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RENAL HEMODYNAMICS AND CARDIORENAL INTEGRATION
1Smooth Muscle Research Group, Faculty of Medicine, University of Calgary, Calgary, Alberta; 2Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, Quebec; and 3Department of Biology and Centre for Biomedical Research, University of Victoria, Victoria, British Columbia, Canada
Submitted 24 April 2007 ; accepted in final form 9 July 2007
Recent studies of renal autoregulation have shown modulation of the faster myogenic mechanism by the slower tubuloglomerular feedback and that the modulation can be detected in the dynamics of the myogenic mechanism. Conceptual and empirical considerations suggest that perfusion pressure may modulate the myogenic mechanism, although this has not been tested to date. Here we present data showing that the myogenic operating frequency, assessed by transfer-function analysis, varied directly as a function of perfusion pressure in the hydronephrotic kidney perfused in vitro over the range from 80 to 140 mmHg. A similar result was obtained in intact kidneys in vivo when renal perfusion pressure was altered by systemic injection of NG-nitro-L-arginine methyl ester (L-NAME). When perfusion pressure was not allowed to increase, L-NAME did not affect the myogenic operating frequency despite equivalent reduction of renal vascular conductance. Blood-flow dynamics were assessed in the superior mesenteric artery before and after L-NAME. In this vascular bed, the operating frequency of the myogenic mechanism was not affected by perfusion pressure. Thus the operating frequency of the renal myogenic mechanism is modulated by perfusion pressure independently of tubuloglomerular feedback, and the data suggest some degree of renal specificity of this response.
dynamics; tubuloglomerular feedback; interaction
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