1. Plasma samples from both renal veins and infrarenal inferior vena cava were studied in 21 patients with unilateral renal artery stenosis and 11 patients without significant renal artery stenosis (essential hypertension), both groups being on unrestricted sodium intake.
2. Whether inactive renin was activated by acid or trypsin, it tended to be increased by 50–100% in unilateral renal ischaemia patients compared with essential hypertension. Active renin was increased two- to four-fold in unilateral renal ischaemia patients compared with those with essential hypertension. Thus the ratio of active to total renin in peripheral venous blood tended to be higher in unilateral renal ischaemia (0.37) than in essential hypertension (0.30) patients.
3. in renal vein blood from the affected kidney in unilateral renal ischaemia, the proportion of active renin to total renin was very high (68% for trypsinized samples and 73% for acidified samples). When affected renal vein blood was compared with infrarenal vena caval blood (equivalent to renal artery blood in amount and proportions of active and inactive renin), there was found to be a marked increase of active renin (ratio 2.83, significance of difference from 1.0, P < 0.001), as expected.
4. Inactive renin was decreased in affected renal vein blood compared with peripheral blood (ratio of renal vein to peripheral blood renin). This occurred whether acidification was used (ratio 0.62 ±0.11, P < 0.01) or trypsin (ratio 0.70 ± 0.13, P < 0.05).
5. The cause of the apparent uptake may be conversion of inactive renin into active renin by protease action in the ischaemic kidney. Urinary excretion or lymphatic drainage would seem unlikely.
Regional angiotensin II production in essential hypertension and renal artery stenosis.