Abstract
Chronic treatment (22 days) of rats with clonidine (0.5 mg/kg s.c. twice a day followed by 20 h of withdrawal) resulted in a significant increase in the specific [3H]WB4101 binding to ventricular and intraventricular septal α1-adrenoceptors but no alteration of the atrial α1-adrenoceptors. Scatchard analysis indicated that the increase in the [3H]WB4101 binding to the clonidine-treated cardiac tissues was due to an enhancement of the α1-adrenoceptor density since there was a significant increase in the Bmax value for the [3H]WB4101 binding to the treated ventricles without a change in the Kd value. The specific [3H]WB4101 binding to cardiac α1-adrenoceptors was not altered by the acute (1 day) or 7 days treatment with clonidine. Chronic treatment with clonidine had no significant effect on the specific [3H](-)DHA binding to the atrial and ventricular β-adrenoceptors. The noradrenaline (NA) concentrations in the clonidine-treated ventricles and intraventricular septae were decreased by 16-20%. These data provide biochemical evidence compatible with a significant reduction of sympathetic outflow to the ventricular myocardium by clonidine.
Original language | English (US) |
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Pages (from-to) | 115-118 |
Number of pages | 4 |
Journal | Naunyn-Schmiedeberg's Archives of Pharmacology |
Volume | 320 |
Issue number | 2 |
DOIs | |
State | Published - Aug 1982 |
Keywords
- Cardiac α-adrenoceptor
- Chronic clonidine treatment
- Noradrenaline concentrations
- Withdrawal syndromes
- [H]WB4101 binding
ASJC Scopus subject areas
- Pharmacology