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Interactions between neural and hormonal mediators of renal vascular tone in anaesthetized rabbits

Published online by Cambridge University Press:  12 March 2003

Sarah-Jane Guild ,
Carolyn J. Barrett ,
Roger G. Evans  and
Simon C. Malpas
Sarah-Jane Guild
Affiliation:
Circulatory Control Laboratory, Departments of Physiology and Electrical and Electronic Engineering, University of Auckland, New Zealand and Department of Physiology, Monash University, Melbourne, Australia
Carolyn J. Barrett
Affiliation:
Circulatory Control Laboratory, Departments of Physiology and Electrical and Electronic Engineering, University of Auckland, New Zealand and Department of Physiology, Monash University, Melbourne, Australia
Roger G. Evans
Affiliation:
Circulatory Control Laboratory, Departments of Physiology and Electrical and Electronic Engineering, University of Auckland, New Zealand and Department of Physiology, Monash University, Melbourne, Australia
Simon C. Malpas
Affiliation:
Circulatory Control Laboratory, Departments of Physiology and Electrical and Electronic Engineering, University of Auckland, New Zealand and Department of Physiology, Monash University, Melbourne, Australia
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Abstract

We investigated how sympathetic nerve activity and vasoactive hormones interact in controlling renal haemodynamics in pentobarbitone-anaesthetized rabbits. Renal blood flow was progressively reduced by electrical stimulation (0.5-3 Hz) of the renal nerves, during renal arterial infusion of saline, vasoconstrictors (angiotensin II and [Phe2,Ile3,Orn8]-vasopressin), or vasodilators (acetylcholine, adrenomedullin and the nitric oxide donor methylamine hexamethylene NONOate (MAHMA NONOate). A frequency-rich stimulus was also applied to test whether the vasoactive agents affect the dynamic control of renal blood flow by sympathetic nerve activity. The vasodilators tended to increase renal blood flow, but only the effect of MAHMA NONOate was statistically significant. [Phe2,Ile3,Orn8]-vasopressin reduced medullary perfusion (by 61 ± 12 %) but not renal blood flow or cortical perfusion. Angiotensin II reduced renal blood flow (33 ± 3 %) and cortical perfusion (14 ± 5 %) but not medullary perfusion. Steady-state responses of renal blood flow and cortical perfusion during renal nerve stimulation were attenuated during infusion of acetylcholine and [Phe2,Ile3,Orn8]-vasopressin, while angiotensin II attenuated responses of medullary perfusion, and MAHMA NONOate and adrenomedullin had no significant effects. The dynamic response to sympathetic nerve activity (renal blood flow responded as a low pass filter with a pure time delay of ~664 ms) was not altered by the vasoactive agents. We conclude that some vasoactive agents can modulate steady-state renal haemodynamic responses to sympathetic nerve activity in a regionally specific manner, independent of their effects on baseline renovascular tone. However, they have little impact on the dynamic response of renal blood flow to sympathetic nerve activity. Experimental Physiology (2003) 88.2, 229-241.

Type
Full Length Papers
Information
Experimental Physiology , Volume 88 , Issue 2 , March 2003 , pp. 229 - 241
Copyright
© The Physiological Society 2003

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