1. One hypothesis to account for altered adrenergic response in hypertensive patients is alteration in adrenergic receptors on responsive cells. We therefore used radioligand binding methods to examine the α2-adrenergic receptors on platelets isolated from 17 normal men and from 19 men with essential hypertension. in these studies we used the α2-selective radioligand [3H]yohimbine to determine receptor number and affinity on intact platelets.

2. The median number of receptors per platelet was 265 for the hypertensive patients versus 246 for the platelets of controls. Likewise there was no difference between hypertensives and controls in the dissociation constant of the receptors for [3H]yohimbine or adrenaline.

3. Anti-hypertensive treatment with the α2-agonist guanabenz or the β-antagonist propranolol did not change the number or affinity of platelet α2-receptors.

4. in untreated hypertensives the receptor number did not correlate with age, blood pressure, or 24 h urinary excretion of catecholamines or Na+.

5. We conclude that neither hypertension nor anti-hypertensive treatment alters the number of α2-adrenergic receptors on human platelets. Furthermore, because therapy with an α2-agonist does not alter the receptor number and because the receptor number did not correlate with urinary excretion of catecholamines (an index of sympathetic-nervous-system activity), we conclude that ‘down-regulation’ of human platelet α2-adrenergic receptors may not readily occur in vivo.

This content is only available as a PDF.
You do not currently have access to this content.