Genetically fixed enhanced G protein activation in essential hypertension.
Recent studies have shown that enhanced Na/H exchanger activity, a frequently observed abnormality in essential hypertension, persists in Epstein-Barr-virus-immortalised lymphoblasts from afflicted patients. This phenomenon is associated with an enhanced proliferation of these cell lines. Studies have ruled out structural changes in the Na/H exchanger protein, but demonstrated a distinct enhancement of intracellular signal transduction in these cell lines. The ultimate cause can be assigned to an obviously genetically fixed increased reactivity of pertussis-toxin-sensitive G proteins, which can easily explain the increased formation of intracellular- second messengers, enhanced Ca2+ signals, and enhanced proliferation of these cell lines. Thus, hypertension in the subset of patients with enhanced Na/H exchanger activity could be caused by increased G protein reactivity.
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Institut für Pharmakologie, Universitätsklinikum Essen, Germany.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002455:Cell Division; D002460:Cell Line; D019204:GTP-Binding Proteins / Q000235:genetics* / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000378:metabolism*; D007424:Intracellular Fluid / Q000378:metabolism; D015398:Signal Transduction; D017923:Sodium-Hydrogen Exchangers / Q000235:genetics / Q000378:metabolism*
D017923:Sodium-Hydrogen Exchangers; D019204:GTP-Binding Proteins; D002118:Calcium