Arterial hemodynamics in human hypertension: Effects of adrenergic blockade

Abstract

Background. Resistance, pulse wave velocity, and wave reflections have been shown to be increased in patients with essential hypertension compared with normotensive controls. These alterations are completely normalized by nitroprusside infusion but exacerbated during β-adrenergic blockade, suggesting an enhanced smooth muscle tone that is in part modulated by adrenergically mediated vasodilation. The present study was performed to examine the extent to which this apparently enhanced smooth muscle tone is a result of α-adrenergically mediated vasoconstriction. Methods and Results. Age-matched normotensive and hypertensive Chinese subjects were instrumented with catheter-tipped micromanometers and an electromagnetic flow velocity sensor positioned in the ascending aorta. Aortic impedance and wave reflection properties were obtained from Fourier analysis of the pressure and flow signals during baseline conditions, after β-blockade with propranolol (0.15 mg/kg i.v.), and after α-blockade with intravenous phentolamine (range, 15-80 mg) that was sufficient to either normalize blood pressure or produce a pressure that could not be further lowered. Compared with normotensives, in the baseline state, hypertensives had elevated resistance (1,962 versus 1,268 dyne · sec/cm5, p<0.001), total power (1,893 versus 1,568 mW, p<0.08), reflected pressure wave component (25.6 versus 13.5 mm Hg, p<0.001), ratio of reflected to forward wave (0.65 versus 0.42, p<0.001), and pulse wave velocity as determined from the frequency of the first zero-crossing of impedance phase angle (4.6 versus 3.5 Hz, p<0.03). During combined α- and β-adrenergic blockade, blood pressure decreased into the normal range (from 162/103 to 131/87 mm Hg) but was still somewhat higher than that in the normotensive subjects. Resistance (1,914 dyne · sec/ cm5, p<0.03), reflected wave (19.5 mm Hg, p<0.01), and ratio of reflected to forward wave (0.61, p<0.001) were, however, persistently elevated above normal values. Conclusions. α-Adrenergically mediated vasoconstriction cannot account for all of the hemodynamic alterations seen in essential hypertension.