BACKGROUND: Muscle metaboreflex control in hypertensive subjects has not been described yet. We investigated the integrity of muscle metaboreflex control of muscle sympathetic nerve activity (MSNA) and blood pressure (BP) in never-treated hypertensive subjects. METHODS: Eighteen hypertensive (42+/-1 years) and 22 normotensive subjects (38+/-1 years) were studied. The MSNA was measured by microneurography and forearm blood flow (FBF) by venous occlusion plethysmography. The BP was noninvasively monitored. RESULTS: Baseline MSNA was significantly increased in hypertensive subjects when compared with normal subjects (34+/-2 v 22+/-2 bursts/min, P<.001). Baseline FBF was significantly decreased in hypertensive subjects (2.66+/-0.2 v 2.05+/-0.1 mL/min/100 mL, P=.04). During moderate handgrip exercise (30% maximal voluntary contraction), MSNA levels were significantly higher in hypertensive subjects. However, MSNA responses were significantly lower in hypertensive subjects (1+/-3 v 10+/-2 bursts/100 heart beats, P = .001). Similarly, FBF responses were significantly lower in hypertensive subjects when compared with normotensive subjects (0.70+/-0.19 v 1.60+/-0.36 mL/min/100 mL, P=.04). During the postexercise circulatory arrest, when the metaboreflex control is isolated, MSNA levels returned toward baseline in hypertensive subjects (58+/-4 v 55+/-3 bursts/100 heart beats, P=.98). In contrast, in normotensive subjects, MSNA levels remained significantly elevated when compared with baseline (48+/-3 v 35+/-1 bursts/100 heart beats, P<.001). CONCLUSIONS: These findings suggest an association between hypertension and decreased muscle metaboreflex control of MSNA.
BACKGROUND: Muscle metaboreflex control in hypertensive subjects has not been described yet. We investigated the integrity of muscle metaboreflex control of muscle sympathetic nerve activity (MSNA) and blood pressure (BP) in never-treated hypertensive subjects. METHODS: Eighteen hypertensive (42+/-1 years) and 22 normotensive subjects (38+/-1 years) were studied. The MSNA was measured by microneurography and forearm blood flow (FBF) by venous occlusion plethysmography. The BP was noninvasively monitored. RESULTS: Baseline MSNA was significantly increased in hypertensive subjects when compared with normal subjects (34+/-2 v 22+/-2 bursts/min, P<.001). Baseline FBF was significantly decreased in hypertensive subjects (2.66+/-0.2 v 2.05+/-0.1 mL/min/100 mL, P=.04). During moderate handgrip exercise (30% maximal voluntary contraction), MSNA levels were significantly higher in hypertensive subjects. However, MSNA responses were significantly lower in hypertensive subjects (1+/-3 v 10+/-2 bursts/100 heart beats, P = .001). Similarly, FBF responses were significantly lower in hypertensive subjects when compared with normotensive subjects (0.70+/-0.19 v 1.60+/-0.36 mL/min/100 mL, P=.04). During the postexercise circulatory arrest, when the metaboreflex control is isolated, MSNA levels returned toward baseline in hypertensive subjects (58+/-4 v 55+/-3 bursts/100 heart beats, P=.98). In contrast, in normotensive subjects, MSNA levels remained significantly elevated when compared with baseline (48+/-3 v 35+/-1 bursts/100 heart beats, P<.001). CONCLUSIONS: These findings suggest an association between hypertension and decreased muscle metaboreflex control of MSNA.
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