1. It has been demonstrated that parathyroid hormone can increase adenylate cyclase activity in the rat papilla, produce a small antidiuretic effect and in vitro can interfere with the action of arginine vasopressin on water transport. Clearance studies were performed in the anaesthetized water diuretic thyroparathyroidectomized rat to evaluate further the effect of parathyroid hormone on urine concentration in the presence and absence of arginine vasopressin. 2. A maximal phosphaturic concentration of rat parathyroid hormone (2 μg/kg) reduced urine flow from 125 ± 7 to 81 ± 9 μl/min within 10 min ( P < 0.01). Addition of a maximal antidiuretic concentration of arginine vasopressin (100 ng/kg) produced a delayed and diminished antidiuretic response when compared with a group of rats not pretreated with parathyroid hormone (47 ± 5 compared with 27 ± 5 μl/min; P < 0.01). However, a supramaximal arginine vasopressin concentration (1000 ng/kg) produced a maximal antidiuretic effect in the presence of parathyroid hormone. 3. To evaluate further the inhibitory effect of parathyroid hormone on arginine vasopressin-induced anti-diuresis, parathyroid hormone (2 μg/kg) was administered to one group of rats and a minimally effective arginine vasopressin concentration (7.5 ng/kg) to another group, which produced a similar antidiuretic effect. However, the subsequent effect of a maximal antidiuretic arginine vasopressin concentration (100 ng/kg) was again significantly blunted in the group pretreated with parathyroid hormone. 4. Parathyroid hormone produced only a small increase in mean plasma calcium concentration, and glomerular filtration rate was not altered by either hormone. 5. These results demonstrate that high physiological concentrations of parathyroid hormone do have a significant antidiuretic effect and can interfere with the action of arginine vasopressin. This suggests that parathyroid hormone may act as a partial agonist to arginine vasopressin in the collecting system.
1. The precise role of prostaglandins in modulating urine concentration and dilution is unclear. Evidence in vitro has recently cast doubt on the accepted theory that renal prostaglandins inhibit the hydro-osmotic effect of vasopressin. 2. Urine clearance studies were performed on indomethacin treated (prostaglandin deficient) and control anaesthetized water diuretic rats both before and during the addition of vasopressin in maximal (10 m-units) and supramaximal (100 m-units) concentrations. 3. Before the addition of vasopressin, indomethacin treatment inhibited the excretion of a water load by 48.7%. The mean papillary sodium concentration was also greater in this group of rats. 4. Vasopressin (10 m-units) increased the urine osmolality in control and indomethacin treated rats; however, the mean urine osmolality was greater in the indomethacin group (1521 ± 103 compared with 1120 ± 98 mosmol/kg; P < 0.01), as was the papillary sodium concentration. A tenfold increase in vasopressin depressed the papillary sodium concentration to a level similar to that in the control group and produced a marked natriuresis. Consequently, the mean urine osmolalities and urine flows were similar in control and indomethacin treated rats. 5. These experiments suggest that a major function of renal prostaglandins is to increase the ability of the kidney to excrete a water load. Renal prostaglandins do not interfere with the vasopressin induced increase in distal nephron water permeability.
1. Dietary magnesium deficiency is commonly associated with significant potassium depletion although the mechanisms responsible are unknown. Because the kidney has an important role in both magnesium and potassium homeostasis, clearance and micropuncture experiments were performed on thyroparathyroidectomized magnesium-deficient, normal and hypermagnesaemic rats to study the effect of body magnesium status on renal potassium handling. 2. Dietary magnesium restriction that reduced total-body magnesium by 30% did not alter renal potassium excretion despite a 10% reduction in total-body potassium. Graded magnesium infusions increased the fractional excretion of potassium in both magnesium-depleted and normal rats. However, the increase in the dietary depleted group was significantly less than in the control group (5-10 and then 13% compared with 7-19 and then 28% respectively). These changes in urine potassium excretion followed alterations in distal-tubule function. Parathyroid hormone did not alter potassium excretion in any of the experimental groups in contrast with its effect on magnesium excretion. 3. These data support the concept of distal tubular control of renal potassium homeostasis. The body magnesium status appears to exert some control over cellular potassium content and to alter indirectly distal-tubule potassium excretion.