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Effects of guanfacine monotherapy on blood pressure, heart rate, plasma renin activity, aldosterone, and catecholamines in hypertensive patients with chronic glomerulonephritis
Author(s) -
Ikeda Toshio,
Gomi Tomoko,
Yuhara Mikio,
Sakurai Jun,
Nakayama Daisuke
Publication year - 1988
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1988.33
Subject(s) - plasma renin activity , guanfacine , blood pressure , medicine , aldosterone , endocrinology , heart rate , renal function , renin–angiotensin system , creatinine , renovascular hypertension , clonidine
Effects of guanfacine, a centrally acting antihypertensive, on blood pressure, heart rate, plasma renin activity, serum aldosterone, plasma norepinephrine, and renal function were evaluated in 16 patients with hypertension with biopsy‐proved chronic glomerulonephritis. Guanfacine monotherapy with a daily dose of 1 to 2.5 mg at bedtime for 6 months brought about a significant reduction in blood pressure (171 ± 2/110 ± 2 to 144 ± 2/89 ± 1 mm Hg; P < 0.01), with concurrent decreases in heart rate (78 ± 2 to 70 ± 2 bpm; P < 0.01), plasma renin activity (1.96 ± 0.12 to 1.21 ± 0.19 ng/ml/hr; P < 0.05), aldosterone (14.6 ± 1.5 to 9.7 ± 0.9 ng/dl; P < 0.05), plasma norepinephrine (220.5 ± 24.2 to 132.8 ± 27.7 pg/ml; P < 0.05). There was no change in serum creatinine, β 2 ‐microglobulin, or endogenous creatinine clearance during guanfacine monotherapy. Our data suggest that guanfacine exerts its antihypertensive effect via the inhibition of sympathetic outflow and in part the suppression of the renin‐angiotensin‐aldosterone system and that guanfacine is suitable for the effective treatment of hypertension associated with chronic glomerulonephritis. Clinical Pharmacology and Therapeutics (1988) 43, 278–282; doi: 10.1038/clpt.1988.33