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To assess whether the pressure-independence of renin release by isolated kidneys of Lyon hypertensive (LH) rats could result from long-term exposure to high blood pressure, sodium retention or an altered regulation of intracellular calcium through L-type voltage operated channels.Renin release was studied in kidneys from LH rats, either controls or chronically (aged 3–7 weeks) treated with hydralazine or deprived of sodium. The influence of L-type calcium channels was studied acutely using a specific activator (BAY K8644) or modulator (verapamil). Lyon low blood pressure (LL) rats served as controls.Kidneys were isolated from LH or LL rats aged 7 weeks and single-pass perfused at three pressure levels: 70, 85 and 160mmHg.LH rat kidneys differed from LL rat kidneys in having elevated vascular resistances, decreased glomerular filtration rate, pressure natriuresis and pressure-dependent renin release. Hydralazine treatment and sodium deprivation did not significantly modify the pressure-independence of renin release by LH rat kidneys. BAY K8644 (1 × 10-8 and 5 × 10-8 mol/l) induced significantly greater vasoconstrictor effects in LH than in LL rat kidneys but did not affect the renin release already stimulated by low perfusion pressure. Verapamil (5 × 10-6 mol/l) dilated LH more than LL rat kidneys. It did not change the renin release observed at low, but enhanced it at high, perfusion pressure. This effect was more marked in LL than in LH rat kidneys.The poor stimulation of renin release by low perfusion pressure in LH rat kidneys does not appear to be a consequence of high blood pressure level, sodium retention and alteration in L-type calcium channels. However, results demonstrate that these channels participate in the increased vascular resistances exhibited by LH rat kidneys.