Nonlinear analysis of renal autoregulation in rats using principal dynamic modes.

V Z Marmarelis; K H Chon; N H Holstein-Rathlou; D J Marsh

Nonlinear analysis of renal autoregulation in rats using principal dynamic modes.

V Z Marmarelis, K H Chon, N H Holstein-Rathlou, D J Marsh

Biomedicinsk Institut

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

20 Citationer (Scopus)

Abstract

Udgivelsesdato: null-null

Originalsprog	Engelsk
Tidsskrift	Annals of Biomedical Engineering
Vol/bind	27
Udgave nummer	1
Sider (fra-til)	23-31
Antal sider	8
ISSN	0090-6964
Status	Udgivet - 1999

Bibliografisk note

Keywords: Animals; Homeostasis; Kidney; Male; Models, Biological; Rats; Rats, Sprague-Dawley

Citationsformater

@article{ea64ced0ab6311ddb5e9000ea68e967b,

title = "Nonlinear analysis of renal autoregulation in rats using principal dynamic modes.",

abstract = "This article presents results of the use of a novel methodology employing principal dynamic modes (PDM) for modeling the nonlinear dynamics of renal autoregulation in rats. The analyzed experimental data are broadband (0-0.5 Hz) blood pressure-flow data generated by pseudorandom forcing and collected in normotensive and hypertensive rats for two levels of pressure forcing (as measured by the standard deviation of the pressure fluctuation). The PDMs are computed from first-order and second-order kernel estimates obtained from the data via the Laguerre expansion technique. The results demonstrate that two PDMs suffice for obtaining a satisfactory nonlinear dynamic model of renal autoregulation under these conditions, for both normotensive and hypertensive rats. Furthermore, the two PDMs appear to correspond to the two main autoregulatory mechanisms: the first to the myogenic and the second to the tubuloglomerular feedback (TGF) mechanism. This allows the study of the separate contributions of the two mechanisms to the autoregulatory response dynamics, as well as the effects of the level of pressure forcing and hypertension on the two distinct autoregulatory mechanisms. It is shown that the myogenic mechanism has a larger contribution and is affected only slightly, while the TGF mechanism is affected considerably by increasing pressure forcing or hypertension (the emergence of a second resonant peak and the decreased relative contribution to the response flow signal).",

author = "Marmarelis, {V Z} and Chon, {K H} and Holstein-Rathlou, {N H} and Marsh, {D J}",

note = "Keywords: Animals; Homeostasis; Kidney; Male; Models, Biological; Rats; Rats, Sprague-Dawley",

year = "1999",

language = "English",

volume = "27",

pages = "23--31",

journal = "Annals of Biomedical Engineering",

issn = "0090-6964",

publisher = "Springer",

number = "1",

}

TY - JOUR

T1 - Nonlinear analysis of renal autoregulation in rats using principal dynamic modes.

AU - Marmarelis, V Z

AU - Chon, K H

AU - Holstein-Rathlou, N H

AU - Marsh, D J

N1 - Keywords: Animals; Homeostasis; Kidney; Male; Models, Biological; Rats; Rats, Sprague-Dawley

PY - 1999

Y1 - 1999

N2 - This article presents results of the use of a novel methodology employing principal dynamic modes (PDM) for modeling the nonlinear dynamics of renal autoregulation in rats. The analyzed experimental data are broadband (0-0.5 Hz) blood pressure-flow data generated by pseudorandom forcing and collected in normotensive and hypertensive rats for two levels of pressure forcing (as measured by the standard deviation of the pressure fluctuation). The PDMs are computed from first-order and second-order kernel estimates obtained from the data via the Laguerre expansion technique. The results demonstrate that two PDMs suffice for obtaining a satisfactory nonlinear dynamic model of renal autoregulation under these conditions, for both normotensive and hypertensive rats. Furthermore, the two PDMs appear to correspond to the two main autoregulatory mechanisms: the first to the myogenic and the second to the tubuloglomerular feedback (TGF) mechanism. This allows the study of the separate contributions of the two mechanisms to the autoregulatory response dynamics, as well as the effects of the level of pressure forcing and hypertension on the two distinct autoregulatory mechanisms. It is shown that the myogenic mechanism has a larger contribution and is affected only slightly, while the TGF mechanism is affected considerably by increasing pressure forcing or hypertension (the emergence of a second resonant peak and the decreased relative contribution to the response flow signal).

AB - This article presents results of the use of a novel methodology employing principal dynamic modes (PDM) for modeling the nonlinear dynamics of renal autoregulation in rats. The analyzed experimental data are broadband (0-0.5 Hz) blood pressure-flow data generated by pseudorandom forcing and collected in normotensive and hypertensive rats for two levels of pressure forcing (as measured by the standard deviation of the pressure fluctuation). The PDMs are computed from first-order and second-order kernel estimates obtained from the data via the Laguerre expansion technique. The results demonstrate that two PDMs suffice for obtaining a satisfactory nonlinear dynamic model of renal autoregulation under these conditions, for both normotensive and hypertensive rats. Furthermore, the two PDMs appear to correspond to the two main autoregulatory mechanisms: the first to the myogenic and the second to the tubuloglomerular feedback (TGF) mechanism. This allows the study of the separate contributions of the two mechanisms to the autoregulatory response dynamics, as well as the effects of the level of pressure forcing and hypertension on the two distinct autoregulatory mechanisms. It is shown that the myogenic mechanism has a larger contribution and is affected only slightly, while the TGF mechanism is affected considerably by increasing pressure forcing or hypertension (the emergence of a second resonant peak and the decreased relative contribution to the response flow signal).

M3 - Journal article

C2 - 9916757

VL - 27

SP - 23

EP - 31

JO - Annals of Biomedical Engineering

JF - Annals of Biomedical Engineering

SN - 0090-6964

IS - 1

ER -