Acute effects of alinidine on heart rate and blood pressure in healthy subjects and patients with hyperkinetic heart syndrome
Author(s) -
Brigitte Stanek,
W Reiterer,
P. Placheta,
G. Raberger
Publication year - 1983
Publication title -
european journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.845
H-Index - 108
eISSN - 1432-1041
pISSN - 0031-6970
DOI - 10.1007/bf00613923
Subject(s) - heart rate , blood pressure , propranolol , clonidine , medicine , catecholamine , tachycardia , endocrinology , anesthesia , cardiology
The effects of a single dose of alinidine (0.5 mg/kg i.v.), the N-allyl-derivative of clonidine, on heart rate and blood pressure were investigated in healthy volunteers and in patients with hyperkinetic heart syndrome, at rest and during bicycle exercise. In healthy volunteers plasma catecholamine levels were also determined. Alinidine did not change heart rate at rest in the healthy volunteers but it did significantly reduce exercise-induced tachycardia, whereas blood pressure and plasma catecholamine levels were not significantly affected by alinidine, either at rest or during exercise. In patients with hyperkinetic heart syndrome, alinidine reduced heart rate at rest and during exercise to a similar extent as propranolol (0.1 mg/kg i.v.). The blood pressure did not change with alinidine but it was significantly reduced by propranolol. The observation that an alinidine-induced reduction of heart rate occurs without a concomitant fall in blood pressure, and without a clonidine-like symphatho-inhibitory action, is in line with experimental findings suggesting a specific bradycardic action of alinidine under short-term conditions.
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