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Nitric oxide, atrial natriuretic factor, and dynamic renal autoregulation
X Wang1, F C Salevsky, W A Cupples
1Lady Davis Institute, Sir Mortimer B. Davis, Jewish General Hospital, Montréal, QC, Canada.
Canadian Journal of Physiology and Pharmacology
|December 10, 1999
Summary
Nitric oxide (NO) synthase inhibition by N(omega)-nitro-L-arginine methyl ester (L-NAME) alters renal blood flow (RBF) dynamics. L-NAME enhances the autoregulatory mechanism, particularly a rate-sensitive component, impacting arterial pressure regulation.
Area of Science:
- Physiology
- Renal Physiology
- Cardiovascular Physiology
Background:
- Nitric oxide (NO) plays a crucial role in regulating arterial pressure (PA) and renal blood flow (RBF).
- Inhibition of NO synthase (NOS) by N(omega)-nitro-L-arginine methyl ester (L-NAME) is a common method to study NO's physiological effects.
- Understanding the impact of NOS inhibition on renal hemodynamics and autoregulation is vital for cardiovascular and renal research.
Purpose of the Study:
- To investigate the effects of L-NAME-induced NO synthase inhibition on the arterial pressure-RBF transfer function.
- To determine the impact of L-NAME on the autoregulatory mechanisms controlling renal blood flow.
- To assess the potential role of cGMP in mediating the observed changes by comparing L-NAME effects with those of atrial natriuretic factor (ANF).
Main Methods:
- Administration of L-NAME to inhibit nitric oxide synthase.
- Analysis of the arterial pressure-renal blood flow transfer function to assess autoregulatory dynamics.
- Infusion of L-arginine to investigate the reversibility of L-NAME's effects.
- Administration of atrial natriuretic factor (ANF) to assess its ability to substitute for NO signaling via cGMP.
Main Results:
- L-NAME increased arterial pressure and reduced renal blood flow.
- L-NAME significantly altered the PA-RBF transfer function, enhancing the approximately 0.2 Hz autoregulatory mechanism.
- A rate-sensitive component of the myogenic system emerged or was augmented following L-NAME administration.
- L-arginine partially reversed the pressor response but not renal vasoconstriction or transfer function changes.
- ANF administration showed additive pressor responses with L-NAME but did not restore RBF or reverse transfer function alterations.
Conclusions:
- Inhibition of NO synthase by L-NAME profoundly alters renal blood flow dynamics.
- L-NAME enhances the rate-sensitive component of the myogenic system, leading to more vigorous autoregulatory responses to rapid PA changes.
- cGMP signaling, as mimicked by ANF, may not fully substitute for NO in maintaining basal renal blood flow and normal autoregulatory transfer function dynamics.
- The study highlights the critical role of NO in modulating renal autoregulation and vascular tone.