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Articles in PresS, published online ahead of print November 23, 2001
Am J Physiol Regu Physiol, 10.1152/ajpregu.00468.2001
Submitted on August 2, 2001
Accepted on November 21, 2001
1 Physiology, University of Mississippi Medical Center, Jackson, MS, USA
2 Physiology, Medical College of Georgia, Augusta, GA, USA
* To whom correspondence should be addressed. E-mail: brandsmcg{at}aol.com.
We demonstrated previously that induction of diabetes in rats treated chronically with the nitric oxide synthase inhibitor, L-NAME, causes a severe, progressive increase in mean arterial pressure. This study tested the role of the sympathetic nervous system in that response. Rats were instrumented with chronic artery and vein catheters and assigned randomly to 4 diabetic groups, pretreated with: vehicle (D), L-NAME (D+L), the 
1- and ß-adrenergic receptor anatagonists, terazosin and propranolol (D+B), or with L-NAME, terazosin and propranolol (D+LB). Following baseline measurements, rats were pretreated as above and 6 days later streptozotocin was administered, followed by 3 weeks of diabetes. The D+L rats had a marked and progressive increase in arterial pressure, which by day 20 was ~60 mmHg greater than in the D rats. The pressor response to L-NAME was significantly attenuated in diabetic rats co-treated with adrenergic blockers. During week 1 of diabetes, plasma renin activity (PRA) increased but then returned to control in the D rats, but there was a progressive increase in PRA in the D+L rats; chronic adrenergic receptor blockade restored the biphasic renin response in the D+LB rats. These results suggest that the sympathetic nervous system may be involved in the hypertensive response to onset of diabetes in L-NAME-treated rats, possibly through control of renin secretion.
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