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[Central and peripheral actions of clonidine causing changes of the adrenal medullary functions in spontaneously
Abstract:
The central and peripheral effects of clonidine on the adrenal medullary function were investigated in the spontaneously hypertensive rats (SHR). Male 20-25 week old SHR of Wistar Okamoto strain were used (body weight 344.9 +/- 5.7 g). SHR were anesthetized with 50 mg/kg alpha-chloralose and 500 mg/kg urethane intraperitoneally. Tracheae were cannulated and connected to a respirator. Blood pressure and heart rate were recorded via left carotid artery. For the analysis of the adrenal function, adrenal venous catecholamine secretion rates and efferent adrenal nerve discharges were determined. Blood samples were collected from the left adrenal vein of the heparinized animal. Catecholamines in adrenal venous plasma were separated by high performance liquid chromatography and measured spectrofluorometrically using the trihydroxyindole method. Intravenous administration of clonidine decreased adrenal venous catecholamine secretion rates and adrenal nerve activity. Intracerebroventricular administration of clonidine also decreased adrenal nerve discharge rates. Furthermore, after acute splanchnicotomy, clonidine produced a significant decrease in epinephrine secretion rate from the denervated adrenal medulla during electrical stimulation of splanchnic nerve. These findings indicate that the adrenal medulla and the spinal and supraspinal structures are the responsible sites of action of clonidine induced adrenal suppressant effect. The fact that the clonidine induced decrease in adrenal catecholamine secretion rates was approximately parallel to the decrease in preganglionic adrenal nerve discharges in the nerve intact SHR, suggests that the central action of clonidine is important in the adrenal suppressant effect relative to its peripheral action.