1987 Volume 51 Issue 10 Pages 1131-1137
The present study was carried out to elucidate the role of epinephrine as a neuromodulator in hypertension. The effects of epinephrine on norepinephrine release form the sympathetic nerve endings were examined in isolated perfused mesenteric arteries of spontaneously hypertensive rats (SHR) and age-matched Wistar Kyoto rats (WKY). Norepinephrine overflow during electrical nerve stimulation (5, 15 Hz) was significantly greater in SHR than in WKY. Low concentration of exogenous epinephrine (5.5×10-9 M) potentiated norepinephrine overflow during nerve stimulation in SHR, and this (at 15 Hz stimulation) was antagonized by propranolol (5.0×10-7 M), whereas, the overflow in WKY was reduced y the same concentration of epinephrine. A high concentration of epinephrine (1.4×10-8 M) decreased norepinephrine overflow in both SHR and WKY, and this change (at 15 Hz stimulation) was antagonized by yohimbine (1.0×10-7 M). Further, magnitudes of the suppression were smaller in SHR than in WKY. These results suggest that altered modulations of norepinephrine release by epinephrine through presynaptic β- and α2-adrenoceptors might induce increased sympathetic nerve activity in SHR.
