiol, the more Emax of phenylephrine decreased without altering ED50 and pD2D also the mount density of α1D adrenergic receptor. To conclude, in the present study it is proved that 17ß-estradiol decreased aortic muscle contractility is associated with the decrease of the density of αD1-adreased aortic smooth muscle contractility which is associated with the decrease of the density of α1-adrenergic receptor.

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Series Title

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Call Number

Jurnal Kedokteran Brawijaya, 24(2):90-96

Publisher

Mataram : Fk. Universitas Brawijaya., 2008

Collation

4p.

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ISBN/ISSN

0216-9347

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Subject(s)

rats
RECEPTOSS, ADRENERGIC
STRADIOL

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