Increased expression of inhibitory guanine nucleotide binding proteins in membranes from renal proximal tubules, but not brain striata, of the normotensive and the spontaneously hypertensive rat

BACKGROUNDDysfunctional dopamine neurotransmission and defective D1A receptor-G protein coupling exist in renal proximal tubules (RPT) of the spontaneously hypertensive rat (SHR). OBJECTIVETo determine whether differential expression G proteins contributes to these anomalous phenomena. METHODSWe exa...

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Veröffentlicht in:Journal of hypertension 1996-11, Vol.14 (11), p.1281-1285
Hauptverfasser: White, Beatrix H, Sidhu, Anita
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Sprache:eng
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Zusammenfassung:BACKGROUNDDysfunctional dopamine neurotransmission and defective D1A receptor-G protein coupling exist in renal proximal tubules (RPT) of the spontaneously hypertensive rat (SHR). OBJECTIVETo determine whether differential expression G proteins contributes to these anomalous phenomena. METHODSWe examined the expression levels of the α-subunits of G proteins, in RPT of SHR and the normotensive Wistar-Kyoto (WKY) rat, as well as in striatal membranes, where dopamine functions and receptor-G protein coupling are known to be normal. RESULTSIn general, rat striatal membranes displayed overall higher expression levels of the different α-subunits, relative to those of RPT membranes. Moreover, no significant differences were observed between G protein levels in rat striata in SHR and WKY rats. However, in RPT, both subunits of Gsα were equally expressed in SHR and WKY rats. Gi1α was expressed in RPT of SHR and WKY rats the same levels, but neither Goα nor Gzα was detected these membranes; higher (50%) expression levels of Gi2α were found in SHR. The largest difference in α-subunit expression levels between SHR and WKY RPT was observed for Gi3α. This protein was present in SHR RPT at levels 4.8-fold higher than those in WKY rat RPT. The only α-subunit which was slightly depressed (by 20%) in SHR was Gqα. CONCLUSIONThe overexpression of Gi2α and Gi3α in SHR RPT may be of importance in the genesis of hypertension in this animal.
ISSN:0263-6352
1473-5598
DOI:10.1097/00004872-199611000-00005