Talk abstract:

Renal Blood Flow Dynamics After NO Synthase Inhibition

William A. Cupples
SMBD-Jewish General Hospital
wcupples@ldi.jgh.mcgill.ca

Inhibition of nitric oxide synthase causes profound renal vasoconstriction that is proportional to the prior blood flow. There are also significant changes in the blood pressure - renal blood flow transfer function, particularly in the myogenic component. These include: 1) increased positive gain in the pressure passive region of the spectrum above 0.25 Hz, 2) emergence of a large resonance peak in gain at the system's operating frequency of (approx) 0.25 Hz, 3) increased amplitude of the phase peak to pi/2 rad, and 4) increased rate of gain roll-off below 0.2 Hz to (approx) 40 dB/decade. These changes are interpreted to indicate uncovering of a significant second order component in the myogenic system. In the mesenteric circulation, which also shows effective autoregulation mediated by a myogenic mechanism, inhibition of nitric oxide synthase has somewhat different effects. The vasoconstriction appears to be less profound, though still proportional to the prior blood flow. Effects on dynamic autoregulation were less apparent in this bed. The resonance peak in gain at (approx) 0.15 Hz remains small, the phase peak remains < pi/2 rad, and the rate of gain roll-off is unchanged at (approx) 20 dB/decade, indicating a predominantly first order system. However gain in the pressure-passive region of the spectrum > 0.2 Hz becomes significantly more positive. This is difficult to explain as positive gain is typically considered to result from vascular compliance which is reduced during strong vasoconstriction such as that evoked by inhibition of nitric oxide synthase.

Back to Workshop Schedule

1998-1999 Mathematics in Biology