JPET xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Podevin, R. A.
Right arrow Articles by Parini, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Podevin, R. A.
Right arrow Articles by Parini, A.

Adrenergic agonists and the Na+-K+-adenosine triphosphatase from rabbit proximal tubules and their basolateral membranes

RA Podevin and A Parini

Laboratoire de Physiologie Renale, Faculte de Medecine Xavier-Bichat Institut National de la Sante et de la Recherche Medicale U.251, Paris, France.

Several studies suggested that catecholamines modulate renal sodium and water excretion by direct stimulation of adrenergic receptors located on the renal proximal tubule. However, neither the mechanism nor the class of adrenoceptor involved in this effect have yet been established definitively. In the present study, we examined the effects of L- norepinephrine (NE) and selective alpha-1, alpha-2 and beta adrenergic agonists on monovalent cation transport and on Na+-K+-adenosine triphosphatase (ATPase) activity from homogenates, intact tubules and highly purified basolateral membranes prepared from superficial rabbit kidney cortex. Our results showed that neither NE nor specific alpha-1, alpha-2 and beta adrenergic agonists (10 microM) modified ouabain- sensitive uptake of 86Rb+ (a K+ analog) in intact proximal tubules. Similarly, it is demonstrated that NE and alpha and beta adrenergic agonists did not affect Na+-K+-ATPase activity from homogenates, intact tubules and basolateral membranes. The integrity of the alpha-2 adrenergic receptor system, the predominant adrenergic subtype in rabbit proximal tubule, was supported by the following findings: 1) maximal binding of [3H] rauwolscine was about 4-fold higher in basolateral membranes than in homogenates; 2) 5'-guanylimidodiphosphate induced a 27-fold increase in the Ki of NE for alpha-2 receptor in basolateral membranes; 3) NE (5 microM) inhibited by 35% parathyroid hormone-stimulated cyclic AMP production in intact tubules. In conclusion, these data fail to demonstrate that NE, as well as other adrenergic agonists, directly increases Na+-K+-ATPase in the rabbit proximal tubule. Further investigations are needed to clarify the interaction of catecholamines with the renal Na+K+ pump.

Volume 250, Issue 2, pp. 672-677, 08/01/1989
Copyright © 1989 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
Am. J. Physiol. Renal Physiol.Home page
S. Abdulnour-Nakhoul, R. N. Khuri, and N. L. Nakhoul
Effect of norepinephrine on intracellular pH in kidney proximal tubule: role of Na+-(HCO-3)n cotransport
Am J Physiol Renal Physiol, July 1, 1998; 275(1): F33 - F45.
[Abstract] [Full Text] [PDF]




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
 Molecular Interventions Drug Metabolism and Disposition

Copyright © 1989 by the American Society for Pharmacology and Experimental Therapeutics.