The effect of potassium infusion on proximal sodium reabsorption and renin release in the dog

The effect of potassium infusion on proximal sodium reabsorption and renin release in the dog. The effect of infusions of potassium chloride (KC1) on sodium reabsorption by the proximal tubule and renal renin release was measured in 18 dogs. Following renal arterial infusions of 8 or 16 µEq/min/kg potassium chloride, fractional and absolute sodium reabsorption by the proximal tubule, measured by micropuncture techniques, was not significantly altered. As compared to five control dogs, urinary sodium excretion was significantly increased following both infusions of KC1. The release of renin was significantly decreased following both rates of potassium infusion. The inhibition of renin release was not associated with consistent changes in either glomerular filtration rate or renal plasma flow. The data indicate that the inhibition of renin release following the infusion of potassium is probably not the result of a marked increase in sodium delivery from the proximal tubule

Catecholamines and phosphate excretion by the remnant kidney

Catecholamines and phosphate excretion by the remnant kidney. The remnant kidney (RK) exhibits an enhanced fractional excretion of phosphate (FEPi) even in the absence of parathyroid hormone (PTH). Thus, factors other than PTH contribute to this adaptive phosphaturia. Dopamine (DA) infusion is phosphaturic, whereas stimulation of adrenoreceptors is antiphosphaturic. Therefore, the hypothesis that alterations in catecholamines by the RK may be associated with the phosphaturia exhibited by this model was tested. Male Sprague-Dawley rats were subjected to right nephrectomy and surgical ablation of the left renal poles. Four weeks later rats with a RK (N = 10) and control rats with intact kidneys (N = 9) were anesthetized and thyroparathy-roidectomized (TPTX). Two hours after TPTX, urine samples were collected for measurements of urinary free DA excretion. Subsequently, 3% inulin in saline was infused for one hour and a 30 minute clearance was taken. The kidneys were then removed and frozen for determination of tissue norepinephrine (NE) and DA concentrations. Glomerular filtration rate was significantly lower in rats with a RK than in controls (0.57 ± 0.07 vs. 0.83 ± 0.08 ml/min/g kidney wt), whereas fractional excretion of phosphate (FEPi) was significantly higher (29.4 ± 4.7 vs. 8.3 ± 3.4%). Tissue NE concentration was significantly lower in the RK than in the control intact kidney (85.10 ± 4.95 vs. 129.60 ± 7.20 ng/g), whereas urinary DA excretion per nephron was significantly higher in the RK (0.12 ± 0.02 vs. 0.04 ± 0.006 pg/min). Infusion of the specific DA-1 receptor antagonist (SCH 23390) in rats with a RK significantly decreased the FEPi when compared to the saline infused control group (Δ-5.2 ± 4.3 vs. +9.5 ± 5.2%), however, urinary c-AMP excretions were not different. We conclude that decreased renal sympathetic nerve tone, unchanged tissue DA levels, and an increased DA synthesis per residual nephron are associated with the enhanced FEPi exhibited by the RK

Escape from the sodium-retaining effects of mineralocorticoids: Role of ANF and intrarenal hormone systems

Chronic exposure to either endogenous or exogenous mineralocorticoid excess results in a syndrome characterized by hypokalemia, metabolic alkalosis, polydipsia, polyuria, and mild arterial pressure elevation. Contrary to what might be expected from the mechanism of action of these hormones, there is only a transient period of positive sodium balance (Fig. 1). The expansion of the extracellular fluid volume is maintained as evidenced by an increase in body weight even after sodium balance is restored. However, this elevation of the extracellular fluid volume is not striking, and congestive heart failure is not part of the syndrome [1]