Sympathetic cardiac influence and arterial blood pressure instability

Previous studies have suggested that sympathetic cardiac blockade enhances baroreflex function, whereas parasympathetic blockade diminishes baroreflex sensitivity and elicits arterial blood pressure (ABP) instability. The aim of this project was to test the hypothesis that sympathetic cardiac blockade was beneficial in maintaining ABP stability during orthostatic challenge. In 8 young healthy subjects, measurements were taken before and after sympathetic cardiac blockade (β1-adrenoceptor blockade via metoprolol) in combination with or without parasympathetic blockade (atropine) at rest and during lower body negative pressure (LBNP). Arterial blood samples were obtained to evaluate plasma renin activity (PRA) and norepinephrine (NE). Power spectral analyses were performed on heart rate (HR) and ABP variability. LBNP −50 Torr significantly decreased systolic blood pressure (SBP, −6±3 mm Hg) and increased PRA (from 0.72±0.23 to 1.75±0.24 ng ml−1 h−1) and NE (from 1.02±0.11 to 2.13±0.32 pg ml−1). Low frequency (LF, 0.04-0.12 Hz) SBP and diastolic blood pressure (DBP) variability were significantly augmented by LBNP (4.1±1.6 vs. 10.8±3.0 mm Hg2, and 3.1±1.0 vs. 7.9±1.9 mm Hg2, respectively). Following metoprolol, arterial baroreflex sensitivity (assessed by the slope of HR interval to SBP during injection with 1 μg kg−1 phenylephrine) increased significantly (9.9±2.2 to 19.6±4.1 ms mm Hg−1). With β1-adrenoceptor blockade, LBNP still decreased SBP (−10±2 mm Hg) and increased NE, but did not significantly augment PRA (0.59±0.22 vs. 1.03±0.18 ng ml−1 h−1), or LF SBP and DBP variability (3.3±0.6 vs. 5.7±1.3 mm Hg2, and 3.1±0.7 vs. 5.4±1.1 mm Hg2, respectively). The increased PRA during LBNP remained non-significant following metoprolol combined with atropine, whereas the augmented LF SBP (2.6±0.7 vs. 9.9±2.8 mm Hg2) and DBP (2.5±0.7 vs. 11.1±3.0 mm Hg2) variability were significantly accentuated compared to both metoprolol alone and control conditions, accompanied by a greater ΔSBP (−17±7 mm Hg) and significantly diminished baroreflex gain (0.91±0.05 ms/mm Hg). These data suggested that removal of sympathetic cardiac influence improved cardiovascular stability as indicated by a diminished LF ABP variability, which was related to an enhanced cardiac responsiveness.