Effect of short-term losartan treatment in patients with primary aldosteronism and essential hypertension.
The aim of this study was to investigate the effect of short-term treatment with losartan, a selective and competitive angiotensin II (AngII) receptor blocker, on vascular endothelial growth factor (VEGF), active renin and kallikrein activity (KA) in patients with essential hypertension and primary aldosteronism. Nine patients with primary aldosteronism (5 with Conn adenoma and 4 with idiopathic hyperaldosteronism) and 9 patients with essential hypertension were included in the study. Systolic and diastolic blood pressure decreased significantly after losartan treatment in both patient groups. Plasma and urinary Kallikrein activity were significantly higher in primary aldosteronism in comparison with essential hypertension. There were no significant changes in the active renin and aldosterone in patients with primary aldosteronism after treatment. Plasma and urinary KA decreased significantly after losartan administration in both groups. Serum VEGF levels in primary aldosteronism were not significantly different from those in essential hypertension and did not change significantly after treatment in either group. In conclusion, losartan, in usual therapeutic doses, lowers blood pressure in patients with primary aldosteronism and essential hypertension. This marked antihypertensive effect in primary aldosteronism could be explained predominantly by blockade of tissue renin-angiotensin system (RAS). The variations in KA could be due to hemodynamic changes. VEGF is not likely to be involved in the action of losartan.
Zacharieva
S
S
Clinical Centre of Endocrinology and Gerontology, Medical University, National Oncological Centre, Sofia, Bulgaria. zacharieva@uheg.medicalnet-bg.org
Atanassova
I
I
Natchev
E
E
Orbetzova
M
M
Tzingilev
D
D
D000284:Administration, Oral; D000367:Age Factors; D000450:Aldosterone / Q000032:analysis; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D016228:Endothelial Growth Factors / Q000032:analysis; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D007610:Kallikreins / Q000652:urine; D019808:Losartan / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D008222:Lymphokines / Q000032:analysis; D008297:Male; D016555:Matched-Pair Analysis; D008875:Middle Aged; D020842:Plasma Kallikrein / Q000032:analysis; D044140:Receptor, Angiotensin, Type 1; D012083:Renin / Q000032:analysis; D012737:Sex Factors; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D016228:Endothelial Growth Factors; D008222:Lymphokines; D044140:Receptor, Angiotensin, Type 1; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D000450:Aldosterone; D007610:Kallikreins; D020842:Plasma Kallikrein; D012083:Renin; D019808:Losartan