1974
DOI: 10.1152/ajplegacy.1974.226.5.1015
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Effects of prostaglandins E1 and E2 on renal sodium reabsorption and Starling forces

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Cited by 70 publications
(15 citation statements)
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“…The pars recta would be an unlikely site since the superficial proximal tubule was not affected. The superficial thin descending limb is also an unlikely site for increased reabsorption of chloride since this portion of the nephron appears to lack capacity for active salt transport and the permeability to sodium is exceedingly low (13 The results ofthe present study when combined with the studies cited above (16)(17)(18)(19)(20) suggest that endogenous renal prostaglandins may play a role in the natriuresis and chloruresis of acute volume expansion by decreasing fractional salt reabsorption in the juxtamedullary nephron preferentially. The majority of the juxtamedullary nephron traverses the renal medulla, an area known to be rich in prostaglandins (21).…”
Section: Discussionmentioning
confidence: 50%
“…The pars recta would be an unlikely site since the superficial proximal tubule was not affected. The superficial thin descending limb is also an unlikely site for increased reabsorption of chloride since this portion of the nephron appears to lack capacity for active salt transport and the permeability to sodium is exceedingly low (13 The results ofthe present study when combined with the studies cited above (16)(17)(18)(19)(20) suggest that endogenous renal prostaglandins may play a role in the natriuresis and chloruresis of acute volume expansion by decreasing fractional salt reabsorption in the juxtamedullary nephron preferentially. The majority of the juxtamedullary nephron traverses the renal medulla, an area known to be rich in prostaglandins (21).…”
Section: Discussionmentioning
confidence: 50%
“…In an additional six experiments unidirectional lumen-to-bath fluxes were measured under conditions identical to the PD experiments (i.e., with the bath pump on). PGE2 inhibited efflux in a similar fashion: 25.5+4.0 (control), 15.1+3.5 (PGE2), and 21.3±4.1 (recovery). The differences are highly significant (P < 0.001).…”
Section: Methodsmentioning
confidence: 61%
“…Since the discovery of large qtuantities of prostaglandins in the renal medulla (4), many attempts have been made to elucidate its mechanisms of action. The general approaches that have been utilized to assess the effect of prostaglandins oIn renal function in the intact kidney include: (a) infuision of prostaglandins into the renal artery (8,9,15,16), (b) infuision of sodium arachidonate into the renal artery to stimulate endogenous prostaglandins (17,18), and (c) reduction of endogenous intrarenal prostaglandins by drugs or dietary deficiency (19,20 (31)(32)(33). Several patients have been reported whose metabolic and pathologic syndrome has been reversed with indomethacin, an inhibitor of' prostaglan(lin synthesis (31,32).…”
Section: Discussionmentioning
confidence: 99%
“…PGE|, however, re duced the rate of fluid absorption from the proximal tubule. On the basis of further studies, they concluded that alterations in physical factors governing transepithelial fluid movement could not account for the results obtained [23], Higashihara et al [24], when studying indomethacin, found no change in either the superficial single-nephron GFR or net chloride absorption in proxi mal nephrons. On the basis of these studies, most inves tigators have concluded that PGE increases salt and water excretion by acting at some site beyond the proxi mal nephron.…”
Section: Renal Prostaglandins and Sodium Excretionmentioning
confidence: 92%
“…Strandhoy et al [23] evaluated the effects of renal artery infusion of PGE| and PGE2 in dogs. They found that PGE2 had no effect on single nephron GFR or on proximal tubular fluid absorption.…”
Section: Renal Prostaglandins and Sodium Excretionmentioning
confidence: 99%