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Effects of epinephrine and dopamine on norepinephrine release from the sympathetic nerve endings in hypertension.

The purpose of the present study was to analyse the regulatory mechanisms of epinephrine and dopamine on norepinephrine release from the sympathetic nerve endings in the resistance vessels in hypertension. The perfused mesenteric arteries were used for the experiment in spontaneously hypertensive rats (SHR; 7-10 weeks old) and age-matched normotensive Wistar-Kyoto (WKY) rats. Norepinephrine overflow during electrical nerve stimulation was significantly greater in SHR than in WKY rats. A low concentration of epinephrine (5.5 X 10(-9) mol/l) potentiated norepinephrine overflow from the nerve endings in SHR, and this was antagonized by propranolol, while this overflow was reduced by the same concentration of epinephrine in WKY rats. Higher concentrations of epinephrine decreased the norepinephrine overflow both in SHR and WKY rats, and this was antagonized by yohimbine. Dopamine reduced the norepinephrine overflow during electrical nerve stimulation, suppression being significantly less in SHR than in WKY rats. These results suggest that in SHR the increased norepinephrine overflow from sympathetic nerve endings may be partly caused by the facilitatory effect of epinephrine (through presynaptic beta-adrenoceptors) and impaired dopamine-mediated inhibition on the nerve terminals, which might contribute to the enhanced adrenergic activity in hypertension.