title: [Autoregulation of renal blood flow and blood pressure variability in the conscious rat].
abstract: It is often proposed that autoregulatory mechanisms prevent acute changes in systemic blood pressure (BP) from being transmitted to the glomerular capillary circulation. However, it is not known whether renal blood flow (RBF) is still autoregulated when the kidney is exposed to exaggerated BP fluctuations, in particular hypertensive episodes. The aim of the present study was therefore to evaluate the efficacy of renal autoregulatory responses in an animal model of BP lability, the sinoaortic denervated (SAD) rat. BP and RBF were simultaneously recorded in 8 SAD (2 wks before study) and 8 baroreceptor intact (INT) Sprague-Dawley rats during approximately 3 h of spontaneous activity. The left kidney used for RBF recordings was denervated to prevent the interference of changes in renal sympathetic tone with autoregulatory responses. The SAD procedure modified neither the mean BP nor the mean RBF levels (111 +/- 1 mmHg and 11.3 +/- 1.3 mL/min in INT rats: 113 +/- 6 mmHg and 11.1 +/- 0.9 mL/min in SAD rats). However, SAD strongly increased the BP variability (coefficient of variation: 5.9 +/- 0.2% and 18.2 +/- 1.1% in INT and SAD rats, respectively). In spite of this marked BP lability, RBF variability was not significantly affected by the SAD procedure (9.1 +/- 0.8% and 12.4 +/- 1.6% in INT and SAD rats, respectively). In SAD rats, spontaneous hypertensive episodes (top 1% of BP values: 174 +/- 10 mmHg) did not induce increases in RBF (10.5 +/- 1.0 ml/min). Fast Fourier transform analysis revealed that in SAD rats, autoregulatory mechanisms attenuated approximately 80% of BP fluctuations in the 0.0015-0.01 Hz frequency range, suggesting a major involvement of the tubuloglomerular feedback. In conclusion, autoregulatory mechanisms have an ample capacity to protect the kidney against spontaneous BP fluctuations in the conscious rat. Consequently, BP variability per se is probably not detrimental to the kidney, as long as autoregulatory mechanisms are normally functioning.
authors.affiliation: CNRS UMR 5014, IFR 39, université Claude-Bernard, 8, av. Rockefeller, 69373 Lyon.
authors.forename: S L
authors.initials: SL
authors.lastname: Pires
authors.forename: C
authors.initials: C
authors.lastname: Barrès
authors.forename: J
authors.initials: J
authors.lastname: Sassard
authors.forename: C
authors.initials: C
authors.lastname: Julien
mesh_terms: D000818:Animals; D001011:Aorta / Q000294:innervation / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D007668:Kidney / Q000098:blood supply*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow; D012849:Sinoatrial Node / Q000294:innervation / Q000502:physiology