title: Synchronization among mechanisms of renal autoregulation is reduced in hypertensive rats.
abstract: We searched for synchronization among autoregulation mechanisms using wavelet transforms applied to tubular pressure recordings in nephron pairs from the surface of rat kidneys. Nephrons have two oscillatory modes in the regulation of their pressures and flows: a faster (100-200 mHz) myogenic mode, and a slower (20-40 mHz) oscillation in tubuloglomerular feedback (TGF). These mechanisms interact; the TGF mode modulates both the amplitude and the frequency of the myogenic mode. Nephrons also communicate with each other using vascular signals triggered by membrane events in arteriolar smooth muscle cells. In addition, the TGF oscillation changes in hypertension to an irregular fluctuation with characteristics of deterministic chaos. The analysis shows that, within single nephrons of normotensive rats, the myogenic mode and TGF are synchronized at discrete frequency ratios, with 5:1 most common. There is no distinct synchronization ratio in spontaneously hypertensive rats (SHR). In normotensive rats, full synchronization of both TGF and myogenic modes is the most probable state for pairs of nephrons originating in a common cortical radial artery. For SHR, full synchronization is less probable; most common in SHR is a state of partial synchronization with entrainment between neighboring nephrons for only one of the modes. Modulation of the myogenic mode by the TGF mode is much stronger in hypertensive than in normotensive rats. Synchronization among nephrons forms the basis for an integrated reaction to blood pressure fluctuations. Reduced synchronization in SHR suggests that the effectiveness of the coordinated response is impaired in hypertension.
authors.affiliation: Department of Physics, The Technical University of Denmark, Kongens Lyngby, Denmark.
authors.forename: Olga V
authors.initials: OV
authors.lastname: Sosnovtseva
authors.forename: Alexey N
authors.initials: AN
authors.lastname: Pavlov
authors.forename: Erik
authors.initials: E
authors.lastname: Mosekilde
authors.forename: Kay-Pong
authors.initials: KP
authors.lastname: Yip
authors.forename: Niels-Henrik
authors.initials: NH
authors.lastname: Holstein-Rathlou
authors.forename: Donald J
authors.initials: DJ
authors.lastname: Marsh
mesh_terms: D000818:Animals; D001160:Arterioles / Q000503:physiopathology; D025461:Feedback, Physiological; D006706:Homeostasis; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000503:physiopathology; D007684:Kidney Tubules / Q000503:physiopathology; D008297:Male; D008954:Models, Biological; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D009399:Nephrons / Q000098:blood supply / Q000503:physiopathology; D009991:Oscillometry; D051381:Rats; D011918:Rats, Inbred SHR; D017207:Rats, Sprague-Dawley; D013997:Time Factors