Effects of acute and chronic estrogenic treatment on vasomotor responses of aortic rings from ovariectomized rats

Paredes-Carbajal, M.C.; Juárez-Oropeza, Marco Antonio; Ortíz-Mendoza, C.M.; Mascher, Dieter

doi:10.1016/0024-3205(95)00281-a

Cited by 35 publications

(30 citation statements)

References 28 publications

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“…This finding is in accordance with previous "ex vivo" studies showing that long-term replacement of estrogen significantly blunted the adrenergic sensitivity of mesenteric arteries (6, 7) and aortic rings (8). In their studies, NO synthase inhibition reverted or lessened the attenuating effect of estrogen on the adrenergic vasoconstrictor responses, suggesting that basal NO release is a major determinant of this phenomenon.…”

Section: Discussionsupporting

confidence: 92%

“…Thus the doses of EV 5 µg and 25 µg used in the present study might have exerted 2.5 and 12.5 times more potent action than the dose used for hormone replacement, respectively. Paredes-Carbajal et al (8) have shown that the contractile responses to phenylephrine in aortic rings excised from OVX rats are not altered before or after (40-60 min) addition of a physiological level of 17β-estradiol (10 9 mol/l), while chronic (11-13 days) treatment with a physiological level of estrogen significantly attenuated the adrenergic vasoconstriction. They speculated that acute administration of estrogen does not increase basal NO release enough to attenuate the adrenergic vasoconstriction, because it takes at least several days for estrogen to increase eNOS mRNA and eNOS activity (21,22).…”

Section: Discussionmentioning

confidence: 97%

“…Estrogen improves vasomotor function of the coronary artery and peripheral vessels in postmenopausal women (4,5). It has also been shown that estrogen attenuates vasoconstrictor responsAlthough some studies have demonstrated that long-term replacement of estrogen attenuates the adrenergic vasoconstrictor responses (6)(7)(8), other studies do not concur (10)(11)(12). This controversy may be in part due to differences in the methods of "ex vivo" measurement of vascular responsiveness and different schemes of estrogen treatment.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Estrogen on Pressor Responses to .ALPHA.1-Adrenoreceptor Agonist in Conscious Female Rats.

et al. 2002

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es to α1-adrenoreceptor agonist (6-8). These effects of estrogen on vasomotor function seem to be largely mediated by augmentation of endothelial nitric oxide (NO) release. Although endothelial NO is released basally as well as in response to various stimuli, including acetylcholine (9), it seems that acute administration of a physiological level of estrogen differently affects basal and stimulated NO release after long-term estrogen withdrawal. Gilligan et al. (4,5) have demonstrated that a physiological level of estrogen rapidly potentiates vasodilator coronary and forearm vascular response to acetylcholine in postmenopausal women. On the other hand, acute administration of physiological level of estrogen does not normalize vasoconstrictor responses to α1-adrenoreceptor agonist, which are largely determined by basal NO release, in ovariectomized (OVX) rats (8).

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Effect of Estrogen on Pressor Responses to .ALPHA.1-Adrenoreceptor Agonist in Conscious Female Rats.

et al. 2002

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“…In previous studies, we demonstrated that the vasorelaxant effects of BcEx are mediated by enhancement of the NO/cGMP system and inhibition of calcium influx into vascular smooth muscle cells [13]. Additionally, carbachol elicits endothelium-dependent, NO-mediated relaxation in isolated rat aortae [29]. In our study, the vasomotor response to carbachol in isolated aortas contracted by NE was reduced in OVX-control rats compared with sham-control rats.…”

Section: Discussionsupporting

confidence: 49%

Black Cohosh (<i>Actaea racemosa</i> L.) Improves Serum Lipid Profiles and Vasomotor Responses in Ovariectomized Rats

Kim¹,

Song²,

Kim³

et al. 2017

JFNR

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We investigated the effects of long-term administration of black cohosh extract (BcEx) on serum lipid profiles and vasomotor responses in ovariectomized (OVX) rats and compared them with those of rats administered 17β-estradiol (E2) or raloxifene, a selective estrogen receptor modulator. Vehicle (OVX-or sham-control), BcEx (0.5 or 3.0 mg/kg/day), E2 (0.5 mg/kg/day), or raloxifene (2.5 mg/kg/day) were injected subcutaneously for 5 weeks, and serum lipid profiles and vasomotor responses were measured at the end of the treatment. BcEx lowered total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels, but did not affect high-density lipoprotein cholesterol or triglyceride (TG) levels. Raloxifene showed a similar effect to that of BcEx, while E2 attenuated the increase in TC and LDL-C levels and significantly increased TG levels. The vascular relaxation induced by carbachol increased significantly in norepinephrine-precontracted aortic rings isolated from BcEx-, E2-, or raloxifene-treated rats. No change in uterine weight was observed in the BcEx-treated group. The raloxifene-treated group showed a similar trend as that of the BcEx-treated group, but E2 significantly increased uterine weight. These results suggest that long-term administration of BcEx behaves similar to the selective estrogen receptor modulator raloxifene.

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“…Notably, short-term hydrocortisone exposure mediated an enhancement of vasoconstrictor response-consistent with the findings of others. 26,27 17␤-Estradiol has previously been demonstrated to "nongenomically" enhance vasorelaxation and attenuate vasoconstriction, 28,29 ie, effects comparable to those of aldosterone. However, these previously reported effects of estradiol were seen at much higher concentrations (nmol/L to mol/L) than those used in the present studies.…”

Section: Discussionmentioning

confidence: 99%

Aldosterone Regulates Vascular Reactivity

et al. 2003

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Background-There is increasing evidence for rapid nongenomic effects of aldosterone. Therefore, we studied the immediate effects of aldosterone on vascular reactivity in rat aortic ring segments and on endothelial and vascular smooth muscle cellular responses. Methods and Results-In endothelium-intact ring segments, aldosterone attenuated phenylephrine-mediated constriction (maximal reduction, 25Ϯ4% below control phenylephrine-mediated constriction). In contrast, in endothelium-denuded vessels, aldosterone mediated a monophasic dose-dependent enhancement of vasoconstrictor response. In endothelial cells, aldosterone caused a phosphatidylinositol 3-kinase (PI3K)-dependent increase in nitric oxide synthase activity as well as PI3K-dependent activation of extracellular signal-regulated kinase 1/2 and p70 S6 kinase. Conclusions-Overall, these data support a novel effect of aldosterone on vascular endothelial and smooth muscle cell function. These rapid effects of aldosterone might be important in both the short-and long-term regulation of peripheral vascular resistance. Furthermore, in the setting of endothelial dysfunction, alterations in aldosterone's short-term vascular responses might contribute to its pathophysiological effects in cardiovascular disease. (Circulation. 2003;108: 2400-2406.)

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Effects of acute and chronic estrogenic treatment on vasomotor responses of aortic rings from ovariectomized rats

Cited by 35 publications

References 28 publications

Effect of Estrogen on Pressor Responses to .ALPHA.1-Adrenoreceptor Agonist in Conscious Female Rats.

Effect of Estrogen on Pressor Responses to .ALPHA.1-Adrenoreceptor Agonist in Conscious Female Rats.

Black Cohosh (<i>Actaea racemosa</i> L.) Improves Serum Lipid Profiles and Vasomotor Responses in Ovariectomized Rats

Aldosterone Regulates Vascular Reactivity

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