Glomerular filtration rate, the renal clearances of sodium, potassium and chloride, and several parameters of urinary acidification were measured separately in the “clamped” and “undamped” kidney of rats after acute (normo-tensive rats) or chronic (hypertensive rats) clamping of one renal artery. Both acute and chronic constriction of one renal artery resulted in a decrease, in the clamped kidney, in GFR, the excretion of sodium, potassium, chloride, ammonium and bicarbonate ions, and the absolute rate of bicarbonate reabsorption. Bicarbonate reabsorption factored by the volume of glomerular filtrate was significantly, though slightly, increased after chronic constriction of a renal artery. Urinary pCO2 was higher than plasma pCO2 in the undamped kidney (positive A pCO2) but not in the clamped kidney (null or negative A pCO2) of renal hypertensive rats. Intravenous injection of carbonic anhydrase abolished the positive A pCO2 present in the undamped kidney. Injection of acetazolamide induced a positive A pCO2 in the clamped kidney. The present data confirm the existence of a glomerular-tubular balance for bicarbonate reabsorption, and possibly for hydrogen secretion, which remains active after constriction of the renal artery. The slight enhancement of bicarbonate reabsorption per unit volume of glomerular filtrate as well as the disappearance of the A pCO2 in the clamped kidney may be due to a relative excess of luminal (brush border) carbonic anhydrase and/or to a prolonged contact time of tubular fluid with this