Isoproterenol amplifies 17β-estradiol-mediated vasorelaxation: role of endothelium/nitric oxide and cyclic AMP

Chan, Hoi Yun; Yao, Xiaoqiang; Tsang, Suk Ying; Bourreau, Jean-Pierre; Chan, F.H.Y.; Huang, Yü

doi:10.1016/s0008-6363(01)00498-9

Cited by 8 publications

(3 citation statements)

References 31 publications

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“…It seems that the reactivity of smooth muscle to NO was therefore not impaired by a maternal low-protein diet. It is known that isoprenaline induced vasodilatation not only by the direct action on smooth muscle cells but also by stimulating endothelial ␤ 2 -adorenoceptors resulting in elevation basal nitric oxide release via a cAMP-dependent mechanism on the endothelium (37,38). But according to some papers, these responses are different depend on vessels or endocrine environment (38,39).…”

Section: Discussionmentioning

confidence: 99%

Does Estrogen Affect the Development of Abnormal Vascular Function in Offspring of Rats Fed a Low-Protein Diet in Pregnancy?

et al. 2006

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It is established that there are gender-related differences in the effects on offspring blood pressure induced by maternal protein restriction in animal studies. Since such effects may depend on estrogen levels, we hypothesized that lower estrogen would induce an earlier onset of hypertension caused by maternal under-nutrition. Wistar rats were fed a diet containing either 18% (C) or 9% (R) casein throughout pregnancy. Half of the offspring in both C and R groups were ovariectomized on day 50 (CX, RX), and the other half underwent a sham operation (CO, RO). On d 175, offspring were killed for small artery reactivity and histologic investigation. Birth weight and later growth were not significantly different between C and R. RX had higher systolic blood pressure than CX on d125, but no difference was seen between RO and CO. On d 175, systolic blood pressure was higher in R than in C, whether or not ovariectomized. Dilator responses to acetylcholine and bradykinin in small mesenteric arteries were significantly attenuated in RX, although responses to SNP and isoprenaline showed no attenuation in R. The ratio of coronary peri-vascular fibrosis to total vascular area was higher in R, and the fibrosis became prominent in ovariectomized rats. These findings suggest that estrogen plays an important role in limiting the elevation of offspring blood pressure induced by maternal under-nutrition, possibly via BK-mediated mechanisms. The processes may underlie gender and life course patterns of hypertension and also the developmental origins of this disease.

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Section: Discussionmentioning

confidence: 99%

Does Estrogen Affect the Development of Abnormal Vascular Function in Offspring of Rats Fed a Low-Protein Diet in Pregnancy?

et al. 2006

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“…These interesting findings reveal a novel intracellular signal transduction pathway different from those being dependent on ERα. On the other hand, it was reported that the estradiol‐elicited acute relaxation of isolated mesenteric arteries is mediated by NO and is abolished by ICI, 182780 and Rp‐cAMPS triethylamine, suggesting that the response is cyclic AMP‐dependent (36). Indeed, estradiol rapidly activates adenylyl cyclase activity and increases cAMP production, which is blocked by an ER antagonist, but not by cyclohexamide, suggesting further that these effects are also mediated via nongenomic, but ER‐linked mechanisms (59,69).…”

Section: Mechanisms Of the Vascular Actions Of Estrogenmentioning

confidence: 99%

Gender‐Specific Regulation of Cardiovascular Function: Estrogen as Key Player

Huang

Kaley

2004

Microcirculation

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This review provides an overview of gender-specific differences in the incidence and development of cardiovascular diseases, including hypertension, atherosclerosis, heart failure and the corresponding myocardial remodeling. The review discusses the possible mechanisms by which estrogen affords a beneficial effect on cardiovascular function via genomic vs non genomic regulation; estrogen receptor-dependent vs estrogen receptor-independent pathways, specific signal transduction cascades, especially those involving protein kinase B (Akt) and mitogen activated protein kinase (MAPK), as well as their downstream targets, such as nitric oxide synthase, cyclooxygenase, cytochrome P450 (CYP), NADPH oxidase and superoxide dismutase. Having considered the essential role of the microcirculation in the control of vascular resistance in vivo, estrogen-related regulation of microvascular function and blood pressure is highlighted. Attention is focused on the effects of estrogen on pressure (myogenic)-dependent and flow/shear stress-dependent mechanisms of arterioles, which contribute significantly to the control of local blood flow and peripheral resistance via alterations in the release of endothelial mediators, such as nitric oxide, prostaglandins and endothelium-derived hyperpolarizing factor.

