Regulation Of Sodium Reabsorption Research Articles

Interactions between ADH and prostaglandins in isolated erythrocyte-perfused rat kidney.

Interactions between antidiuretic hormone (ADH) and renal prostaglandins in the regulation of sodium reabsorption and urinary concentrating ability were studied in isolated erythrocyte-perfused rat kidneys (IEPK). In this model, hemodynamic characteristics are comparable to those found in vivo, and tubular morphology is preserved throughout the period of perfusion. [Deamino]-D-arginine vasopressin (dDAVP) markedly reduced fractional sodium excretion (FE Na) in the IEPK from 3.5 +/- 0.6 to 0.45 +/- 0.14%. After indomethacin, FE Na fell still further to 0.08 +/- 0.02%. In the absence of dDAVP indomethacin had no effect on sodium excretion; FE Na was 2.4 +/- 0.6% in control and 2.0 +/- 0.4% in indomethacin-treated groups. dDAVP increased urine osmolality in the IEPK to 741 +/- 26 mosmol/kg. When prostaglandin synthesis was blocked with indomethacin, urinary osmolality increased further to 1,180 +/- 94 mosmol/kg. In isolated kidneys perfused without erythrocytes (IPK), dDAVP decreased FENa from 14.5 +/- 1.8% to 9.6 +/- 1.2%; addition of indomethacin had no further effect. dDAVP increased urine osmolality only modestly to 350 +/- 12 mosmol/kg in the IPK and indomethacin did not increase concentrating ability further (342 +/- 7 mosmol/kg). Thus the IEPK (unlike the IPK) can excrete a markedly hypertonic urine in response to ADH. ADH also enhances tubular reabsorption of sodium in the IEPK. Prostaglandins inhibit both these actions of ADH but do not directly affect sodium excretion in the absence of the hormone.

Factors relating to aldosterone secretion rate, the excretions of aldosterone 18-glucuronide, and the plasma aldosterone concentration in cirrhosis.

In a group of eight patients with cirrhosis the rate of renal excretion of the 18-glucuronide metabolite of aldosterone (U Aldo V) was found to be closely related to the aldosterone secretion rate (ASR). U Aldo V was therefore used as an index of ASR in a further group of fifty patients in order to evaluate the possible importance of factors known to regulate aldosterone secretion. U Aldo V showed statistically significant relationships to both plasma renin activity (PRA) and the plasma sodium concentration (P Na), but not to the plasma potassium concentration (PK) or the renal excretion of cortisol (U Cort V), the latter sued as an index of adrencorticotrophic hormone activity. The plasma aldosterone concentration (P Aldo) was determined in fifty-eight patients and also found to show statistically significant relationships to PRA and P Na. P Aldo showed a weak, though statistically significant, relationship to PK, but not to U Cort V. These findings are in keeping with a role for the renin-angiotensin system in the control of aldosterone secretion in cirrhosis although evidence from other studies suggest other factors to be involved also. Whether P Na was another determinant of ASR, or whether aldosterone was a determinant of P Na through regulating sodium reabsorption by the proximal tubule of the nephron, is uncertain.

Effect of parathyroid hormone secretion on sodium reabsorption by the proximal tubule.

To determine if an increase in the endogenous secretion of parathyroid hormone could decrease sodium reabsorption by the proximal tubule, the ionized calcium concentration of blood perfusing the parathyroid gland of eight unilaterally thyroid parathyroidectomized dogs (TPTX) was reduced by infusion of an isotonic sodium citrate plus sodium chloride solution into the blood supply of the parathyroid gland. The fractional clearance of phosphate increased significantly (+9.3 +/- 2.8 ml/min per 100 ml GFR), while fractional sodium reabsorption by the proximal tubule decreased (-.06 +/- .02; P less than .025). In seven normal control dogs that received isotonic sodium chloride infusion, neither fractional sodium reabsorption by the proximal tubule nor the fractional clearance of phosphate was significantly altered. In five bilaterally TPTX dogs that received a sodium citrate plus sodium chloride infusion, sodium reabsorption by the proximal tubule was not significantly altered. There were no significant changes in glomerular filtration rate or renal plasma flow in any of these groups. The data demonstrate that alterations in endogenous parathyroid hormone secretion can play a significant role in the regulation of sodium reabsorption by the proximal tubule.

Suppressive action of prolactin on renal response to volume expansion.

The effects of prolactin on rat renal sodium and water handling during volume expansion were studied using clearance techniques. Both control and experimental adult male Wistar rats were prehydrated with an oral water load of volume equal to 2.5% body weight (BW). At least 3 h later, a continuous intravenous infusion of ovine prolactin (NIH-P-S8), 7.1 mug/h per 100 g, was started in the experimental group. After a 1-h steady-state period, the rats were given an intravenous expansion infusion of either hypotonic saline (2.5% BW), isotonic saline (2.5% and 7.5% BW), or blood (2.5% BW). In all control hypotonic and isotonic saline-expanded animals, within 1 h the rats excreted a volume of urine equal to over 50% of the volume of saline infused. The diuretic and natriuretic responses to saline expansion of prolactin-treated rats were significantly smaller than controls. In contrast to the effects of prolactin on the renal response to saline infusions, it did not alter the natriuretic or diuretic response to blood infusion. Prolactin may be counteracting the effects of physical factors on the regulation of sodium reabsorption in the proximal tubule.

Regulation of sodium reabsorption by the proximal tubules in the dog.

Micropuncture studies of the proximal tubules suggest that fractional reabsorption is maintained at a constant level by the mechanism of glomerular–tubule balance, best explained at present by changes in intratubular volume which are proportional to and result from changes in the glomerular filtration rate. The precise role of the macula densa renin–angiotensin system in intrarenal regulation of sodium reabsorption has not been critically defined. The important factor in determining the value of fractional reabsorption in the proximal tubule appears to depend upon changes in body fluid volume balance, volume depletion enhancing the rate of reabsorption and volume expansion depressing it. Aldosterone may be an additional regulator of sodium reabsorption in the proximal tubules.