Orchidectomy enhances the expression of endothelin-1 and ET&lt;sub&gt;B&lt;/sub&gt; receptors in rat portal vein

Rossignoli, Patrícia de Souza; Lábio, Roger Willian de; Payão, Spencer Luíz Marques; Pereira, Oduvaldo Câmar Marques; Chies, Agnaldo Bruno

doi:10.1540/jsmr.50.85

Cited by 6 publications

(5 citation statements)

References 20 publications

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“…This effect is abolished by progestins, suggesting that progestins may oppose the beneficial effects of estrogen on the arterial wall [110]. In portal veins, expression of ET B receptors and ET-1 levels are enhanced in orchidectomized rats, and testosterone-replacement therapy completely reversed this effect [111]. …”

Section: Sex Differences In the Et-1 Systemmentioning

confidence: 99%

Role of the endothelin system in sexual dimorphism in cardiovascular and renal diseases

et al. 2016

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Epidemiological studies of blood pressure in men and women and in experimental animal models point to substantial sex differences in the occurrence of arterial hypertension as well as in the various manifestations of arterial hypertension, including myocardial infarction, stroke, retinopathy, chronic kidney failure, as well as hypertension-associated diseases (e.g. diabetes mellitus). Increasing evidence demonstrates that the endothelin (ET) system is a major player in the genesis of sex differences in cardiovascular and renal physiology and diseases. Sex differences in the ET system have been described in the vasculature, heart and kidney of humans and experimental animals. In the current review, we briefly describe the role of the ET system in the cardiovascular and renal systems. We also update information on sex differences at different levels of the ET system including synthesis, circulating and tissue levels, receptors, signaling pathways, ET actions, and responses to antagonists in different organs that contribute to blood pressure regulation. Knowledge of the mechanisms underlying sex differences in arterial hypertension can impact therapeutic strategies. Sex-targeted and/or sex-tailored approaches may improve treatment of cardiovascular and renal diseases.

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Section: Sex Differences In the Et-1 Systemmentioning

confidence: 99%

Role of the endothelin system in sexual dimorphism in cardiovascular and renal diseases

et al. 2016

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“…Testosterone treatment increased ET-1 constriction of porcine coronary artery rings [45]. ORX increased expression of ET A and ET B receptors in the rat portal veins, and this increase was completely reversed by testosterone replacement [46]. Human data suggest that androgen suppression improves skin microcirculatory vasodilator responsiveness to local heating in polycystic ovary syndrome via ET A and ET B receptors [47].…”

Section: Discussionmentioning

confidence: 99%

Afferent arteriole responsiveness to endothelin receptor activation: does sex matter?

et al. 2019

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BackgroundThe pathogenesis of hypertension is distinct between men and women. Endothelin-1 (ET-1) is a potential contributor to sex differences in the pathophysiology of hypertension. ET-1 participates in blood pressure regulation through activation of endothelin A (ETA) and endothelin B (ETB) receptors including those in the vasculature. Previous studies demonstrated that sex and sex hormones evoke discrepancies in ET-1-mediated control of vascular tone in different vascular beds. However, little is known about sex- and sex hormone-related differences in ET-1-dependent renal microvascular reactivity. Accordingly, we hypothesized that loss of sex hormones impairs afferent arteriole reactivity to ET-1.MethodsMale and female Sprague Dawley rats were subjected to gonadectomy or sham surgery (n = 6/group). After 3 weeks, kidneys from those rats were prepared for assessment of renal microvascular responses to ET-1 (ETA and ETB agonist, 10−12 to 10−8 M) and sarafotoxin 6c (S6c, ETB agonist, 10−12 to 10−8 M) using the blood-perfused juxtamedullary nephron preparation.ResultsControl afferent arteriole diameters at 100 mmHg were similar between sham male and female rats averaging 14.6 ± 0.3 and 15.3 ± 0.3 μm, respectively. Gonadectomy had no significant effect on control arteriole diameter. In sham males, ET-1 produced significant concentration-dependent decreases in afferent arteriole diameter, with 10−8 M ET-1 decreasing diameter by 84 ± 1%. ET-1 induced similar concentration-dependent vasoconstrictor responses in sham female rats, with 10−8 M ET-1 decreasing the diameter by 82 ± 1%. The afferent arteriolar vasoconstrictor responses to ET-1 were unchanged by ovariectomy or orchiectomy. Selective ETB receptor activation by S6c induced a concentration-dependent decline in afferent arteriole diameter, with 10−8 M S6c decreasing diameter by 77 ± 3 and 76 ± 3% in sham male and female rats, respectively. Notably, ovariectomy augmented the vasoconstrictor response to S6c (10−12 to 10−9 M), whereas orchiectomy had no significant impact on the responsiveness to ETB receptor activation.ConclusionThese data demonstrate that sex does not significantly influence afferent arteriole reactivity to ET receptor activation. Gonadectomy potentiated the responsiveness of the afferent arteriole to ETB-induced vasoconstriction in females, but not males, suggesting that female sex hormones influence ETB-mediated vasoconstriction in the renal microcirculation.

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“…[49][50][51] Thus, it appears that ET system is modulated in maternal HFD exposure model and may contribute to the cerebrovascular dysfunction, but specific receptor distribution, receptor affinity, signaling cascades mediating contraction have not been studied. Although maternal diet-induced programing of ET-1 system may be associated with the changed plasma gonadal hormone level, 52 stress hormone 53 and glucose metabolism, 21 the underlying mechanisms remain to be fully established.…”

Section: Discussionmentioning

confidence: 99%

Maternal high-fat diet programs cerebrovascular remodeling in adult rat offspring

Lin

Zhou

et al. 2017

J Cereb Blood Flow Metab

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Maternal environmental factors such as diet have consequences on later health of the offspring. We found that maternal high-fat diet (HFD) exposure renders adult offspring brain more susceptible to ischemic injury. The present study was further to investigate whether HFD consumption during rat pregnancy and lactation influences the cerebral vasculature in adult male offspring. Besides the endothelial damage observed in the transmission electron microscopy, the MCAs of offspring from fat-fed dams fed with control diet (HFD/C) also displayed increased wall thickness and media/lumen ratio, suggesting that cerebrovascular hypertrophy or hyperplasia occurs. Moreover, smaller lumen diameter and elevated myogenic tone of the MCAs over a range of intralumenal pressures indicate inward cerebrovascular remodeling in HFD/C rats, with a concomitant increase in vessel stiffness. More importantly, both wire and pressure myography demonstrated that maternal HFD intake also enhanced the MCAs contractility to ET-1, accompanied by increases in ET types A receptor (ETR) but not B (ETR) density in the arteries. Furthermore, ETR antagonism but not ETR antagonism restored maternal HFD-induced cerebrovascular dysfunction in adult offspring. Taken together, maternal diet can substantially influence adult offspring cerebrovascular health, through remodeling of both structure and function, at least partially in an ET-1 manner.

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Orchidectomy enhances the expression of endothelin-1 and ET<sub>B</sub> receptors in rat portal vein

Cited by 6 publications

References 20 publications

Role of the endothelin system in sexual dimorphism in cardiovascular and renal diseases

Role of the endothelin system in sexual dimorphism in cardiovascular and renal diseases

Afferent arteriole responsiveness to endothelin receptor activation: does sex matter?

Maternal high-fat diet programs cerebrovascular remodeling in adult rat offspring

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