Are cardiac G-proteins altered in rat models of hypertension?


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Abstract

Objective:To determine whether alterations in cardiac G-protein number or function, or both, are involved in the desensitization of adenylate cyclase responsiveness in the hypertensive stateDesign:Quantitation of G-protein subunits in myocardial membranes from four different rat models of hypertension in comparison with respective normotensive ratsMethods:We compared male and female adult spontaneously hypertensive rats (SHR) with age- and sex-matched Wistar-Kyoto (WKY) rats, rats from the highest-pressure quartile from an F2 generation of WKY x SHR hybrids with those from the lowest-pressure quartile, and one-kidney, one clip renal hypertensive with shamoperated rats. The function of G was quantitated by reconstitution of cardiac cholate extracts into cyc—cell membranes with subsequent measurement of NaF-stimulated adenylate cyclase activity. The amounts of immunodetectable C, G,G, and Gβ were determined from quantitative Western blotting experiments with[125l]-protein A detectionResults:None of the parameters investigated differed significantly between hypertensive and normotensive rats in any of the models investigatedConclusion:We conclude that major quantitative alterations in cardiac Gs, Gj or Gq are not a general feature of the hypertensive state

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