1999
DOI: 10.1161/01.hyp.34.4.931
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Gender Differences in Ca 2+ Entry Mechanisms of Vasoconstriction in Wistar-Kyoto and Spontaneously Hypertensive Rats

Abstract: Abstract-We investigated whether putative vascular protection against hypertension in females reflects differences in the Ca 2ϩ mobilization mechanisms of vasoconstriction depending on the gender and the status of the gonads. Active stress and 45 Ca 2ϩ influx were measured in aortic strips isolated from intact and gonadectomized male and female Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR

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Cited by 43 publications
(62 citation statements)
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“…Consistent with results reported by others in rat aorta [15][16][17], we demonstrated a higher maximal relaxation to acetylcholine, and a lower contractile response to phenylephrine and less sensitivity to angiotensin II in aortae from females compared to males. Estrogen deficiency was shown to augment contractions to angiotensin II, with AT 1 receptor overexpression, and phenylephrine, which is reversed by estrogen substitution therapy, in isolated aortic rings from female rats [16,17]. Administration of estrogen for 7 days to male and female rats was demonstrated to increase endothelial relaxation or suppress the contractions most likely by increasing production of endothelial nitric oxide [22][23][24].…”
Section: Discussionsupporting
confidence: 93%
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“…Consistent with results reported by others in rat aorta [15][16][17], we demonstrated a higher maximal relaxation to acetylcholine, and a lower contractile response to phenylephrine and less sensitivity to angiotensin II in aortae from females compared to males. Estrogen deficiency was shown to augment contractions to angiotensin II, with AT 1 receptor overexpression, and phenylephrine, which is reversed by estrogen substitution therapy, in isolated aortic rings from female rats [16,17]. Administration of estrogen for 7 days to male and female rats was demonstrated to increase endothelial relaxation or suppress the contractions most likely by increasing production of endothelial nitric oxide [22][23][24].…”
Section: Discussionsupporting
confidence: 93%
“…Moreover, the female sex hormone estrogen seems to be involved in the regulation of vascular tension because estrogen, at physiological concentrations, causes relaxation by activating nitric oxide synthesis, which may lead to gender-related differences [21]. Consistent with results reported by others in rat aorta [15][16][17], we demonstrated a higher maximal relaxation to acetylcholine, and a lower contractile response to phenylephrine and less sensitivity to angiotensin II in aortae from females compared to males. Estrogen deficiency was shown to augment contractions to angiotensin II, with AT 1 receptor overexpression, and phenylephrine, which is reversed by estrogen substitution therapy, in isolated aortic rings from female rats [16,17].…”
Section: Discussionsupporting
confidence: 91%
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“…In comparison, ER-mediated relaxation in the carotid, mesenteric, and renal artery appears to mainly involve an endothelium-independent mechanism in VSM because 1) E 2 -, PPT-, DPN-, and G1-induced relaxation of the carotid, mesenteric, and renal artery was not blocked by L-NAME, indomethacin, TEA, or endothelium removal; 2) ER agonist-induced relaxation was still greater in the mesenteric and renal artery and in the carotid artery than in the aorta even after treatment with blockers of endothelium-derived vasodilators or endothelium removal; and 3) immunohistochemistry showed ER␣, ER␤, and GPER in the tunica media and VSM of the aorta, carotid artery, mesenteric artery, and renal artery of pregnant rats. These data are consistent with reports that E 2 causes relaxation of the endothelium-denuded aorta and coronary artery (13,14,31), and inhibits Phe-and PGF 2␣ -induced contraction in VSM cells from the rat aorta and porcine coronary artery (60,61).…”
Section: Pregnancy-and E 2 /Er-related Adaptations In Vascular Functionsupporting
confidence: 92%
“…Membrane depolarization by high KCl mainly stimulates Ca 2+ entry from the extracellular space (28). Reports that KCl-induced smooth muscle contraction, Ca 2+ infl ux and [Ca 2+ ] i are greater in males than females further support possible gender differences in the Ca 2+ -entry mechanisms (29,30). These results support our observation.…”
Section: Discussionmentioning
confidence: 95%