Estrogen therapy may counterbalance eutrophic remodeling of coronary arteries and increase bradykinin relaxation in a rat model of menopausal hypertension

Abstract

Objective:Hypertension causes adverse remodeling and vasomotor alterations in coronaries. Hormones such as estrogen may help counterbalance some of these effects. The aim of this study was to analyze the effects of ovariectomy and estrogen therapy in a rat model of menopausal hypertension induced by angiotensin II (AII).Methods:We investigated diameter, tone, and mechanics of intramural coronaries taken from ovariectomized female rats (n = 11) that received chronic AII treatment to induce hypertension, and compared the results with those found in female rats that were also given estrogen therapy (n = 11). The “hypertensive control” group (n = 11) underwent an abdominal sham operation, and received AII. After 4 weeks of AII treatment, side branches of left anterior descendent coronary (approximately 200 μm in diameter) were isolated, cannulated with plastic microcannulas at both ends, and studied in vitro in a vessel chamber. The inner and outer diameter of the arteries were measured by microangiometry, and spontenuous tone, wall thickness, wall cross-sectional area, tangential stress, incremental distensibility, circumferential incremental elastic modulus, thromboxane agonist-induced tone, and bradykinin-induced dilation were calculated.Results:In hypertension, intramural small coronaries show inward eutrophic remodeling after ovariectomy comparing with hypertensive controls. Estrogen therapy had an opposite effect on vessel diameter. Hormone therapy led to an increase in spontaneous tone, allowing for greater dilatative capacity.Conclusions:Estrogen may therefore be considered to counterbalance some of the adverse changes seen in the wall of intramural coronaries in the early stages of chronic hypertension.

Sexual dimorphic response to rituximab treatment: A longitudinal observational study in a large cohort of patients with primary membranous nephropathy and persistent nephrotic syndrome

“…Indeed, female hormones such as estrogens have profound effects on the renin-angiotensin (Baylis, 2009(Baylis, , 2012Xue et al, 2013;Herak-Kramberger et al, 2015;Pringle et al, 2015;Kafami et al, 2016;Lu et al, 2016;Mompeón et al, 2016) and endothelin (Kittikulsuth et al, 2013) systems, thus affecting glomerular hemodynamic. Other potential mechanisms include the receptor-mediated effects of estrogens on TGF-β signaling (Kim et al, 2014), which in turn regulates glomerular cell proliferation (Kim et al, 2016), matrix accumulation (Li et al, 2014), apoptosis (Doublier et al, 2011), and antioxidant capacity (Pérez-Torres et al, 2009;Matrai et al, 2016). In line with this evidence, selective estrogen receptor modulators ameliorated the progression of kidney disease in animal models (Gracelli et al, 2012;Tazumi et al, 2016) and postmenopausal females (Silbiger, 2009;Suzuki and Kondo, 2012;Pollow et al, 2015).…”

Development and External Validation of a Nomogram for Predicting the Effect of RTX on the Treatment of Membranous Nephropathy

“…Other potential mechanisms include receptor-mediated effects of estrogen on TGF-β signaling, 19 which in turn regulates glomerular cell proliferation, matrix accumulation, apoptosis, and antioxidant capacity. [20][21][22][23] Interim studies are needed to investigate this interesting question further, and more direct evidences are needed to explain the influence of gender on this outcome.…”

Additive damage in the thromboxane related vasoconstriction and bradykinin relaxation of intramural coronary resistance arterioles in a rodent model of andropausal hypertension

“…Of course, this protective effect is assumed to start at the onset of hormone deficiency. In an analogue situation of women the positive effects of menopausal hormone replacement are noticeable only if hormone replacement is started within 5 years of the onset of menopause [ 6 ]. Beyond 10 years, definitive vascular damage develops, and complications outweigh the benefits of treatment [ 60 ].…”

“…It has long been established that in women menopausal estrogen deficiency significantly increases cardiovascular risk [ 6 , 7 ]. It is also well known that testosterone deficiency (men with hypogonadism/andropause) also increases cardiovascular risk [ 8 , 9 ].…”