[Arterial hypertension. Density of alpha 1 and alpha 2 adrenergic receptors in blood platelets, beta adrenergic receptors in the lymphocytes and serum catecholamine levels]
- PMID: 1666134
[Arterial hypertension. Density of alpha 1 and alpha 2 adrenergic receptors in blood platelets, beta adrenergic receptors in the lymphocytes and serum catecholamine levels]
Abstract
The influence of the sympathetic nervous system on blood pressure is mediated predominantly by catecholamines norepinephrine and epinephrine acting on alpha- and beta-adrenoceptors. The study of human alpha-adrenergic and beta-adrenergic receptors in hypertension is hampered by the lack of easily accessible cardiovascular tissues. Therefore numerous investigators have used platelets as a model system to study alpha-adrenergic receptors and lymphocytes to study beta-adrenergic receptors in humans. During the last decade some studies with small patient numbers have been published, that generally did not detect significant differences in platelet alpha 2-adrenergic receptor density between normotensive and hypertensive subjects, however, most investigators have described higher density of beta-receptors in lymphocytes from hypertensive patients than in cells from normotensive control subjects. This study was carried out to analyse density of alpha 1- and alpha 2-adrenoceptors in platelet membrane preparations and beta-adrenoreceptors in lymphocytes before and after physiological increase in plasma catecholamines. It was found that density of alpha 1- and alpha 2-adrenoreceptors in platelet membranes of patients with stable blood hypertension was similar to that in the healthy individuals while beta-adrenergic receptors density in lymphocytes was higher. In normotensives posture induced rise in plasma catecholamines correlated with reduced alpha 1- and alpha 2-adrenoreceptors density as well as beta-adrenoreceptor density. Hypertensive subjects had similar rise in plasma catecholamines with upright posture, but no changes in receptor density was observed. These suggest that in hypertension alpha-adrenergic and beta-adrenergic regulation by agonist may be disturbed.
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