Neuropeptide y shifts the equilibrium between the [alpha] - and [beta] - adrenergic tonus in proximal tubule cells.. Holtb[umlaut]ack, Ulla, Yoshiyuki Ohtomo, Petter F[diaeresis]orberg, Bo Sahlgren, and Anita Aperia. Dept. Woman and Child Health, Pediatric unit, Karolinska Institute, Stockholm, Sweden
APStracts 5:0056F, 1998.
Renal sympathetic nerves play a central role in the regulation of tubular Na+ reabsorption. Norepinephrine (NE) and neuropeptide Y (NPY) are co-localized in renal sympathetic nerve endings. The purpose of this study is to examine the integrated effects of these neurotransmitters on the regulation of Na+,K+-ATPase, the enzyme responsible for active Na+ reabsorption in renal tubular cells. Studies were performed on proximal tubular segments which express adrenergic [alpha]- and [beta]-receptors as well as NPY-Y2 receptors. It was found that [alpha]- and [beta]-adrenergic agonists had opposing effects on Na+,K+-ATPase activity. [beta]-adrenergic agonists induced a dose-dependent inhibition of the Na+,K+-ATPase activity, whereas [alpha]-adrenergic agonists stimulated the enzyme. NPY abolished [beta]-agonist-induced deactivation of Na+,K+-ATPase and enhanced [alpha]-agonist-induced activation of Na+,K+-ATPase. The [beta]-adrenergic agonist appeared to inhibit Na+,K+-ATPase activity via a cAMP pathway. NPY antagonized [beta]-agonist-induced accumulation of cAMP. In our preparation NE alone had no net effect, but stimulated the Na+,K+-ATPase activity in the presence of [beta] -adrenergic antagonists as well as in the presence of NPY. The results indicate that, in renal tissue, NPY determines the net effect of its co-localized transmitter, NE, by its ability to attenuate the [beta]- and enhance the [alpha]-adrenergic effect. 

Received 9 July 1997; accepted in final form 19 February 1998.
APS Manuscript Number F224-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 9 March 1998