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Cortisol and alpha 2 adrenergic regulation of sympathoneural activity



Cortisol and alpha 2 adrenergic regulation of sympathoneural activity



Biogenic Amines 7(5): 445-454



Alpha-2 adrenoceptor regulation of sympathoneural function was assessed in conscious, unrestrained Wistar-Kyoto rats during chronic glucocorticoid treatment. Cortisol administered for seven days via a subcutaneous reservoir pump increased blood pressure, decreased body weight and decreased plasma norepinephrine (NE) levels. In untreated animals, intravenous administration of the alpha-2 adrenoceptor antagonist, yohimbine, increased plasma levels of NE and of dihydroxyphenylglycol (DHPG), the main intraneuronal metabolite of NE. Cortisol treatment abolished these responses to yohimbine. Intravenous administration of clonidine, an agonist at alpha-2 adrenoceptors, decreased plasma NE levels; cortisol treatment did not affect the proportionate decreases in NE and DHPG levels produced by clonidine or alter the inhibitory effect of clonidine on reflexive catecholamine responses induced by sodium-nitroprusside. The results suggest that hypercortisolemia suppresses sympathetic activity and may also interfere indirectly with central neural noradrenergic mechanisms regulating sympathoneural outflow.

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