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1 Department of Internal Medicine and Physiology & Biophyscis, University of Iowa College of Medicine, Iowa City, Iowa, USA
2 Department of Internal Medicine and Physiology & Biophyscis, University of Iowa College of Medicine, Iowa City, Iowa, USA; Internal Medicine, Veterans Administration Medical Center, Iowa City, Iowa, USA
* To whom correspondence should be addressed. E-mail: gerald-dibona{at}uiowa.edu.
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 reninangiotensin 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 reninangiotensin 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 high) sodium diet rats and that this was reversed by losartan administration. Thus, physiological increases in endogenous reninangiotensin 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.
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