Open AccessNitric oxide, cGMP, and hormone regulation of active sodium transport.
Author(s) -
Mary McKee,
Cristóforo Scavone,
James A. Nathanson
Publication year - 1994
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.91.25.12056
Subject(s) - nitric oxide , microbiology and biotechnology , chemistry , cgmp dependent protein kinase , second messenger system , hormone , intracellular , regulator , endocrinology , medicine , kidney , sodium , protein kinase a , biophysics , kinase , biology , biochemistry , organic chemistry , gene , cyclin dependent kinase 2
The inter- and intracellular regulator nitric oxide (NO) has been suggested to play a role in the modulation of cellular excitability, but the mechanism(s) by which this occurs remain unclear. Using the kidney as a model system, we report here evidence that NO, produced in response to various hormones and cytokines, can effect long-term alterations in the activity of the membrane sodium pump. This regulation of Na, K-ATPase, which occurs in a system of NO-containing renal tubules, involves cGMP and cGMP-dependent protein kinase. Na, K-ATPase can also be regulated by alterations of cGMP initiated through NO-independent factors, such as atriopeptin, and in nonrenal tissues, such as cerebellum. Regulation of the membrane sodium pump by NO and cGMP, therefore, represents a mechanism for hormonal modulation of ion gradients, not only in kidney but also in other organs, including brain, where NO and cGMP play a prominent role in cellular function.