Hepatoportal bumetanide-sensitive K+-sensor mechanism controls urinary K+ excretion

Author:

Morita Hironobu1,Fujiki Nobuhiro1,Miyahara Taro1,Lee Ken1,Tanaka Kunihiko1

Affiliation:

1. Department of Physiology, Gifu University School of Medicine, Gifu 500-8705, Japan

Abstract

To determine whether a K+-sensor mechanism exists in the hepatoportal region, periarterial hepatic afferent nerve activity responses to intraportal injection of KCl were examined in anesthetized rats. Hepatic afferent nerve activity increased in response to intraportal injection in a K+ concentration-dependent manner, and the increase was attenuated by inhibition of the Na+-K+-2Cl cotransporter by bumetanide in a dose-dependent manner. These results suggest that a bumetanide-sensitive K+-sensor mechanism exists in the hepatoportal region. Stimulation of this mechanism by intraportal KCl infusion elicited an immediate and powerful kaliuresis with no significant change in the plasma K+ concentration; this was significantly greater than the kaliuresis induced by intravenous KCl infusion and was attenuated by severing the periarterial hepatic nervous plexus. These results indicate that a hepatoportal bumetanide-sensitive K+-sensor mechanism senses the portal venous K+ concentration and that stimulation of this sensor mechanism causes kaliuresis, which is mainly mediated by the periarterial hepatic nervous plexus.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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