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Plasma catecholamines and adrenoceptors in young hypertensive patients
R Müller1, H M Steffen, P Weller
1Medizinische Klinik II, Köln, Germany.
Insights
Young patients with essential hypertension show elevated plasma catecholamines and reduced beta2-adrenoceptors. This suggests increased sympathetic activity and an adrenoceptor imbalance contribute to high blood pressure.
Area of Science:
- Cardiology
- Endocrinology
- Pharmacology
Background:
- Essential hypertension pathogenesis may involve elevated sympathoadrenal tone.
- Imbalances in postsynaptic alpha- and beta-adrenoceptor function are implicated.
Purpose of the Study:
- To investigate plasma catecholamines and adrenoceptor function in young essential hypertension patients.
- To compare these markers between hypertensive individuals and normotensive controls.
Main Methods:
- Measured plasma noradrenaline and adrenaline levels.
- Assessed thrombocyte alpha2-adrenoceptor and lymphocyte beta2-adrenoceptor density.
- Included 16 newly diagnosed essential hypertension patients and 26 age-matched controls.
Main Results:
- Hypertensive patients had significantly elevated plasma noradrenaline and adrenaline.
- Lymphocyte beta2-adrenoceptor density was markedly reduced in hypertensive patients.
- Thrombocyte alpha2-adrenoceptor density showed a nonsignificant decrease.
Conclusions:
- Elevated plasma catecholamines support a role for increased sympathetic activity in young hypertension.
- Reduced beta2-adrenoceptors and potential alpha2-adrenoceptor imbalance suggest a postsynaptic adrenoceptor dysfunction.
- This dysfunction may promote sympathetic system pressor effects in essential hypertension.
Abstract:
An elevated sympathoadrenal tone and an imbalance in postsynaptic alpha- and beta-adrenoceptor function are discussed as factors in the pathogenesis of essential hypertension. This study examined plasma catecholamines, thrombocyte alpha2-adrenoceptors and lymphocyte beta2-adrenoceptors in 16 young patients with newly detected essential hypertension and 26 normotensive age matched controls (27.1 +/- 4.5 vs. 24.8 +/- 2.8 years; NS). Plasma noradrenaline (276 +/- 34 vs. 216 +/- 18 pg/ml, P < 0.05) and plasma adrenaline (96 +/- 15 vs. 31 +/- 4 pg/ml, P < 0.0001) were significantly elevated in hypertensive patients. Thrombocyte alpha2-adrenoceptor density was only nonsignificantly decreased (230 +/- 37 vs. 311 +/- 36 fmol/mg protein, NS), whereas lymphocyte beta2-adrenoceptor density was markedly reduced (15.3 +/- 2.3 vs. 22.6 +/- 1.8 fmol/mg protein, P < 0.01) in hypertensive patients. Elevated plasma catecholamines are consistent with a pathophysiological role for increased sympathetic neural activity in young hypertensive patients. Assuming that results of adrenoceptor studies on blood elements are applicable on vascular receptors, our results are consistent with an imbalance of postsynaptic adrenoceptor functions which promotes the pressor effects of the sympathetic system.