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“…Another explanation is that raloxifene is directly able to potentiate vasodilator effectiveness. Interaction between agonists to influence positively endothelial function has been demonstrated (Bell et al , 1995; Wang et al , 1995, 1996; Chan et al , 2002).…”

Section: Introductionmentioning

confidence: 99%

Therapeutic concentrations of raloxifene augment nitric oxide‐dependent coronary artery dilatation in vitro

Leung

Yung

Leung

et al. 2007

British J Pharmacology

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Background and purpose: Raloxifene improves cardiovascular function. This study examines the hypothesis that therapeutic concentrations of raloxifene augment endothelium-dependent relaxation via up-regulation of eNOS expression and activity in porcine coronary arteries. Experimental approach: Isometric tension was measured in rings from isolated arteries. Intracellular Ca 2 þ concentrations ([Ca 2 þ ] i ) in arterial endothelial cells were detected by Ca 2 þ fluorescence imaging. Phosphorylation of eNOS at Ser-1177 was assayed by Western blot analysis. Key results: In arterial rings pre-contracted with 9,11-dideoxy-11a,9a-epoxy-methano-prostaglandin F 2a (U46619), treatment with raloxifene (1-3 nM) augmented bradykinin-or substance P-induced relaxation and this effect was antagonized by ICI 182,780, an estrogen receptor antagonist. The enhanced relaxation was abolished in rings treated with inhibitors of nitric oxide/cyclic GMP-dependent dilation, N G -nitro-L-arginine methyl ester (L-NAME) plus 1H-[1,2,4]oxadizolo[4,3-a]quinoxalin-1-one (ODQ). In contrast, effects of raloxifene were unaffected after inhibition of endothelium-derived hyperpolarizing factors by charybdotoxin plus apamin. Raloxifene (3 nM) did not influence endothelium-independent relaxation to sodium nitroprusside. 17 -Estradiol (3-10 nM) also enhanced bradykinin-induced relaxation, which was inhibited by ICI 182,780. Treatment with raloxifene (3 nM) did not affect bradykinin-stimulated rise in endothelial cell [Ca 2 þ ] i . Raloxifene, 17 -estradiol, and bradykinin increased eNOS phosphorylation at Ser-1177 and ICI 182,780 prevented effects of raloxifene or 17 -estradiol but not that of bradykinin. Raloxifene had neither additive nor antagonistic effects on 17 -estradiol-induced eNOS phosphorylation. Conclusions and implications: Raloxifene in therapeutically relevant concentrations augmented endothelial function in porcine coronary arteries in vitro through ICI 182,780-sensitive mechanisms that were associated with increased phosphorylation of eNOS but independent of changes in endothelial cell [Ca 2 þ ] i .

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Isoproterenol amplifies 17β-estradiol-mediated vasorelaxation: role of endothelium/nitric oxide and cyclic AMP

Cited by 8 publications

References 31 publications

Does Estrogen Affect the Development of Abnormal Vascular Function in Offspring of Rats Fed a Low-Protein Diet in Pregnancy?

Does Estrogen Affect the Development of Abnormal Vascular Function in Offspring of Rats Fed a Low-Protein Diet in Pregnancy?

Gender‐Specific Regulation of Cardiovascular Function: Estrogen as Key Player

Therapeutic concentrations of raloxifene augment nitric oxide‐dependent coronary artery dilatation in vitro

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