Mechanisms involved in the relaxant effect of estrogens on rat aorta strips

Rodríguez, J.; Boto, María José García de; Hidalgo, Agustı́n

doi:10.1016/0024-3205(95)02330-5

Cited by 31 publications

(10 citation statements)

References 33 publications

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“…These findings are consistent with previous studies demonstrating that micromolar concentrations of estradiol had minimal effect on aorta strips precontracted with 127 mmol/l KCl [17]. Therefore, estrogen-induced relaxation of rat aorta requires the presence of physiological gradients of potassium and further suggests that this vascular response to estrogen involves potassium channel activity, i.e.…”

Section: Discussionsupporting

confidence: 82%

Estradiol Relaxes Rat Aorta via Endothelium-Dependent and -Independent Mechanisms

Abou-Mohamed¹,

Elmarakby²,

Carrier³

et al. 2003

Pharmacology

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The effects of estrogen on arterial function are heterogeneous with respect to vessel and/or species. We have investigated 17β-estradiol-induced relaxation in isolated rat aorta with regard to the role of the vascular endothelium and ionic mechanisms. Estrogen induced a concentration-dependent relaxation of 46.5 ± 7.9% and 70.1 ± 12.2% (10^–8 and 10^–7M), which was reduced by endothelial denudation. Furthermore, L-nitroarginine methyl ester completely abrogated this effect; however, estradiol did not relax KCl-contracted rings. Tetraethyl ammonium (1 mmol/l) completely blocked estradiol-induced relaxation. Estradiol increased [cGMP] in isolated aortic rings via NO, but did not significantly affect NOS activity in endothelial cells. Thus, estrogen can relax rat aorta in vitro via both endothelium-dependent and -independent mechanisms involving the NO/cGMP and potassium channel signaling system.

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Section: Discussionsupporting

confidence: 82%

Estradiol Relaxes Rat Aorta via Endothelium-Dependent and -Independent Mechanisms

Abou-Mohamed¹,

Elmarakby²,

Carrier³

et al. 2003

Pharmacology

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“…This effect could be related to the aromatase conversion of androgens to estrogens, and, in fact, testosterone treatment reduces estrogen receptor levels in the male rabbit aorta [11]. We have also observed that the synthetic estrogen diethylstilbestrol induces relaxation of male rat aorta strips via endothelium-dependent mechanisms [12] and via direct effects on smooth muscle cells [13]. These effects are produced at pharmacological concentrations, compatible with the one reported for other vascular areas in vitro [14].…”

Section: Introductionsupporting

confidence: 71%

“…The acute relaxation after diethylstilbestrol has components that are endothelium and smooth muscle dependent [12]. The present data demonstrated the influence of the hormonal environment on diethylstilbestrol-induced, NO-mediated, endothelium-dependent relaxation in isolated rat aortae.…”

Section: Discussionmentioning

confidence: 52%

Gonadectomy Eliminates Endothelium-Dependent Diethylstilbestrol-Induced Relaxant Effect in Rat Aorta

Martı́nez¹,

López²,

Hidalgo

et al. 2003

Pharmacology

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The effects of gender and castration of rats on diethylstilbestrol-induced, endothelium-dependent and endothelium-independent relaxation in rat aorta strips were studied. For this, male and female control and castrated rats were used. Diethylstilbestrol elicited a concentration-dependent (1–30 µmol/l) relaxation of isolated rat aorta. The effect was significantly higher in the presence of endothelium in aorta strips of the control group and also in female as compared with male rats. This effect is NO-dependent, since it is inhibited by N^G-methyl-L-arginine. Castration of the rats suppressed the endothelium-dependent relaxation, and it was similar to that induced in the absence of endothelium. Acetylcholine-induced relaxation was not suppressed by castration. The acetylcholine-induced relaxation was decreased in aorta strips previously relaxed by diethylstilbestrol. There are no gender differences in the diethylstilbestrol-induced, endothelium-independent component of the relaxation, nor is it modified by the hormonal environment. Therefore, diethylstilbestrol-induced, endothelium-dependent relaxation in rat aorta strips is modulated by the hormonal status of the rats.

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“…For these authors, the vasorelaxant effect of βES seemed to be more gifted than PRG, however they did not find statistical differences between the IC 50 values calculated for the inhibitory action of the female hormones. In opposition, Rodriguez et al showed that 17α-estradiol, but not βES, relaxes calcium-dependent contractions in rat aortic strip [36] . On the other hand, we previously showed that testosterone and cholesterol also relax rat aorta by inhibiting LTCC [37] .…”

Section: Discussionmentioning

confidence: 99%

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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Mechanisms involved in the relaxant effect of estrogens on rat aorta strips

Cited by 31 publications

References 33 publications

Estradiol Relaxes Rat Aorta via Endothelium-Dependent and -Independent Mechanisms

Estradiol Relaxes Rat Aorta via Endothelium-Dependent and -Independent Mechanisms

Gonadectomy Eliminates Endothelium-Dependent Diethylstilbestrol-Induced Relaxant Effect in Rat Aorta

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

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