Low-dose estrogen is as effective as high-dose treatment in rats with postmenopausal hypertension.

: This study was conducted to test the hypothesis that 17ß-estradiol therapy improves redox balance by decreasing reactive oxygen species production and increasing nitric oxide (NO) bioavailability, favoring Akt pathway activation and resulting in a better autonomic vascular control. Ovariectomized female Wistar rats were divided into 4 groups: (1) vehicle (VL) and animals treated with a pellet of 17ß-estradiol for 21 days; (2) low dose (LE; 0.05 mg); (3) medium dose (ME; 0.2 mg); and (4) high dose (HE; 0.5 mg). Arterial pressure and its sympathetic nervous system modulation were evaluated by spectral analysis. Nitric oxide synthase and NADPH oxidase (Nox) activities, H2O2 concentration, redox status (GSH/GSSG), protein expression of Trx-1 and p-Akt/Akt were evaluated in the aorta, whereas NO metabolites were measured in the serum. Estrogen-treated groups showed a significant decrease in arterial pressure and sympathetic vascular drive. Redox status was significantly improved and NADPH oxidase and H2O2 were decreased in all estrogen-treated groups. Estrogen also induced an enhancement in NO metabolites, nitric oxide synthase activity, and Akt phosphorylation. This study demonstrated that estrogen treatment to ovariectomized rats induced cardioprotection, which was evidenced by reduced blood pressure variability and vascular sympathetic drive. These effects were associated with an improved redox balance and Akt activation, resulting in an enhanced NO bioavailability.

Exercise improves cardiovascular control in a model of dislipidemia and menopause.

The present study investigated the effects of exercise training on arterial pressure, baroreflex sensitivity, cardiovascular autonomic control and metabolic parameters on female LDL-receptor knockout ovariectomized mice. Mice were divided into two groups: sedentary and trained. Trained group was submitted to an exercise training protocol. Blood cholesterol was measured. Arterial pressure (AP) signals were directly recorded in conscious mice. Baroreflex sensitivity was evaluated by tachycardic and bradycardic responses to AP changes. Cardiovascular autonomic modulation was measured in frequency (FFT) and time domains. Maximal exercise capacity was increased in trained as compared to sedentary group. Blood cholesterol was diminished in trained mice (191+/-8mg/dL) when compared to sedentary mice (250+/-9mg/dL, p<0.05). Mean AP and HR were reduced in trained group (101+/-3mmHg and 535+/-14bpm, p<0.05) when compared with sedentary group (125+/-3mmHg and 600+/-12bpm). Exercise training induced improvement in bradycardic reflex response in trained animals (-4.24+/-0.62bpm/mmHg) in relation to sedentary animals (-1.49+/-0.15bpm/mmHg, p<0.01); tachycardic reflex responses were similar between studied groups. Exercise training increased the variance (34+/-8 vs. 6.6+/-1.5ms(2) in sedentary, p<0.005) and the high-frequency band (HF) of the pulse interval (IP) (53+/-7% vs. 26+/-6% in sedentary, p<0.01). It is tempting to speculate that results of this experimental study might represent a rationale for this non-pharmacological intervention in the management of cardiovascular risk factors in dyslipidemic post-menopause women.

Impairment on cardiac output and blood flow adjustments to exercise in L-NAME-induced hypertensive rats.

The objective of the present study was to investigate cardiovascular adjustments at rest, during exercise, and 1 hour after exercise among nitric oxide (NO) blockade-induced hypertensive rats. Male Wistar rats (308 +/- 9 g) assigned as normotensive (n = 9) and hypertensive (N(omega)-nitro-L-arginine methyl ester, n = 11) underwent a bout of exercise. Arterial pressure (AP) and blood oxygen saturation were measured. Colored microspheres were used to evaluate blood flow and cardiac output (CO). Hypertensive rats (143 +/- 5 vs. 102 +/- 4 mmHg in normotensive rats), who presented reduced CO (57 +/- 6 vs. 102 +/- 7 mL/min in normotensive), also presented diminished blood flow in kidney, lung, and muscles at rest in comparison with normotensive rats. Exercise increased AP (20%), heart rate (40%), and CO (32%) among the normotensive rats, whereas the hypertensive rats presented an increased heart rate (40%) accompanied by a reduced venous oxygen saturation (45.5 +/- 2.1% vs. 75 +/- 0.7% in normotensive rats). Muscle vasodilatation, which was observed among the normotensive rats and is considered a hallmark adjustment to exercise, was not observed among the hypertensive rats. After a 1-hour interval from exercise most of the evaluated parameters returned to basal values. In conclusion, exercise did not cause an increase in CO, AP, or blood flow to skeletal muscle in hypertensive rats. However, it was associated with a significant increase in the arterio-venous oxygen content difference in NO-blocked rats, thus suggesting that hypertension associated with impairment in NO release induced different cardiovascular adjustments to exercise.