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1 Department of Medicine, Wayne State University, Detroit, MI, USA; Department of Physiology, University of Gdansk, Gdansk, Poland
2 Department of Physiology, Wayne State University, Detroit, MI, USA
3 Department of Medicine, Wayne State University, Detroit, MI, USA; Department of Physiology, Wayne State University, Detroit, MI, USA; Department of Medicine, John D. Dingell VAMC, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: nrossi{at}intmed.wayne.edu.
Little is known about baroreflex control of renal nerve sympathetic activity (RSNA) or the effect of angiotensin II (Ang II) on the baroreflex in diabetes. We examined baroreflex control of RSNA and heart rate (HR) in conscious, chronically instrumented rats 2-wk after citrate vehicle (normal) or streptozotocin 55 mg/kg iv (diabetic) before and after losartan (5 mg/kg iv) or enalapril (2.5 mg/kg iv). Resting HR and RSNA were lower in diabetic vs normal rats. The range of baroreflex control of HR and the gain of baroreflex-mediated bradycardia were impaired in diabetic rats. Maximum gain was unchanged. The baroreflex control of RSNA was reset to lower pressures in diabetics, but remained otherwise unchanged. Losartan decreased mean arterial pressure (MAP) and increased HR and RSNA in both groups, but had no influence on the baroreflex. Enalapril decreased MAP only in normal rats, yet the increase in HR and RSNA was similar in both groups. Thus, in diabetic rats enalapril produced a pressure-independent increase in HR and RSNA. Enalapril exerted no effect on baroreflex control of HR or RSNA in either group. These data indicate that in conscious rats resting RSNA is lower but baroreflex control of RSNA is preserved after 2-wk diabetes. At this time, the baroreflex control of HR is already impaired and blockade of endogenous Ang II does not improve this dysfunction.
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