Peripheral neural mechanism of hypertension in rat models--peripheral sympathetic neurotransmission in hypertension.

To investigate the peripheral neural mechanism of hypertension, norepinephrine release from sympathetic nerve endings was evaluated in various hypertensive rat models. The isolated mesenteric vasculatures were prepared in 7-9-week-old and 20-22-week-old spontaneously hypertensive rats (SHR), DOCA-salt hypertensive rats (DOCA-HT), two-kidney, one clip renal hypertensive rats (2K1C-HT) and their age-matched normotensive controls. The vasoconstrictor responses to exogenous norepinephrine (EN) were significantly enhanced in all hypertensive rat models compared with their age-matched normotensive controls. The pressor responses to electrical nerve stimulation (NS) were greater in SHR than age-matched Wistar-Kyoto (WKY) rats, and were also increased in DOCA-HT. The norepinephrine overflow during NS was significantly greater in young SHR and chronic DOCA-HT than in the normotensive controls. In 2K1C-HT, the norepinephrine overflow by NS was somewhat reduced compared with sham-operated normotensive controls. Inhibition by calcium-antagonist (verapamil) of the pressor responses and norepinephrine overflow during NS was significantly greater in young SHR and chronic DOCA-HT than in their controls. The facilitatory effect on the norepinephrine overflow exerted by the alpha 2-adrenoceptor antagonist, yohimbine, during NS was significantly less in young SHR and chronic DOCA-HT.