Effects of a calcium-antagonist on vascular sympathetic nerve activity in salt-dependent hypertension

The purpose of the present study was to investigate the effects of a Ca2(+)-antagonist on vascular sympathetic nerve activity in salt-dependent hypertension. Isolated mesenteric vasculature preparations from reduced renal mass-salt hypertensive and age-matched normotensive control rats were used to examine the effects of diltiazem on vascular responsiveness and norepinephrine release from sympathetic nerve endings. Pressor responses and endogenous norepinephrine release during electrical nerve stimulation were significantly greater in preparations from salt-dependent hypertensive rats than from normotensive control rats. Diltiazem inhibited both stimulation-evoked pressor responses and norepinephrine release in a dose-dependent manner. The attenuation of these responses was more pronounced in preparations from rats with salt-dependent hypertension than in those from control rats. These results indicate that norepinephrine release from vascular adrenergic neurons is enhanced in the mesenteric vasculatures of rats with salt-dependent hypertension. The marked reduction of stimulation-evoked pressor responses and norepinephrine release by diltiazem suggests that enhanced Ca2(+)-dependent adrenergic transmission may contribute to the exaggerated vascular sympathetic tone in salt-dependent hypertension.