This review focuses on the effects of thyroid hormones in vascular and renal systems. Special emphasis is given to the mechanisms by which thyroid hormones affect the regulation of body fluids, vascular resistance and, ultimately, blood pressure. Vascular function is markedly affected by thyroid hormones that produce changes in vascular reactivity and endothelial function in hyper- and hypothyroidism. The hypothyroid state is accompanied by a marked decrease in sensitivity to vasoconstrictors, especially to sympathetic agonists, alteration that may play a role in the reduced blood pressure of hypothyroid rats, as well as in the preventive effects of hypothyroidism on experimental hypertension. Moreover, in hypothyroid rats, the endothelium-dependent and nitric oxide donors vasodilation is reduced. Conversely, the vessels from hyperthyroid rats showed an increased endothelium-dependent responsiveness that may be secondary to the shear-stress induced by the hyperdynamic circulation, and that may contribute to the reduced vascular resistance characteristic of this disease. Thyroid hormones also have important effects in the kidney, affecting renal growth, renal haemodynamics, and salt and water metabolism. In hyperthyroidism, there is a resetting of the pressure-natriuresis relationship related to hyperactivity of the reninangiotensin system, which contributes to the arterial hypertension associated with this endocrine disease. Moreover, thyroid hormones affect the development and/or maintenance of various forms of arterial hypertension. This review also describes recent advances in our understanding of thyroid hormone action on nitric oxide and oxidative stress in the regulation of cardiovascular and renal function and in the long-term control of blood pressure.

This study analysed and compared the effects of chronic oral treatment with quercetin or verapamil on systolic blood pressure and vascular function in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Quercetin and verapamil inhibited the development of DOCA-salt-induced hypertension in a similar manner. DOCA-salt-hypertensive rats showed potassium depletion and oxidative stress, prevented only by concomitant quercetin administration. Quercetin and verapamil treatments reduced the endothelium-independent hyper-reactivity to KCl observed in the aorta of DOCA-salt-hypertensive rats, but only quercetin increased the contractile responses to angiotensin II, improved endothelial dysfunction and restored basal aortic Cu/Zn SOD expression, altered in DOCA-salt-treated rats. In conclusion, quercetin and verapamil show similar antihypertensive effects in mineralocorticoid hypertension, but quercetin was superior to verapamil in improving endothelial-dependent aortic dilatation, suggesting a better vascular protection in this volume expansion hypertension model.

This study analyzed whether hypertension induced by N(omega)-nitro-l-arginine methyl ester (L-NAME) is associated with dysregulation of the main antioxidant enzymes (superoxide dismutase [SOD], catalase, glutathione peroxidase [GPX], and glutathione reductase [GR]) and whether chronic administration of tempol ameliorates this hypertension. Four groups of male Wistar rats were used: 1) control rats; 2) rats treated with L-NAME (35 mg/100 mL in drinking fluid); 3) rats treated with tempol (18 mg/100 mL in drinking fluid); and 4) rats treated with L-NAME plus tempol. All treatments were maintained for 6 weeks. Body weight, systolic blood pressure (BP) determined by the tail-cuff method, and heart rate were measured once per week. At the end of the experimental period, direct BP and morphologic, metabolic, plasma, and renal variables were measured. Enzymatic activities were measured in the kidney (cortex and medulla) and heart (right and left ventricles). Rats with L-NAME-induced hypertension showed increased copper-zinc (Cu-Zn) SOD activity in the renal cortex and medulla and the left and right ventricles, which was reduced by tempol administration. The manganese (Mn) SOD activity was increased by L-NAME and reduced by tempol in the renal cortex but was unchanged in other tissues. Catalase activity was not affected by L-NAME or tempol treatments in any tissue. Both GPX and GR activities were increased by L-NAME and reduced by tempol in the renal cortex and medulla but were not affected in the ventricles. Tempol reduced BP and total urinary excretion of 8-hydroxy-2'-deoxyguanosine in L-NAME-treated animals but did not affect either variable in controls. We conclude that L-NAME-induced hypertension is associated with an upregulation of antioxidant SOD, GPX, and GR activities. Moreover, the results indicate that tempol attenuates hypertension on nitric oxide-deficient rats and that oxidative stress participates in the established phase of this type of hypertension.

The aim of this study was to examine female sexual functioning and its association with the impact of the symptoms of menopause among Spanish postmenopausal women. A total of 182 postmenopausal women (65.59 ± 7.93 years) participated in this cross-sectional study. The female sexual function index (FSFI) and the menopause rating scale (MRS) were used to analyze sexual function and severity of menopausal symptoms, respectively. Age, education, area of residence, occupation, and depression (Hospital Anxiety and Depression Scale) were considered as possible confounders. The results of a linear multivariate regression analysis showed that the severity of urogenital menopause-related symptoms was associated with lower values in the FSFI total score and the lubrication, satisfaction, arousal, and orgasm domains. These last three subscales were also linked to severe psychological impact, while the MRS total score was only related to the desire domain. Regarding confounders, being younger, working, and residing in a rural area were all linked to better sexual function. All effect sizes were large (adjusted R² > 0.35). In conclusion, after controlling for possible confounders, postmenopausal women who experience a severe impact of menopausal symptoms endure poorer sexual function, particularly when said symptoms are urogenital or psychological in nature.