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Am J Physiol Renal Physiol 287: F1171-F1178, 2004. First published August 3, 2004; doi:10.1152/ajprenal.00201.2004
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Effect of endogenous angiotensin II on the frequency response of the renal vasculature

Gerald F. DiBona and Linda L. Sawin

Departments of Internal Medicine and Physiology and Biophysics, University of Iowa College of Medicine, and Veterans Administration Medical Center, Iowa City, Iowa 52242

Submitted 1 June 2004 ; accepted in final form 27 July 2004

The renal vasculature functions as an efficient low-pass filter of the multiple frequencies contained within renal sympathetic nerve activity. This study examined the effect of angiotensin II on the frequency response of the renal vasculature. Physiological changes in the activity of the endogenous renin-angiotensin system were produced by alterations in dietary sodium intake. The frequency response of the renal vasculature was evaluated using pseudorandom binary sequence renal nerve stimulation, and the role of angiotensin II was evaluated by the administration of the angiotensin II AT1-receptor antagonist losartan. In low-sodium-diet rats with increased renin-angiotensin system activity, losartan steepened the renal vascular frequency response (i.e., greater attenuation); this was not seen in normal- or high-sodium-diet rats with normal or decreased renin-angiotensin system activity. Analysis of the transfer function from arterial pressure to renal blood flow, i.e., dynamic autoregulation, showed that the tubuloglomerular feedback but not the myogenic component was enhanced in low- and normal- but not in high-sodium-diet rats and that this was reversed by losartan administration. Thus physiological increases in endogenous renin-angiotensin activity inhibit the renal vascular frequency response to renal nerve stimulation while selectively enhancing the tubuloglomerular feedback component of dynamic autoregulation of renal blood flow.

renal sympathetic nerves; renal blood flow; angiotensin II AT1 receptors



Address for reprint requests and other correspondence: G. F. DiBona, Dept. of Internal Medicine, Univ. of Iowa College of Medicine, 200 Hawkins Dr., Iowa City, IA 52242 (E-mail: gerald-dibona{at}uiowa.edu)




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