Effects of nephrectomy and adrenalectomy on the renin-angiotensin system of transgenic rats TGR(mRen2)27.

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Abstract
The transgenic rat TGR(mRen2) develops severe hypertension with high renin activity in the adrenal and low renin activity in the kidney. To clarify the role of the adrenal gland as a source of circulating renin in TGR rats, we investigated the effects of nephrectomy (NEPEX) and adrenalectomy (ADX) on the adrenal and plasma renin-angiotensin system. TGR rats had a high basal plasma renin concentration (PRC; 18.2 +/- 1.0 ng angiotensin-I (AngI)/ml.h) compared with Harlan Sprague-Dawley (SD) rats (7.4 +/- 0.5 ng AngI/ml.h; P < 0.01) and SD rats of the Hannover strain from which the TGR rat was derived (5.3 +/- 0.6 ng AngI/ml.h, P < 0.01); TGR rats also had high adrenal renin (83.3 +/- 8.9) compared with Harlan SD rats (5.5 +/- 0.7; P < 0.01) and Hanover SD rats (6.1 +/- 0.6 ng AngI/ml.h). NEPEX markedly increased PRC (82.4 +/- 18.8 ng AngI/ml.h, P < 0.01) and adrenal renin levels (386.3 +/- 43.9 ng AngI/adrenal.h; P < 0.01) in TGR rats. ADX significantly lowered control levels of PRC and plasma AngII in the TGR rats (19.0 +/- 1.2 to 7.7 +/- 1.2 ng AngI/ml.h and 33.5 +/- 5.6 to 12.8 +/- 2.1 pg/ml, respectively) and suppressed the increases in PRC (119.4 +/- 20.2 to 61.8 +/- 4.0 ng AngI/ml.h) and plasma AngII (95.8 +/- 9.8 to 55.1 +/- 4.3 pg/ml; P < 0.01) caused by NEPEX in TGR rats. However, the levels of PRC and plasma AngII remained high after NEPEX/ADX in TGR rats. Our results suggest that the adrenal gland is one of the main sources of circulating renin in the TGR rat, but other extrarenal sources of plasma renin also exist in these animals.

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