Open AccessChanges in Plasma Norepinephrine Concentration and Thrombocyte α2-Adrenoceptor Density During Long-Term Antihypertensive Therapy with Nitrendipine and Captopril
Author(s) -
Ralf Müller,
H. Steffen,
P Weller,
Claudia Kugel,
Thorsten Freiheit,
Wilhelm Krone
Publication year - 1994
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-199409000-00011
Subject(s) - captopril , nitrendipine , medicine , endocrinology , norepinephrine , blood pressure , angiotensin converting enzyme , angiotensin ii , pharmacology , chemistry , dopamine
Antihypertensive drugs influence the sympathetic nervous system in different ways that may cause adverse or beneficial effects. We treated 48 hypertensive patients with either nitrendipine (10-20 mg twice daily, b.i.d.) or captopril (25-50 mg b.i.d.) for 16 weeks to evaluate changes in plasma catecholamines, platelet alpha 2- and lymphocyte beta 2-adrenoceptors. Blood pressure (BP) decreased from 153/95 to 135/87 mm Hg with captopril and from 155/99 to 137/89 mm Hg with nitrendipine. Treatment with nitrendipine significantly stimulated plasma norepinephrine (NE) from 327 +/- 37 to 446 +/- 50 pg/ml, and treatment with captopril resulted in a significant reduction in platelet alpha 2-adrenoceptor density from 265 +/- 39 to 171 +/- 26 fmol/mg protein. Despite having equal BP-lowering properties, captopril and nitrendipine have different effects on the sympathetic nervous system. Stimulation of plasma NE during long-term treatment with nitrendipine may contribute to possible adverse effects, whereas reduction in alpha 2-adrenoceptors induced by captopril may contribute to the vasodilating effect of angiotensin-converting enzyme (ACE) inhibition.