1. Studies were performed to evaluate the mechanism involved in the hypertension of moderate renal failure in partially (five-sixths) nephrectomized rats. Cardiac index (CI) was studied by means of the microsphere technique, and systemic vascular resistance (SVR) calculated from the mean arterial resistance MAP/CI, in four groups of experimental animals: (A) partially nephrectomized rats; (B) group A rats chronically treated with the calcium channel blocker verapamil; (C) sham-operated rats; (D) sham-operated rats treated with verapamil. 2. The results demonstrate a significant increase in MAP in group A rats, which was due to a 72% increase in SVR as compared with groups C and D. In group B rats, MAP decreased significantly owing to a marked decrease in SVR (40%) as compared with group A. However, MAP remained higher in group B than in group C. 3. The vascular responsiveness to noradrenaline was studied in group A, group C and group A rats after parathyroidectomy (group A1). An increased pressor responsiveness to noradrenaline was indicated by a shift of the noradrenaline dose-response curve to the left in group A rats as compared with group C rats. This change was corrected after partial nephrectomy. 4. We conclude that hypertension in nephrectomized rats is due to an increase in SVR, and that an increased pressor responsiveness to catecholamines may play a role in this phenomenon. Furthermore, verapamil reduced the hypertension, and parathyroidectomy improved the abnormal sensitivity to noradrenaline in group A rats. 5. These results raise the possibility that an abnormality in calcium metabolism, possibly due to secondary hyperparathyroidism, may be implicated in the hypertension of mildly uraemic rats.
1. The effect of extracellular volume expansion (ECVE) during water diuresis, and of water diuresis alone, on the formation of free water in man was compared. 2. ECVE reduced free water formation at any given rate of distal delivery compared with water diuresis. Thus, ECVE depresses distal sodium chloride reabsorption. 3. This attenuation of free water formation occurred both when urine flow ( V /100 ml glomerular filtration rate) and distal chloride delivery [( C water + C Cl )/100 ml glomerular filtration rate] were used as the terms for distal delivery. 4. We suggest that the distal depression of sodium chloride reabsorption after ECVE is probably due to a direct inhibition of distal sodium chloride transport mechanisms, and not to the flooding of the diluting site by the poorly reabsorbable bicarbonate ion.