G protein mRNA expression in renal microvessels from spontaneously hypertensive and Wistar-Kyoto rats

The American Journal of Physiology
R MokkapattiE K Jackson

Abstract

The exaggerated sensitivity of spontaneously hypertensive rat (SHR) renal microvasculature to angiotensin II (ANG II) may be due to an imbalance between the effectiveness of G alpha s-utilizing vasodilator pathways and vasoconstrictor pathways activated by ANG II (mediated by G alpha i-1, G alpha i-2, G alpha i-3, and G alpha q). Because the alteration appears to be distal to the hormone receptors and proximal to the effector adenylyl cyclase, we hypothesized that SHR have altered amounts of signal-transducing G proteins. This was examined by quantifying the steady-state mRNA levels of specific G alpha subunits in renal microvessels of 12- to 14-wk-old SHR and control Wistar-Kyoto (WKY) rats, using a quantitative-competitive polymerase chain reaction technique coupled to reverse transcription. No significant differences were detected in the absolute levels of G alpha s (0.96 +/- 0.35 vs. 0.74 +/- 0.25 amol/50 ng RNA) or in the relative levels of G alpha i-1 (0.44 +/- 0.05 vs. 0.48 +/- 0.13). G alpha i-2 (40.9 +/- 7.8 vs. 45.2 +/- 8.9), or G alpha i-3 (0.79 +/- 0.05 vs. 0.82 +/- 0.15) normalized to the level of G alpha s for WKY vs. SHR, respectively. The ratio of G alpha q to G alpha s tended to be higher in SHR, but this diffe...Continue Reading

References

Nov 23, 1992·FEBS Letters·C Thibault, M B Anand-Srivastava
Dec 1, 1990·Proceedings of the National Academy of Sciences of the United States of America·M Strathmann, M I Simon
Jun 1, 1986·Proceedings of the National Academy of Sciences of the United States of America·H ItohK Suzuki
Mar 28, 1995·Proceedings of the National Academy of Sciences of the United States of America·C ChatziantoniouW J Arendshorst
Apr 1, 1993·Journal of Hypertension·M C MichelP A Insel

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