18 research outputs found
Alterations in carotid baroreflex control of arterial blood pressure during the menstrual cycle in young women [abstract]
Limited studies have suggested that menstrual cycle variations in sex hormones may influence arterial baroreflex control of heart rate (HR) and sympathetic nerve activity, however, results are equivocal. In addition, the baroreflex control of blood pressure (BP) has not been directly examined as pharmacological perturbations were mainly used to assess baroreflex function
Selective attenuation of carotid-cardiac responses to hypertension at the onset of static handgrip in humans [abstract]
Previous studies have indicated that at the onset of exercise cardiac baroreflex function is reduced in an intensity-dependent manner, which appears to be mediated by a blunted ability to buffer hypertensive challenges. However, whether cardiac baroreflex responses to a hypotensive stimulus are altered at exercise onset is unclear
Statin therapy lowers muscle sympathetic nerve activity and oxidative stress in patients with heart failure
Despite standard drug therapy, sympathetic nerve activity (SNA) remains high in heart failure (HF) patients making the sympathetic nervous system a primary drug target in the treatment of HF. Studies in rabbits with pacing-induced HF have demonstrated that statins reduce resting SNA, in part, due to reductions in reactive oxygen species (ROS). Whether these findings can be extended to the clinical setting of human HF remains unclear. We first performed a study in seven statin-naïve HF patients (56 ± 2 yr; ejection fraction: 31 ± 4%) to determine if 1 mo of simvastatin (40 mg/day) reduces muscle SNA (MSNA). Next, to control for possible placebo effects and determine the effect of simvastatin on ROS, a double-blinded, placebo-controlled crossover design study was performed in six additional HF patients (51 ± 3 yr; ejection fraction: 22 ± 4%), and MSNA, ROS, and superoxide were measured. We tested the hypothesis that statin therapy decreases resting MSNA in HF patients and this would be associated with reductions in ROS. In study 1, simvastatin reduced resting MSNA (75 ± 5 baseline vs. 65 ± 5 statin bursts/100 heartbeats; P < 0.05). Likewise, in study 2, simvastatin also decreased resting MSNA (59 ± 5 placebo vs. 45 ± 6 statin bursts/100 heartbeats; P < 0.05). In addition, statin therapy significantly reduced total ROS and superoxide. As expected, cholesterol was reduced after simvastatin. Collectively, these findings indicate that short-term statin therapy concomitantly reduces resting MSNA and total ROS and superoxide in HF patients. Thus, in addition to lowering cholesterol, statins may also be beneficial in reducing sympathetic overactivity and oxidative stress in HF patients