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

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.