Acute administration of 17β-estradiol reduces endothelin-1 release during pacing-induced ischemia

Rosano, Giuseppe; Gebara, Otávio; Sheiban, Imad; Silvestri, Antonello; Wajngarten, Maurı́cio; Vitale, Cristiana; Aldrighi, José Mendes; Ramires, Antônio F; Mercuro, Giuseppe

doi:10.1016/j.ijcard.2006.03.025

Cited by 9 publications

(7 citation statements)

References 39 publications

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“…The mitogenic contributions of the ET receptor subtypes are different in different types of tumors. Several groups have demonstrated that in epithelial tumors in vitro, the ET-1-induced mitogenic effect is mediated via the ETAR and in nonepithelial tumors in vitro ETBR is involved in this process [17,35,39,41]. The present study showed that even though both ETAR and ETBR are found in LNCaP and PC-3 cells, the mitogenic effect and calcium signaling of ET-1 these cells were mediated predominantly by ETAR.…”

Section: Discussionsupporting

confidence: 48%

“…The results of the present study showed that spontaneous proliferation of unstimulated PC-3 cells was inhibited by the ETAR antagonist BQ123, but not by ETBR antagonist BQ788, suggesting that ET-1 is an autocrine growth factor involved in the regulation of prostate cancer cell proliferation. ET-1 and ETAR not only influence cell proliferation directly but also act synergistically with polypeptide growth factors that are relevant to cancer progression, such as EGF and its receptors [38][39][40]. ET-1 is known to exert its action through activation of ETAR and ETBR, both of which are expressed in many tumor cells.…”

Section: Discussionmentioning

confidence: 99%

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Involvement of Ion Channels in Endothelin-1-induced Signalling in Human Prostate Cancer Cells

Vancauwenberghe¹,

Lallet-Daher²,

Derouiche³

et al. 2016

J Cell Signal

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Section: Discussionsupporting

confidence: 48%

Section: Discussionmentioning

confidence: 99%

Involvement of Ion Channels in Endothelin-1-induced Signalling in Human Prostate Cancer Cells

Vancauwenberghe¹,

Lallet-Daher²,

Derouiche³

et al. 2016

J Cell Signal

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“…56 Estrogen-associated effects estrogens decrease systemic vascular resistance, restore and improve impaired coronary and peripheral endothelial function in postmenopausal women, [57][58][59] and prevent coronary artery spasm and reduce endothelin release from the coronary circulation in women with and without coronary atherosclerosis. 57,[60][61][62] estrogens are also thought to have an effect on vascular tone and development of CVD in men, since estrogen receptor beta (eRβ) expression increases in male animals following vascular balloon injury, 63,64 and men with mutations that result in defective estrogen synthesis or estrogen receptors have reduced endothelial function and premature development of athero sclerosis. [65][66][67][68] estrogen levels in men are greatly dependent on, and derived from, androgen production: nearly 80% of plasma 17β-estradiol derives from aromatization of testo sterone and andro stenedione ( Figure 2).…”

Section: Direct Cardiovascular Effectsmentioning

confidence: 99%

Gender differences in the cardiovascular effect of sex hormones

Vitale

Mendelsohn

Rosano³

2009

Nat Rev Cardiol

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297

194

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The higher incidence of cardiovascular disease in men than in women of similar age, and the menopause-associated increase in cardiovascular disease in women, has led to speculation that gender-related differences in sex hormones have a key role in the development and evolution of cardiovascular disease. Compelling data have indicated that sex differences in vascular biology are determined not only by gender-related differences in sex steroid levels, but also by gender-specific tissue and cellular differences that mediate sex-specific responses. In this Review, we describe the sex-specific effects of estrogen and testosterone on cardiovascular risk, direct vascular effects of these sex hormones, and how these effects influence development of atherosclerosis. Cardiovascular effects of exogenous hormone administration are also discussed. Importantly, evidence has indicated that estrogens alone or in combination with progestins in postmenopausal women increase cardiovascular risk if started late after menopause, but that it possibly has beneficial cardiovascular effects in younger postmenopausal women, although data on long-term testosterone therapy are lacking. Hormone therapy should not be considered solely for primary prevention or treatment of cardiovascular disease at this time.

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“…ET-1 has not only been shown to be derived from endothelial cells, but from cardiomyocytes [28] and is thought to be involved in exercise mediated cardiac hypertrophy [29]. Its main function is to act as a potent and long lasting vasoconstrictor that plays a key role in the regulation of vascular tonus [30,31], therefore changes often reflect variations in blood pressure regulation and blood flow.…”

Section: Discussionmentioning

confidence: 99%

Changes in Endothelial Markers during a Summer Ultra-Endurance Road Cycling Event in the Heat

BR¹

2016

Int J Sports Exerc Med

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Purpose: To assess the impact of completing a 164 km road cycling event performed in a hot environment (Wichita Falls, Texas in August), on endothelial biomarkers and resultant risk of blood clots in men and women.Methods: 37 event participants (28 men and 9 women; 51.8 ± 9.5 y) completed the ride. Plasma samples were collected in the morning before (PRE) and immediately after (IP) completing the ride. Concentrations of endothelial cell markers -endothelin-1 (ET-1), p-selectin, and intercellular adhesion molecule 1 (ICAM1), were measured and associations between changes from PRE-to IP-ride were examined as a function of race event completion time and participant characteristics (demographics and anthropometrics). Results:All of the endothelial cell markers (ET-1, p-selectin, and I-CAM1) increased significantly from PRE to IP. After controlling for PRE values, completion time was positively correlated with ET-1 (r = 0.42, p < 0.01) and negatively related to p-selectin (r = -0.42, p < 0.05). Waist circumference was positively related to ICAM1 (r = 0.34, p < 0.01). In addition, males had greater concentrations of ICAM1 (d = 1.32, p < 0.01) and p-selectin (d = 0.84, p < 0.05) than females. Conclusion:Completing a 164 km road cycling event in hot conditions resulted in increased concentrations of endothelial cell markers in men and women. Although this result may suggest endothelial cell injury, it is unclear whether this response is indicative of an increased risk of blood clot formation.

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Acute administration of 17β-estradiol reduces endothelin-1 release during pacing-induced ischemia

Cited by 9 publications

References 39 publications

Involvement of Ion Channels in Endothelin-1-induced Signalling in Human Prostate Cancer Cells

Involvement of Ion Channels in Endothelin-1-induced Signalling in Human Prostate Cancer Cells

Gender differences in the cardiovascular effect of sex hormones

Changes in Endothelial Markers during a Summer Ultra-Endurance Road Cycling Event in the Heat

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