In many experimental models, acute increases in sympathetic nerrous system activity produce disproportionately greater vasoconstriction in the renal vascular bed than occurs in most other vascular beds. Since increased sympathetic nervous system activity has been implicated in the patbogenesis of DOCA-salt hypertension in the rat, we hypothesized that an attenuation of renal sympathetic tone would delay the development of this form of hypertension. Renal denervation was carried out in 5-week-old unlnephrectomized male Sprague-Dawley rats 1 week before beginning DOCA-salt treatment. Systolic blood pressures using the tailcuff method in 32 sham-operated rats were significantly (p < 0.05) elevated above control by Day five (115 ± 3 vs 128 ± 3 mm Hg) of DOCA-salt administration and continued to rise, reaching a platean by Day 21 (192 ± 5 mm Hg). In contrast, DOCA-salt administration in 32 renal denervated rats did not result In a significant elevation of blood pressure above control until Day 17 (121 ± 3 TS 135 ± 3 mm Hg, p < 0.05). During the first 2 weeks of DOCA-salt treatment, fractional urinary sodium excretion was significantly greater (p < 0.05) in renal denervated rats than in sham animals. During the third week of DOCA-salt administration, renal denervated rats had a rapid rise in blood pressure and a fall in fractional urinary sodium excretion to the level of the sham-operated animals. Coincident with the development of hypertension was a threefold increase in renal norepinephrine content (5.3 ± 0.4 ng/g on Day 14 vs 17.7 ± 3.0 ng/g on Day 24, p < 0.01), suggesting reinnervation. These data suggest that increased renal sympathetic tone in the DOCA-salt rat facilitates sodium retention and is necessary for the development of the hypertension. © 1980 American Heart Association, Inc.
