Effects of aldosterone and potassium-sparing diuretics on electrical potential differences across the distal nephron.

175

We have used rat cortical collecting tubules perfused in vitro to study the effects of antidiuretic hormone (ADH) and desoxycorticosterone (DOCA) on the unidirectional fluxes of sodium. We found that in the basal state, lumen-to-bath flux (Jib) and bath-to-lumen flux (JbJ) of 22Na were approximately equal, 39.5±3.9 and 41.8±11.0 pmol min-1 mm-', respectively, resulting in no net flux. Addition of 100 1U/ml ADH to the bath produced a stable increase in Jib to 583±4.7 pmol* min-' * mm-'. Addition of ADH to a tubule from a DOCA-pretreated rat caused an increase in Jib to 144.1±12.0 pmol* min-' mm-'. Neither hormone had an effect on Jbi. Thus ADH produced a greater absolute and fractional increase in Jib when the animal was pretreated with DOCA, and the ADH-induced increase over baseline was greater than the DOCA-induced increase. Both the ADHand DOCA-induced stimulation of Jib were completely abolished by 10-5 M luminal amiloride, suggesting that the route of sodium transport stimulated by both hormones involves apical sodium channels. However, ADH and DOCA have very different time courses of action; ADH acted within minutes, while aldosterone and DOCA are known to require 90-180 min. The facilitating action of ADH on DOCA-induced stimulation of sodium transport may be important for maximal sodium reabsorption and for the ability to achieve a maximally concentrated urine.

Section: Resultscontrasting

confidence: 99%

Sodium transport by rat cortical collecting tubule. Effects of vasopressin and desoxycorticosterone.

Reif¹,

Troutman²,

Schafer³

1986

175

“…Thus, it is likely that in the present study, aldosterone increased sodium and potassium transport in these segments of the distal tubule. Little is known about the function ofthe distal convoluted tubule: however, the available data suggest that aldosterone is without effect on sodium and potassium transport by this segment (19,21,27,45).…”

Section: Discussionmentioning

confidence: 99%

Regulation by adrenal corticosteroids of sodium and potassium transport in loop of Henle and distal tubule of rat kidney.

Stanton

1986

“…This work was presented, in part, at the 9th Annual Meeting of the American Society of Nephrology, [21][22][23] November is the segment sensitive to aldosterone (2,3) and in this way is capable of regulating sodium reabsorption. Rapid natriuresis in response to a variety of stimuli such as acute volume expansion cannot be explained fully by inhibition of aldosterone because of its long duration of action.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of sodium transport by prostaglandin E2 across the isolated, perfused rabbit collecting tubule.

Stokes¹,

Kokko²

1977

Self Cite

348

151

A B S T RAC T This study was designed to examine whether prostaglandin E2 can directly affect sodium transport across isolated perfused rabbit renal collecting tubules. Changes in transepithelial potential and isotopic sodium fluxes in response to peritubular prostaglandin E2 were measured. In addition, changes in transepithelial potential of the outer medullary collecting tubule in response to prostaglandin E2 were also measured. With few exceptions, all rabbits received 5 mg/day desoxycorticosterone acetate for 4-11 days before experimentation. The results ofthe experiments show that: (a) prostaglandin E2 inhibits the negative transepithelial potential in the cortical collecting tubule as well as the outer medullary collecting tubule; (b) prostaglandin E2 inhibits net sodium transport out of the lumen by inhibiting efflux while backflux is unaffected; (c) prostaglandin E2 produces this inhibition within 15 min, and the effects are dose dependent and reversible. These results suggest that prostaglandin E2 may modulate sodium transport in vivo and may contribute to the final regulation of sodium excretion.