Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta

Castillo, Carlos; Ceballos, Guillermo; Rodríguez, Daniel; Villanueva, Cleva; Medina, R.; López, Jorge Góngora; Méndez, Enrique; Castillo, Enrique

doi:10.1152/ajpcell.00556.2005

Cited by 24 publications

(16 citation statements)

References 24 publications

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“…Also, in endothelium-denuded microvessels, ER agonists inhibited the maintained constriction and [Ca 21 ] i induced by high KCl, supporting inhibition of Ca 21 entry into VSM through voltage-gated Ca 21 channels. This is consistent with reports that E2 decreased KCl-induced Ca 21 influx in an endothelium-denuded rat aorta and coronary artery and rat aortic VSM cells (Freay et al, 1997;Crews and Khalil, 1999;Murphy and Khalil, 2000) and reduced capacitative Ca 21 influx through inhibition of L-type voltage-gated Ca 21 channels (Castillo et al, 2006 (Unemoto et al, 2003). Also, E2 increases BK Ca open probability in uterine artery myocytes and E2-induced uterine artery dilation is attenuated by the K 1 channel blocker TEA (Rosenfeld et al, 2000).…”

Section: Discussionsupporting

confidence: 92%

Estrogen Receptor Subtypes Mediate Distinct Microvascular Dilation and Reduction in [Ca²⁺]_i in Mesenteric Microvessels of Female Rat

Mazzuca

Mata

et al. 2014

J Pharmacol Exp Ther

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Estrogen interacts with estrogen receptors (ERs) to induce vasodilation, but the ER subtype and post-ER relaxation pathways are unclear. We tested if ER subtypes mediate distinct vasodilator and intracellular free Ca 21 concentration ([Ca 21 ] i ) responses via specific relaxation pathways in the endothelium and vascular smooth muscle (VSM). Pressurized mesenteric microvessels from female Sprague-Dawley rats were loaded with fura-2, and the changes in diameter and [Ca 21 ] i in response to 17b-estradiol (E2) (all ERs), PPT (4,49,-pyrazole-1,3,5-triyl]-tris-phenol) (ERa), diarylpropionitrile (DPN) (ERb), and G1 [(6)-1-[(3aR*,4S*,9bS*)-4-(6-bromo-1,3-benzodioxol-5-yl)-3a,4,5,9b-tetrahydro:3H-cyclopenta(c)quinolin-8-yl]-ethanon] (GPR30) were measured. In microvessels preconstricted with phenylephrine, ER agonists caused relaxation and decrease in [Ca 21 ] i that were with E2 5 PPT . DPN . G1, suggesting that E2-induced vasodilation involves ERa . ERb . GPR30. Acetylcholine caused vasodilation and decreased [Ca 21 ] i , which were abolished by endothelium removal or treatment with the nitric oxide synthase blocker N v -nitro-L-arginine methyl ester (L-NAME) and the K 1 channel blockers tetraethylammonium (nonspecific)

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Section: Discussionsupporting

confidence: 92%

Estrogen Receptor Subtypes Mediate Distinct Microvascular Dilation and Reduction in [Ca²⁺]_i in Mesenteric Microvessels of Female Rat

Mazzuca

Mata

et al. 2014

J Pharmacol Exp Ther

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“…In the present study, ER agonists inhibited KCl-induced contraction in the endothelium-denuded carotid, mesenteric, and renal artery of virgin and pregnant rats, supporting inhibition of Ca 2ϩ entry into VSM. This is consistent with reports that E 2 decreased KCl-induced Ca 2ϩ influx in the endothelium-denuded rat aorta, coronary artery, and rat aortic VSM cells (13,22,61) and inhibited Phe-induced capacitative Ca 2ϩ influx in the rat aorta (8) and that E 2 , PPT, and DPN caused relaxation of KCl-induced contraction in endothelium-denuded cephalic, thoracic, and abdominal vessels (72) and vasodilation and decreased [Ca 2ϩ ] i in mesenteric vessels of female rats (51). Importantly, PPT-induced relaxation of KCl-induced contraction was greater in the mesenteric artery of pregnant versus virgin rats, suggesting specific enhancement of ER␣-mediated inhibition of Ca 2ϩ entry mechanisms of vasoconstriction in the mesenteric circulation during pregnancy.…”

Section: Er-mediated Inhibition Of Ca 2ϩsupporting

confidence: 93%

Adaptive increases in expression and vasodilator activity of estrogen receptor subtypes in a blood vessel-specific pattern during pregnancy

