A Discrepancy Between Platelet α2-Receptor Density and Functional Circulatory Changes in Hypertensives

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Abstract
To investigate whether differences exist in peripheral .alpha.2-adrenoceptors between normotensive and hypertensive subjects, we determined platelet .alpha.2-adrenoceptor density in 10 (7 males) untreated essential hypertensives (mean age of 51.1 years, range of 44-59 years) and in 10 age- and sex-matched normotensive controls. Moreover, in hypertensive patients, we examined the relationship between receptor density and cardiovascular reactivity to mental arithmetic, static handgrip, and bicycle exercise, to verify the hypothesis that .alpha.2-adrenoceptors might play a role in modulation of hemodynamic response to sympathetic stimuli. .alpha.2-Adrenoceptor density, as calculated by binding of [3H]yohimbine to platelets, was significantly higher in essential hypertensives (314.8 .+-. 38.7 fmol/mg) than in normotensive subjects (213.6 .+-. 34.7 fmol/mg) (p < 0.05), whereas receptor affinity was similar in both groups (4.0 .+-. 0.5 nM hypertensives, 4.3 .+-. 0.5 nM normotensives; p > 0.05). Mental arithmetic increased mean arterial pressure (MAP) by 21.5% from basal values and heart rate (HR) by 13.2%. During isometric exercise, MAP increased by 38.1% and HR by 24.7%, while during bicycle ergometry, mean increases in MAP and HR from baseline were 27.2 and 54.3%, respectively. No correlation was found between platelet .alpha.2-adrenoceptor density and percent changes in MAP induced by all tests, or between adrenoceptors and absolute basal and peak MAP values. Our findings suggest that in hypertensive patients, peripheral .alpha.2-adrenoceptors are increased with respect to matched normotensives, but these receptors seem not to be involved in the modulation of cardiovascular adaptation to enhanced sympathetic activity.