title: The step response: a method to characterize mechanisms of renal blood flow autoregulation.
abstract: Response of renal vasculature to changes in renal perfusion pressure (RPP) involves mechanisms with different frequency characteristics. Autoregulation of renal blood flow (RBF) is mediated by the rapid myogenic response, by the slower tubuloglomerular feedback (TGF) mechanism, and, possibly, by an even slower third mechanism. To evaluate the individual contribution of these mechanisms to RBF autoregulation, we analyzed the response of RBF to a step increase in RPP. In anesthetized rats, the suprarenal aorta was occluded for 30 s, and then the occlusion was released to induce a step increase in RPP. Three dampened oscillations were observed; their oscillation periods ranged from 9.5 to 13 s, from 34.2 to 38.6 s, and from 100.5 to 132.2 s, respectively. The two faster oscillations correspond with previously reported data on the myogenic mechanism and the TGF. In accordance, after furosemide, the amplitude of the intermediate oscillation was significantly reduced. Inhibition of nitric oxide synthesis by Nomega-nitro-l-arginine methyl ester significantly increased the amplitude of the 10-s oscillation. It is concluded that the parameters of the dampened oscillations induced by the step increase in RPP reflect properties of autoregulatory mechanisms. The oscillation period characterizes the individual mechanism, the dampening is a measure for the stability of the regulation, and the square of the amplitudes characterizes the power of the respective mechanism. In addition to the myogenic response and the TGF, a third rather slow mechanism of RBF autoregulation exists.
authors.affiliation: Johannes Müller Institut für Physiologie, Humboldt-Universität (Charité), Berlin, Germany. thomas.wronski@charite.de
authors.forename: T
authors.initials: T
authors.lastname: Wronski
authors.forename: E
authors.initials: E
authors.lastname: Seeliger
authors.forename: P B
authors.initials: PB
authors.lastname: Persson
authors.forename: C
authors.initials: C
authors.lastname: Forner
authors.forename: C
authors.initials: C
authors.lastname: Fichtner
authors.forename: J
authors.initials: J
authors.lastname: Scheller
authors.forename: B
authors.initials: B
authors.lastname: Flemming
mesh_terms: D000818:Animals; D001011:Aorta / Q000502:physiology; D001794:Blood Pressure; D004232:Diuretics / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005246:Feedback; D005665:Furosemide / Q000494:pharmacology; D006706:Homeostasis; D007678:Kidney Glomerulus / Q000187:drug effects / Q000502:physiology; D007684:Kidney Tubules / Q000187:drug effects / Q000502:physiology; D008955:Models, Cardiovascular; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009398:Nephrology / Q000379:methods*; D009569:Nitric Oxide / Q000037:antagonists & inhibitors; D009991:Oscillometry; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology*
chemical_list: D004232:Diuretics; D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D005665:Furosemide; D019331:NG-Nitroarginine Methyl Ester