In normotensive postmenopausal women, chronic transdermal ERT decreases SND without augmenting arterial baroreflexes and causes a small but statistically significant decrease in ambulatory BP. Sympathetic inhibition is evident only with chronic rather than acute estrogen administration, implying a genomic mechanism of action. Because the effects of transdermal ERT are larger than those of oral ERT, the route of administration may be an important consideration in optimizing the beneficial effects of ERT on BP and overall cardiovascular health.

Abstract-A large body of clinical investigation implicates an important role for the sympathetic nervous system in linking obesity with hypertension. However, the experimental support for this hypothesis is derived from strictly white cohorts. The goal of this study was to determine whether being overweight begets sympathetic overactivity in black Americans, the ethnic minority at highest risk for hypertension. We recorded postganglionic sympathetic nerve discharge with microelectrodes in muscle nerve fascicles of the peroneal nerve in 92 normotensive young adult black men and women within a wide range of body mass index. The same experiments were performed in a control group of 45 normotensive white men and women of similar ages and body mass indices. The major new findings are 2-fold. First, in young, normotensive, overtly healthy black women, being overweight begets sympathetic overactivity (rϭ0.45, Pϭ0.0009), a putative intermediate phenotype for incident hypertension. Second, in black men, sympathetic nerve discharge is dissociated from body mass index (rϭ0.03, PϭNS). This dissociation is explained in part by a 20% to 40% higher rate of sympathetic nerve discharge in lean black men compared with lean white men and lean black and white women (28Ϯ3 versus 18Ϯ2, 21Ϯ2, and 17Ϯ2 bursts/min, respectively; PϽ0.05). Sympathetic nerve discharge in lean black men is comparable to that of overweight black men and women as well as white men and women. These data provide the first microneurographic evidence for tonic central sympathetic overactivity in blacks, both adiposity-related sympathetic overactivity in black women and adiposity-independent sympathetic overactivity in black men. Key Words: obesity Ⅲ sympathetic nervous system Ⅲ blacks Ⅲ blood pressure O besity is firmly established to be a major risk factor for hypertension, and a large body of clinical investigation implicates an important role for the sympathetic nervous system in linking adiposity with hypertension. [1][2][3][4][5][6] In numerous studies of normotensive young adults, increasing adiposity is accompanied by increased sympathetic nerve discharge (SND) to skeletal muscle, a major site of energy expenditure. 5-7 Overweight-related sympathetic overactivity is hypothesized to be a compensatory mechanism to burn fat and minimize weight gain but at the cost of increased sympathetic discharge to the peripheral vasculature, which could predispose to hypertension. 2,8 However, the experimental support for this hypothesis is derived from strictly white cohorts. 5,6 The importance of inclusion of minority subjects in this field of clinical investigation is underscored by recent studies of Pima Indians, an ethnic minority with a high prevalence of obesity but a comparatively low prevalence of hypertension. 4 Basal levels of skeletal muscle SND are lower in normotensive male Pima Indians than in whites and do not track with adiposity. This relative sympathetic underactivity constitutes a potential explanation for the surprisingly low prevalence of hypertensio...

In postmenopausal women, oral but not transdermal ET increased CRP by a first-pass hepatic effect. An increase in CRP levels is accompanied by a reduction in IGF-1, an anti-inflammatory growth factor. Because CRP is a powerful predictor of an adverse prognosis in otherwise healthy postmenopausal women, the route of administration may be an important consideration in minimizing the adverse effects of ET on cardiovascular outcomes.

Sympathetic overactivity in chronic renal failure is caused by neurohormonal mechanisms arising in the failing kidney. Future clinical studies are needed to determine whether normalization of sympathetic activity should constitute an important therapeutic goal in this high-risk patient population.

Background Patients with chronic kidney disease (CKD) are at increased risk of life‐threatening cardiovascular arrhythmias. Although these arrhythmias are usually secondary to structural heart diseases that are commonly associated with CKD, a significant proportion of cases with sudden cardiac death have no obvious structural heart disease. This study aims to explore the relationship of cardiac repolarization in patients with CKD and worsening kidney function. Hypothesis There is cardiac repolarization abnormalities among patients with chronic kidney disease. Methods This was a retrospective, chart‐review study of admissions or clinic visits to a university hospital between 2005 and 2010 by patients with a diagnosis of CKD. Inclusion criteria selected patients who had 12‐lead surface electrocardiography (ECG), renal function tests within 24 hours, and transthoracic echocardiography within 6 months. Cases with a documented etiology for the corrected Qt (Qtc) interval prolongation including structural heart disease, QT prolonging drugs, or relevant disease conditions, were excluded. Results Our sample size was 154 ECGs. Two‐thirds of patients with CKD had QTc interval prolongation, and about 20% had a QTc interval >500 ms. QTc interval was significantly different and increased with each successive stage of CKD using the Bazett (P < 0.006) or Fridericia (P = 0.03) formula. QTc interval correlated significantly with serum creatinine (P = 0.01). These finding were independent of age, gender, potassium, and calcium concentrations. Conclusions The progression of CKD resulted in a significant delay of cardiac repolarization, independent of other risk factors. This effect may potentially increase the risk of sudden cardiac death, and may also increase the susceptibility of drug‐induced arrhythmia.