(Hypertension. 1999;34:1012-1015.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Cardiovascular Effects of Clonidine-Like Drugs in Pithed Rabbits
From the Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil, and the Laboratoire de Neurobiologie et Pharmacologie Cardiovasculaire, Faculté de Médecine, ULP, Strasbourg, France.
Correspondence to Maria Cristina O. Salgado, PhD, Department of Pharmacology, School of Medicine-USP, 14049-900 Ribeirão Preto, SP, Brazil. E-mail mcdosalg{at}fmrp.usp.br
Abstract—Administration (3 to
100 µg/kg IV) of clonidine, rilmenidine, and an imidazoline
derivative, 2-(2-chlorophenylamino)imidazoline, in pithed nonstimulated
rabbits caused a dose-dependent increase in mean arterial
pressure without affecting heart rate. Prazosin (0.1 mg/kg IV) almost
abolished the pressor responses to 2-(2-chlorophenylamino)imidazoline,
partially inhibited those induced by clonidine, but failed to affect
those elicited by rilmenidine. In contrast, yohimbine (1 mg/kg IV)
blunted the pressor responses of the 3 drugs. In sympathetically
stimulated pithed rabbits, 2-(2-chlorophenylamino)imidazoline induced
only pressor effects, whereas clonidine and rilmenidine caused a
transient pressure increase followed by a dose-dependent depressor
effect. Yohimbine abolished the depressor effect of both drugs, which
may have involved presynaptic 
2-adrenoceptors. In
conclusion, peripheral effects of
2-(2-chlorophenylamino)imidazoline and clonidine involved at least
1- and 2-adrenoceptor activation, whereas
pressor and depressor effects of rilmenidine were mediated by
2-adrenoceptors.
Key Words: adrenergic receptors • sympathetic • antihypertensive agents