Pharmacologic reduction of sympathetic drive increases platelet alpha-2–receptor number

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Abstract
Several lines of evidence implicate sympathetic nervous system involvement in the pathophysiology of essential hypertension in man. Extrapolations are frequently made from in vitro measurements of plasma catecholamine levels to the physiologic role of the sympathetic system in hypertension. We assessed the utility and validity of such extrapolation from in vitro to in vivo measures of adrenergic function. Addition of guanadrel to diuretic therapy in 11 patients with essential hypertension reduced supine intra-arterial blood pressure from 135 .+-. 14/76 .+-. 9 to 127 .+-. 13/67 .+-. 5 mm Hg (P < 0.02). Supine heart rate was also reduced, from 77 .+-. 14 to 63 .+-. 13 bpm (P < 0.001). Plasma norepinephrine levels fell from 303 .+-. 107 to 170 .+-. 46 pg/ml (P < 0.01). Platelet .alpha.2-receptor number ([3H]yohimbine maximal binding) increased from 204 .+-. 77 to 301 .+-. 150 fmol/mg (P < 0.02). The pupillary mydriatic response to phenylephrine and the forearm arterial vasoconstrictor response to intra-arterial norepinephrine did not change. Thus guanadrel reduced blood pressure by decreasing sympathetic tone. In this milieu of low sympathetic activity the platelet .alpha.-receptor number increased, but physiologic responses to exogenous .alpha.-agonists did not change. Caution is therefore advised when extrapolation from in vitro measurement of plasma catecholamine levels and platelet .alpha.2-receptor number to the in vivo physiologic significance.

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