Circulation Research. 2002;90:1316-1324
Published online before print May 30, 2002, doi: 10.1161/01.RES.0000024262.11534.18
Published online before print May 30, 2002, doi: 10.1161/01.RES.0000024262.11534.18
© 2002 American Heart Association, Inc.
Integrative Physiology |
Renal Myogenic Response
Kinetic Attributes and Physiological Role
From the Smooth Muscle Research Group (R.L., L.C.), Department of Pharmacology and Therapeutics, The University of Calgary, Calgary, Alberta, Canada; and the Division of Nephrology and Hypertension (A.B.), Department of Medicine, Loyola University, Chicago, Hines Veteran’s Administration Medical Center, Maywood, Ill.
Correspondence to Rodger D. Loutzenhiser, PhD, Dept of Pharmacology and Therapeutics, The University of Calgary, Health Sciences Centre, 3330 Hospital Dr NW, Calgary, Alberta T2N 4N1, Canada. E-mail rloutzen{at}ucalgary.ca
The kinetic attributes of the afferent arteriole myogenic response were investigated using the in vitro perfused hydronephrotic rat kidney. Equations describing the time course for pressure-dependent vasoconstriction and vasodilation, and steady-state changes in diameter were combined to develop a mathematical model of autoregulation. Transfer functions were constructed by passing sinusoidal pressure waves through the model. These findings were compared with results derived using data from instrumented conscious rats. In each case, a reduction in gain and increase in phase were observed at frequencies of 0.2 to 0.3 Hz. We then examined the impact of oscillating pressure signals. The model predicted that pressure signals oscillating at frequencies above the myogenic operating range would elicit a sustained vasoconstriction the magnitude of which was dependent on peak pressure. These predictions were directly confirmed in the hydronephrotic kidney. Pressure oscillations presented at frequencies of 1 to 6 Hz elicited sustained afferent vasoconstrictions and the magnitude of the response depended exclusively on the peak pressure. Elevated systolic pressure elicited vasoconstriction even if mean pressure was reduced. These findings challenge the view that the renal myogenic response exists to maintain glomerular capillary pressure constant, but rather imply a primary role in protecting against elevated systolic pressures. Thus, the kinetic features of the afferent arteriole allow this vessel to adjust tone in response to changes in systolic pressures presented at the pulse rate. We suggest that the primary function of this mechanism is to protect the glomerulus from the blood pressure power that is normally present at the pulse frequency.
Key Words: renal hemodynamics • myogenic vasoconstriction • frequency domain analysis • renal autoregulation • mathematical modeling
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