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 (beta1-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 mug kg(-1) phenylephrine) increased significantly (9.9+/-2.2 to 19.6+/-4.1 ms mm Hg(-1)). With beta1-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 delta SBP (-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.

Aging and arterial blood pressure variability during orthostatic challenge.

BACKGROUND: It has been demonstrated that a decrease in vagal cardiac function compromises arterial blood pressure (ABP) stability during orthostatic challenge. Augmentations in low-frequency (LF) ABP oscillations are indicative of this change in autonomic hemodynamic control. Aging is associated with diminished arterial baroreflex sensitivity and vagal cardiac dysfunction. However, the effect of aging on the stability of ABP during an orthostatic challenge remains to be elucidated. OBJECTIVE: The purpose of this study was to investigate ABP stability with aging during central hypovolemia induced by lower-body negative pressure (LBNP). METHODS: Graded LBNP up to -40 mm Hg was applied in 16 older (65 +/- 3 years of age) and 16 younger (25 +/- 3 years of age) healthy adults. ABP variability was analyzed by fast Fourier transform. LF spectral density (0.04-0.15 Hz) was extracted to provide an index of vasomotor responsiveness. RESULTS: Both LF systolic blood pressure (SBP) variability and diastolic blood pressure variability were augmented with LBNP. The rate of increase in LF SBP variability was augmented significantly greater in older as compared with younger subjects (p = 0.049). In addition, LF SBP variability was inversely correlated with decreases in pulse pressure in both age groups (r = -0.84, p = 0.01). The magnitude of the decreases in SBP and pulse pressure during LBNP was significantly affected by age, with the largest changes occurring in older subjects. The altered ABP response that manifested in older individuals was associated with a significant diminution in the reflex tachycardiac response elicited by LBNP. CONCLUSIONS: Induction of central hypovolemia via graded LBNP augments LF ABP variability. This increased ABP variability is significantly greater in older individuals. Our data suggest that aging is associated with ABP instability during orthostatic challenge.