AJP - Renal Physiology, Vol 273, Issue 6 877-F882, Copyright © 1997 by American Physiological Society

ARTICLES

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

R. Mokkapatti, S. J. Vyas and E. K. Jackson
Department of Pharmacology, University of Pittsburgh School of Medicine, Pennsylvania 15213, USA.

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 difference did not achieve statistical significance (0.41 +/- 0.08 vs. 1.04 +/- 0.32, P = 0.08). In conclusion, the steady-state levels of G alpha s, G alpha i-1, G alpha i-2, G alpha i-3, and G alpha q are similar in SHR and WKY renal microvasculature, suggesting that other components of the ANG II signal transduction mechanism are responsible for the enhanced renal vascular responsiveness in SHR.

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