Chaos and non-linear phenomena in renal vascular control.

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Chaos and non-linear phenomena in renal vascular control. / Yip, K P; Holstein-Rathlou, N H.

I: Cardiovascular Research, Bind 31, Nr. 3, 1996, s. 359-70.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Yip, KP & Holstein-Rathlou, NH 1996, 'Chaos and non-linear phenomena in renal vascular control.', Cardiovascular Research, bind 31, nr. 3, s. 359-70.

APA

Yip, K. P., & Holstein-Rathlou, N. H. (1996). Chaos and non-linear phenomena in renal vascular control. Cardiovascular Research, 31(3), 359-70.

Vancouver

Yip KP, Holstein-Rathlou NH. Chaos and non-linear phenomena in renal vascular control. Cardiovascular Research. 1996;31(3):359-70.

Author

Yip, K P ; Holstein-Rathlou, N H. / Chaos and non-linear phenomena in renal vascular control. I: Cardiovascular Research. 1996 ; Bind 31, Nr. 3. s. 359-70.

Bibtex

@article{7d9c4340abeb11ddb5e9000ea68e967b,
title = "Chaos and non-linear phenomena in renal vascular control.",
abstract = "Renal autoregulation of blood flow depends on the functions of the tubuloglomerular feedback (TGF) system and the myogenic response of the afferent arteriole. Studies of the dynamic aspects of these control mechanisms at the level of both the single nephron and the whole kidney have revealed a variety of non-linear phenomena. In halothane-anesthetized, normotensive rats the TGF system oscillates regularly at 2-3 cycles/min because of the non-linearities and the time delays within the feedback system. Oscillations are present in single nephron blood flow, tubular pressure and flow, and in the tubular solute concentrations. Nephrons deriving their afferent arteriole from the same cortical radial artery are entrained, and consequently oscillate at the same frequency. Experimental studies have shown that the synchronization is due to an interaction of the TGF between nephrons. A necessary condition for the interaction is that the nephrons derive their blood supply from the same cortical radial artery. Development of hypertension is associated with a shift from periodic oscillations of tubular pressure to random-like fluctuations. Numerical analyses indicate that these fluctuations are an example of deterministic chaos. Experimental studies show that the development of hypertension is associated with an increase in strength of the interaction between nephrons. Mathematical models suggest that an increased nephron-nephron interaction could cause a bifurcation in the dynamics of TGF from periodic oscillations to deterministic chaos. In addition to the TGF mediated oscillation, experimental studies have also demonstrated the presence of a faster oscillation, this having a frequency of 120-160 mHz. This is caused by a mechanism intrinsic to the vascular wall, and presumably represents the well-known phenomenon of vasomotion. Using newly developed non-linear analytical methods non-linear interactions between vasomotion and the TGF mediated oscillation were detected both in single nephron and in whole kidney blood flow. The physiological significance of these non-linear phenomena in renal vascular control is discussed.",
author = "Yip, {K P} and Holstein-Rathlou, {N H}",
note = "Keywords: Animals; Hemodynamics; Homeostasis; Humans; Hypertension; Models, Biological; Nonlinear Dynamics; Rats; Regional Blood Flow; Renal Circulation",
year = "1996",
language = "English",
volume = "31",
pages = "359--70",
journal = "Cardiovascular Research",
issn = "0008-6363",
publisher = "Oxford University Press",
number = "3",

}

RIS

TY - JOUR

T1 - Chaos and non-linear phenomena in renal vascular control.

AU - Yip, K P

AU - Holstein-Rathlou, N H

N1 - Keywords: Animals; Hemodynamics; Homeostasis; Humans; Hypertension; Models, Biological; Nonlinear Dynamics; Rats; Regional Blood Flow; Renal Circulation

PY - 1996

Y1 - 1996

N2 - Renal autoregulation of blood flow depends on the functions of the tubuloglomerular feedback (TGF) system and the myogenic response of the afferent arteriole. Studies of the dynamic aspects of these control mechanisms at the level of both the single nephron and the whole kidney have revealed a variety of non-linear phenomena. In halothane-anesthetized, normotensive rats the TGF system oscillates regularly at 2-3 cycles/min because of the non-linearities and the time delays within the feedback system. Oscillations are present in single nephron blood flow, tubular pressure and flow, and in the tubular solute concentrations. Nephrons deriving their afferent arteriole from the same cortical radial artery are entrained, and consequently oscillate at the same frequency. Experimental studies have shown that the synchronization is due to an interaction of the TGF between nephrons. A necessary condition for the interaction is that the nephrons derive their blood supply from the same cortical radial artery. Development of hypertension is associated with a shift from periodic oscillations of tubular pressure to random-like fluctuations. Numerical analyses indicate that these fluctuations are an example of deterministic chaos. Experimental studies show that the development of hypertension is associated with an increase in strength of the interaction between nephrons. Mathematical models suggest that an increased nephron-nephron interaction could cause a bifurcation in the dynamics of TGF from periodic oscillations to deterministic chaos. In addition to the TGF mediated oscillation, experimental studies have also demonstrated the presence of a faster oscillation, this having a frequency of 120-160 mHz. This is caused by a mechanism intrinsic to the vascular wall, and presumably represents the well-known phenomenon of vasomotion. Using newly developed non-linear analytical methods non-linear interactions between vasomotion and the TGF mediated oscillation were detected both in single nephron and in whole kidney blood flow. The physiological significance of these non-linear phenomena in renal vascular control is discussed.

AB - Renal autoregulation of blood flow depends on the functions of the tubuloglomerular feedback (TGF) system and the myogenic response of the afferent arteriole. Studies of the dynamic aspects of these control mechanisms at the level of both the single nephron and the whole kidney have revealed a variety of non-linear phenomena. In halothane-anesthetized, normotensive rats the TGF system oscillates regularly at 2-3 cycles/min because of the non-linearities and the time delays within the feedback system. Oscillations are present in single nephron blood flow, tubular pressure and flow, and in the tubular solute concentrations. Nephrons deriving their afferent arteriole from the same cortical radial artery are entrained, and consequently oscillate at the same frequency. Experimental studies have shown that the synchronization is due to an interaction of the TGF between nephrons. A necessary condition for the interaction is that the nephrons derive their blood supply from the same cortical radial artery. Development of hypertension is associated with a shift from periodic oscillations of tubular pressure to random-like fluctuations. Numerical analyses indicate that these fluctuations are an example of deterministic chaos. Experimental studies show that the development of hypertension is associated with an increase in strength of the interaction between nephrons. Mathematical models suggest that an increased nephron-nephron interaction could cause a bifurcation in the dynamics of TGF from periodic oscillations to deterministic chaos. In addition to the TGF mediated oscillation, experimental studies have also demonstrated the presence of a faster oscillation, this having a frequency of 120-160 mHz. This is caused by a mechanism intrinsic to the vascular wall, and presumably represents the well-known phenomenon of vasomotion. Using newly developed non-linear analytical methods non-linear interactions between vasomotion and the TGF mediated oscillation were detected both in single nephron and in whole kidney blood flow. The physiological significance of these non-linear phenomena in renal vascular control is discussed.

M3 - Journal article

C2 - 8681323

VL - 31

SP - 359

EP - 370

JO - Cardiovascular Research

JF - Cardiovascular Research

SN - 0008-6363

IS - 3

ER -

ID: 8439672