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1 Physics, Danish Technical University, Lyngby, Denmark
2 Physics, Saratov State University, Saratov, Russian Federation
3 Department of Physics, Technical University of Denmark, 2800 Kgs. Lyngby, Denmark
4 Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida, United States; Molecular Pharmacology and Physiology , University of South Florida, College of Medicine MDC 8, Tampa, Florida, United States
5 Department of Medical Physiology, The Panum Instititute, Copenhagen N, Denmark
6 Molecular Pharmacology, Physiology, and Biotechnology, Brown University, Providence, Rhode Island, United States
* To whom correspondence should be addressed. E-mail: marsh{at}ash.biomed.brown.edu.
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). 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 neighbouring 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.
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