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Am J Physiol Heart Circ Physiol 284: H1601-H1611, 2003. First published January 9, 2003; doi:10.1152/ajpheart.00578.2002
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Vol. 284, Issue 5, H1601-H1611, May 2003

Effect of blockade of endogenous angiotensin II on baroreflex function in conscious diabetic rats

Maria Maliszewska-Scislo1,3, Tadeusz J. Scislo3, and Noreen F. Rossi1,2

1 Departments of Medicine and Physiology, Wayne State University and 2 John D. Dingell Veterans Affairs Medical Center, Detroit, Michigan 48201; and 3 Department of Physiology, University of Gdansk, 80-822 Gdansk, Poland

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 55 mg/kg iv streptozotocin (diabetic) before and after losartan (5 mg/kg iv) or enalapril (2.5 mg/kg iv). Resting HR and RSNA were lower in diabetic versus 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 the diabetic rats 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 the 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 of diabetes. At this time, the baroreflex control of HR is already impaired and blockade of endogenous ANG II does not improve this dysfunction.

baroreceptors; enalapril; heart rate; losartan; renal sympathetic nerve activity


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