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RENAL HEMODYNAMICS AND CARDIORENAL INTEGRATION

Tubuloglomerular feedback-dependent modulation of renal myogenic autoregulation by nitric oxide

¹Biology Department, Concordia University, and ²Lady Davis Institute for Medical Research, SMBD-Jewish General Hospital, Montreal, Quebec; ³Smooth Muscle Research Group, Faculty of Medicine, University of Calgary, Calgary, Alberta; ⁵Centre for Biomedical Research and Department of Biology, University of Victoria, Victoria, British Columbia, Canada; and ⁴Departments of Biomedical Engineering and Physiology, State University of New York Stony Brook, Stony Brook, New York

Submitted 16 May 2005 ; accepted in final form 14 November 2005

Nonselective inhibition of nitric oxide (NO) synthase (NOS) augments myogenic autoregulation, an action that implies enhancement of pressure-induced constriction and dilatation. This pattern is not explained solely by interaction with a vasoconstrictor pathway. To test involvement of the Rho-Rho kinase pathway in modulation of autoregulation by NO, the selective Rho kinase inhibitor Y-27632 and/or the NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME) were infused into the left renal artery of anesthetized rats. Y-27632 and L-NAME were also infused into isolated, perfused hydronephrotic kidneys to assess myogenic autoregulation over a wide range of perfusion pressure. In vivo, L-NAME reduced renal vascular conductance and augmented myogenic autoregulation, as shown by increased slope of gain reduction and associated phase peak in the pressure-flow transfer function. Y-27632 (10 µmol/l) strongly dilated the renal vasculature and profoundly inhibited autoregulation in the absence or presence of L-NAME in vivo and in vitro. Afferent arteriolar constriction induced by 30 mmol/l KCl was reversed (–92 ± 3%) by Y-27632. Phenylephrine caused strong renal vasoconstriction but did not affect autoregulation. Inhibition of neuronal NOS by N⁵-(1-imino-3-butenyl)-L-ornithine (L-VNIO) did not cause significant vasoconstriction but did augment myogenic autoregulation. Thus vasoconstriction is neither necessary (L-VNIO) nor sufficient (phenylephrine) to explain the augmented myogenic autoregulation induced by L-NAME. The effect of L-VNIO implicates tubuloglomerular feedback (TGF) and neuronal NOS at the macula densa in regulation of the myogenic mechanism. This conclusion was confirmed by the demonstration that systemic furosemide removed the TGF signature from the pressure-flow transfer function and significantly inhibited myogenic autoregulation. In the presence of furosemide, augmentation of myogenic autoregulation by L-NAME was significantly reduced. These results provide a potential mechanism to explain interaction between myogenic and TGF-mediated autoregulation.

kidney; blood flow; dynamics

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