Mata

Reslan

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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RA. Adaptive increases in expression and vasodilator activity of estrogen receptor subtypes in a blood vessel-specific pattern during pregnancy. Am J Physiol Heart Circ Physiol 309: H1679 -H1696, 2015. First published September 25, 2015 doi:10.1152/ajpheart.00532.2015.-Normal pregnancy is associated with adaptive hemodynamic, hormonal, and vascular changes, and estrogen (E 2) may promote vasodilation during pregnancy; however, the specific E 2 receptor (ER) subtype, post-ER signaling mechanism, and vascular bed involved are unclear. We tested whether pregnancy-associated vascular adaptations involve changes in the expression/ distribution/activity of distinct ER subtypes in a blood vessel-specific manner. Blood pressure (BP) and plasma E 2 were measured in virgin and pregnant (day 19) rats, and the thoracic aorta, carotid artery, mesenteric artery, and renal artery were isolated for measurements of ER␣, ER␤, and G protein-coupled receptor 30 [G protein-coupled ER (GPER)] expression and tissue distribution in parallel with relaxation responses to E 2 (all ERs) and the specific ER agonist 4,4=,4Љ-(4-propyl-[1H]-pyrazole-1,3,5-triyl)-tris-phenol (PPT; ER␣), diarylpropionitrile (DPN; ER␤), and G1 (GPER). BP was slightly lower and plasma E 2 was higher in pregnant versus virgin rats. Western blots revealed increased ER␣ and ER␤ in the aorta and mesenteric artery and GPER in the aorta of pregnant versus virgin rats. Immunohistochemistry revealed that the increases in ERs were mainly in the intima and media. In phenylephrineprecontracted vessels, E 2 and PPT caused relaxation that was greater in the aorta and mesenteric artery but similar in the carotid and renal artery of pregnant versus virgin rats. DPN-and G1-induced relaxation was greater in the mesenteric and renal artery than in the aorta and carotid artery, and aortic relaxation to G1 was greater in pregnant versus virgin rats. The nitric oxide synthase inhibitor N -nitro-L-arginine methyl ester with or without the cyclooxygenase inhibitor indomethacin with or without the EDHF blocker tetraethylammonium or endothelium removal reduced E 2, PPT, and G1-induced relaxation in the aorta of pregnant rats, suggesting an endothelium-dependent mechanism, but did not affect E 2-, PPT-, DPN-, or G1-induced relaxation in other vessels, suggesting endothelium-independent mechanisms. E 2, PPT, DPN, and G1 caused relaxation of Ca 2ϩ entry-dependent KCl contraction, and the effect of PPT was greater in the mesenteric artery of pregnant versus virgin rats. Thus, during pregnancy, an increase in ER␣ expression in endothelial and vascular smooth muscle layers of the aorta and mesenteric artery is associated with increased ER␣-mediated relaxation via endothelium-derived vasodilators and inhibition of Ca 2ϩ entry into vascular smooth muscle, supporting a role of aortic and mesenteric arterial ER␣ in pregnancyassociated vasodilation. GPER may contribute to aortic relaxation while enhanced ER␤ expression could mediate other genomic vascular effects during pregnancy.

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“…However, these steroids can also relax arterial smooth muscle via endothelium-independent mechanisms, mainly involving modulation of membrane ionic flux [10,11] . This direct vasodilator effect of PRG and βES has been observed in different arteries from different species such as aorta [12,13] , coronary arteries [8,10,14] , cerebral arteries [15] , omental artery [16] , tail artery [17] and mesenteric artery [9,18,19] . The inhibition of Ca 2+ channels and the activation of K + channels was suggested as a leading cause of the sex horNon-genomic vasorelaxant effects of 17β-estradiol and progesterone on rat aorta are mediated by Ltype Ca…”

Section: Introductionmentioning

confidence: 80%

Non-genomic vasorelaxant effects of 17β-estradiol and progesterone in rat aorta are mediated by L-type Ca2+ current inhibition

et al. 2012

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Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta

Abstract: . Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta.

Cited by 24 publications

References 24 publications

Estrogen Receptor Subtypes Mediate Distinct Microvascular Dilation and Reduction in [Ca²⁺]_i in Mesenteric Microvessels of Female Rat

Estrogen Receptor Subtypes Mediate Distinct Microvascular Dilation and Reduction in [Ca²⁺]_i in Mesenteric Microvessels of Female Rat

Adaptive increases in expression and vasodilator activity of estrogen receptor subtypes in a blood vessel-specific pattern during pregnancy

Non-genomic vasorelaxant effects of 17β-estradiol and progesterone in rat aorta are mediated by L-type Ca2+ current inhibition

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Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta

Abstract: . Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta.

Cited by 24 publications

References 24 publications

Estrogen Receptor Subtypes Mediate Distinct Microvascular Dilation and Reduction in [Ca2+]i in Mesenteric Microvessels of Female Rat

Estrogen Receptor Subtypes Mediate Distinct Microvascular Dilation and Reduction in [Ca2+]i in Mesenteric Microvessels of Female Rat

Adaptive increases in expression and vasodilator activity of estrogen receptor subtypes in a blood vessel-specific pattern during pregnancy

Non-genomic vasorelaxant effects of 17β-estradiol and progesterone in rat aorta are mediated by L-type Ca2+ current inhibition

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Estrogen Receptor Subtypes Mediate Distinct Microvascular Dilation and Reduction in [Ca²⁺]_i in Mesenteric Microvessels of Female Rat

Estrogen Receptor Subtypes Mediate Distinct Microvascular Dilation and Reduction in [Ca²⁺]_i in Mesenteric Microvessels of Female Rat