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Intravenous Pinacidil in the Acute Treatment of Hypertension
Author(s) -
Rijk M. C. M.,
Thien Th.
Publication year - 1987
Publication title -
the journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.92
H-Index - 116
eISSN - 1552-4604
pISSN - 0091-2700
DOI - 10.1002/j.1552-4604.1987.tb03051.x
Subject(s) - pinacidil , plasma renin activity , blood pressure , heart rate , vasodilation , medicine , renin–angiotensin system , metabolite , aldosterone , anesthesia , chemistry , pharmacology , endocrinology , glibenclamide , diabetes mellitus
Pinacidil (N“‐cyano‐N‐4‐pyridyls‐N′‐1,2,2‐trimethyl‐propyl guanidine, monohydrate), a recently developed direct‐acting vasodilator, was given intravenously in a dosage of 0.1‐0.2 mg/kg body weight to ten untreated hypertensive patients. Pinacidil caused a fall of blood pressure from 170/108 ± 6/3 to 156/80 ± 5/4 mm Hg (mean ± SE). The proportional decrease of mean arterial pressure (MAP) was 13.7 ± 1.6%. Together with the decrease of blood pressure an increase of heart rate by 29.7 ± 6.2% occurred. The heart rate increased by 13.6 beats/min per 10 mm Hg decrease of MAP. Pinacidil also caused significant rise of plasma noradrenaline and plasma renin activity, whereas plasma adrenaline and aldosterone remained unchanged. The serum concentrations of pinacidil and its major metabolite pinacidil‐N‐oxyde were within the expected limits. The authors conclude that intravenously administered pinacidil causes a rapid decrease of blood pressure, but at the cost of a considerable increase of heart rate, and thus does not offer advantages over other vasodilators.