GTP-binding proteins and post-receptor components in hypertension.
Alterations in neurohormonal response are a widely-observed feature in various forms of hypertension. Such responses depend not only on levels of hormones/neurotransmitters, but also on receptors and post-receptor components. With respect to G protein-coupled receptors, such as those for catecholamines, angiotensin II, and bradykinin, it is possible that G-proteins or G protein-coupled effector molecules are altered in hypertension. In this article, several classes of G alpha proteins and effectors which link to these proteins are briefly discussed. Evidence is presented in support of the concept that signal amplification in G protein-coupled receptor systems occurs at the level of receptor activation of the G proteins. Limited data are as yet available that directly assess whether changes in the amount or properties of particular G alpha proteins or G-protein-linked effectors, are altered in hypertension. The availability of antibody, cDNA and other genetic probes should prove highly useful in testing the hypothesis that such alterations are important for the pathogenesis and maintenance of the hypertensive state.
Insel
P A
PA
Department of Pharmacology, University of California, San Diego, La Jolla 92093.
D000818:Animals; D004195:Disease Models, Animal; D019204:GTP-Binding Proteins / Q000378:metabolism*; D006973:Hypertension / Q000378:metabolism*; D007473:Ion Channels / Q000502:physiology; D011941:Receptors, Adrenergic / Q000378:metabolism*; D015398:Signal Transduction
D007473:Ion Channels; D011941:Receptors, Adrenergic; D019204:GTP-Binding Proteins