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Aim： The sex hormones 17β-estradiol （13ES） and progesterone （PRG） induce rapid non-genomic vasodilator effects which could be protective for the cardiovascular system. The purpose of this study was to analyze the mechanisms underlying their vasodilator effect in rat aortic smooth muscle preparations. Methods： Endothelium-denuded aorta artery rings were prepared from male Wistar rats and incubated in an organ bath. The contractions of the preparation were recorded through isometric transducers. The effects of the hormones on K^＋ current and L-type Ca^2＋ current （LTCC） were analyzed by using the whole cell voltage-clamp technique in A7r5 cells. Results： Both βES and PRG （1-100 pmol/L） concentration-dependently relaxed the endothelium-denuded aortic rings contracted by （-）-Bay K8644 （0.1 IJmol/L） or by KCl （60 mmol/L）. The IC5o values of the two hormones were not statistically different. The Kvchannel blocker 4-aminopyridine （2 mmol/L）, BKca channel blocker tetraethylammonium （lmmol/L） and KATP channel blocker glibenclamide （10 pmol/L） did not significantly modify the relaxant effect of the hormones. On the other hand, the blockage of the intracellular 13ES and PRG receptors with estradiol receptor antagonists ICI 182,780 （1 pmol/L） and PRG receptor antagonist mifepristone （30 pmol/L）, respectively, did not significantly modify the relaxant action of the hormones. In A7r5 cells, both the hormones （1-100 pmol/L） rapidly and reversibly inhibited the basal and BAY-stimulated LTCC. However, these hormones had no effect on the basal K^＋ current. Conclusion： The vasorelaxant effects of 13ES and PRG are due to the inhibition of LTCC. The K^＋ channels are not involved in the effects.

Aim: The sex hormones 17β-estradiol (βES) and progesterone (PRG) induce rapid non-genomic vasodilator effects which could be protective for the cardiovascular system. The purpose of this study was to analyze the mechanisms underlying their vasodilator effect in rat aortic smooth muscle preparations. Methods: Endothelium-denuded aorta artery rings were prepared from male Wistar rats and incubated in an organ bath. The contractions of the preparation were recorded through isometric transducers. The effects of the hormones on K + current and L-type Ca 2+ current (LTCC) were analyzed by using the whole cell voltage-clamp technique in A7r5 cells. Results: Both βES and PRG (1–100 μmol/L) concentration-dependently relaxed the endothelium-denuded aortic rings contracted by (–)-Bay K8644 (0.1 μmol/L) or by KCl (60 mmol/L). The IC 50 values of the two hormones were not statistically different. The K V channel blocker 4-aminopyridine (2 mmol/L), BK Ca channel blocker tetraethylammonium (1mmol/L) and K ATP channel blocker glibenclamide (10 μmol/L) did not significantly modify the relaxant effect of the hormones. On the other hand, the blockage of the intracellular βES and PRG receptors with estradiol receptor antagonists ICI 182,780 (1 μmol/L) and PRG receptor antagonist mifepristone (30 μmol/L), respectively, did not significantly modify the relaxant action of the hormones. In A7r5 cells, both the hormones (1–100 μmol/L) rapidly and reversibly inhibited the basal and BAY-stimulated LTCC. However, these hormones had no effect on the basal K + current. Conclusion: The vasorelaxant effects of βES and PRG are due to the inhibition of LTCC. The K + channels are not involved in the effects.

Aim: The sex hormones 17 beta -estradiol ( beta ES) and progesterone (PRG) induce rapid non-genomic vasodilator effects which could be protective for the cardiovascular system. The purpose of this study was to analyze the mechanisms underlying their vasodilator effect in rat aortic smooth muscle preparations. Methods: Endothelium-denuded aorta artery rings were prepared from male Wistar rats and incubated in an organ bath. The contractions of the preparation were recorded through isometric transducers. The effects of the hormones on K super(+) current and L-type Ca super(2+) current (LTCC) were analyzed by using the whole cell voltage-clamp technique in A7r5 cells. Results: Both beta ES and PRG (1-100 mu mol/L) concentration-dependently relaxed the endothelium-denuded aortic rings contracted by (-)-Bay K8644 (0.1 mu mol/L) or by KCl (60 mmol/L). The IC sub(50) values of the two hormones were not statistically different. The K sub(V) channel blocker 4-aminopyridine (2 mmol/L), BK sub(Ca) channel blocker tetraethylammonium (1mmol/L) and K sub(ATP) channel blocker glibenclamide (10 mu mol/L) did not significantly modify the relaxant effect of the hormones. On the other hand, the blockage of the intracellular beta ES and PRG receptors with estradiol receptor antagonists ICI 182,780 (1 mu mol/L) and PRG receptor antagonist mifepristone (30 mu mol/L), respectively, did not significantly modify the relaxant action of the hormones. In A7r5 cells, both the hormones (1-100 mu mol/L) rapidly and reversibly inhibited the basal and BAY-stimulated LTCC. However, these hormones had no effect on the basal K super(+) current. Conclusion: The vasorelaxant effects of beta ES and PRG are due to the inhibition of LTCC. The K super(+) channels are not involved in the effects.

The sex hormones 17[beta]-estradiol ([beta]ES) and progesterone (PRG) induce rapid non-genomic vasodilator effects which could be protective for the cardiovascular system. The purpose of this study was to analyze the mechanisms underlying their vasodilator effect in rat aortic smooth muscle preparations. Endothelium-denuded aorta artery rings were prepared from male Wistar rats and incubated in an organ bath. The contractions of the preparation were recorded through isometric transducers. The effects of the hormones on K(+) current and L-type Ca(2+) current (LTCC) were analyzed by using the whole cell voltage-clamp technique in A7r5 cells. Both [beta]ES and PRG (1-100 μmol/L) concentration-dependently relaxed the endothelium-denuded aortic rings contracted by (-)-Bay K8644 (0.1 μmol/L) or by KCl (60 mmol/L). The IC(50) values of the two hormones were not statistically different. The K(V) channel blocker 4-aminopyridine (2 mmol/L), BK(Ca) channel blocker tetraethylammonium (1 mmol/L) and K(ATP) channel blocker glibenclamide (10 μmol/L) did not significantly modify the relaxant effect of the hormones. On the other hand, the blockage of the intracellular [beta]ES and PRG receptors with estradiol receptor antagonists ICI 182,780 (1 μmol/L) and PRG receptor antagonist mifepristone (30 μmol/L), respectively, did not significantly modify the relaxant action of the hormones. In A7r5 cells, both the hormones (1-100 μmol/L) rapidly and reversibly inhibited the basal and BAY-stimulated LTCC. However, these hormones had no effect on the basal K(+) current. The vasorelaxant effects of [beta]ES and PRG are due to the inhibition of LTCC. The K(+) channels are not involved in the effects.