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Renal function during reflexly activated catecholamine flow through an adrenorenal rete

R E Katholi, S P Bishop, S Oparil

The American Journal of Physiology

|January 1, 1981

Summary

Two kidney reflex mechanisms, renal sympathetic nerves and catecholamine flow, help maintain vascular volume during hypotension. Neither reflex mechanism depends on intrarenal angiotensin II activity.

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Area of Science:

Nephrology
Physiology
Cardiovascular Research

Background:

Kidney function is regulated by complex reflex mechanisms.
Renal vasoconstriction can be mediated by sympathetic nerves or catecholamine release.
Understanding these reflexes is crucial for managing renal blood flow and volume homeostasis.

Purpose of the Study:

To compare the effects of two distinct kidney reflex mechanisms on renal function.
To investigate the role of intrarenal angiotensin II in these reflex responses.
To determine the contribution of these reflexes to maintaining vascular volume.

Main Methods:

Inducing transient hypotension via atrial fibrillation in anesthetized dogs.
Measuring renal plasma flow, glomerular filtration rate, and urinary sodium excretion.

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Blocking intrarenal angiotensin II activity using [Sar1,Ala8]angiotensin II.

Main Results:

Activation of either reflex mechanism caused significant decreases in renal plasma flow and glomerular filtration rate.
Both reflexes led to a marked reduction in urinary sodium excretion and an increase in filtration fraction.
Blocking intrarenal angiotensin II did not alter the magnitude or direction of the observed renal functional changes.

Conclusions:

Both renal sympathetic nerve activation and adrenorenal catecholamine flow are significant mechanisms for maintaining vascular volume.
These reflex pathways effectively regulate kidney function during hypotensive stress.
Intrarenal angiotensin II activity is not essential for the function of these two critical renal reflexes.