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1 Physiology, University of Minnesota, Minneapolis, MN, USA
* To whom correspondence should be addressed. E-mail: osbor003{at}umn.edu.
Centrally-mediated hyperactivity of the autonomic nervous system contributes to deoxycorticosterone acetate (DOCA) hypertension but the targeted peripheral vascular bed(s) remain unclear. We propose that if renal sympathetic activity is a factor in the development of DOCA-salt hypertension, then renal denervation (RDNX) should attenuate the hypertensive response. In Protocol 1, uniphrectomized RDNX (n=9) and sham-denervated (n=6) Sprague-Dawley rats were allowed free access to 0.9% NaCl solution and 0.1% NaCl diet. Mean arterial pressure (MAP) and heart rate (HR) were telemetrically recorded for 4 days prior to and 36 days following DOCA (100 mg/rat) implantation; sodium and water balances were recorded daily. Protocol 2 was similar except that saline intake in sham rats (n=7) was matched to that observed in RDNX rats of Protocol 1 for 30 days; for the last 10 days, rats were allowed free access to saline. Prior to DOCA in Protocol 1, MAP was lower (P<0.05) in RDNX (99±1 mmHg) compared to SHAM (111±3) rats but HR, sodium and water balances were similar between groups. RDNX attenuated the MAP response to DOCA by approximately 50% (
MAP= 22±3 mmHg) compared to SHAM (MAP= 38±6) rats. RDNX rats consumed significantly less saline than SHAM rats and cumulative sodium and water balances were reduced by 33% and 23%, respectively. In Protocol 2, a similar pattern in MAP elevation was observed in RDNX and saline restricted sham-denervated rats even when saline restriction was removed. These results indicate that the renal sympathetic nerves are important in hypertension development but other factors are also involved.
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