The ability of angiotensin to enhance the field-stimulation induced release of 3H-norepinephrine from the superfused rat portal vein was examined in vessels obtained from animals fed a normal (0.5%Na+) or low sodium diet (0.05%Na+). Angiotensin was seen to enhance the field-stimulation (480 pulses 2Hz) induced release of 3H-norepinephrine from vessels obtained from Sprague-Dawley

Wistar

Wistar-Kyoto and the Spontaneously Hypertensive Rat (SHR) maintained on a normal sodium diet. In contrast

the effect of angiotensin was attenuated when examined in vessels obtained from animals maintained on the low sodium diet. The selectivity of sodium depletion for angi-otensin was demonstrated by a lack of effect of low sodium diet in altering the facilitory effect of isoproterenol on adrenergic neurotransmission and an enhanced response to the a2 selective antagonist

yohimbine. The simultaneous treatment of rats with a low sodium diet plus captopril (50mg /kg/day for 7 days) prevented the attenuation of the angiotensin-induced enhancement of adrenergic neurotransmission seen by sodium depletion alone. These results are consistent with the hypothesis that sodium depletion increases circulating angiotensin levels which lead to a down-regulation of the angiotensin receptor located on adrenergic nerve varicosities.