Effects of prostaglandins E 1 , A 1 , and F 2   on renal handling of salt and water

Jb, Gross; Barter, FC

doi:10.1152/ajplegacy.1973.225.1.218

Cited by 112 publications

(51 citation statements)

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“…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%

“…No evidence currently exists to implicate prostaglandins in renal epithelial transport of salt though such evidence does exist for the jejunum (5), frog corneal epithelium (6), and toad bladder (7). It is difficult to interpret the effects of prostaglandins on renal epithelial transport with clearance techniques because of their well-demonstrated effects on renal blood flow (8,9) and on vasopressin-induced osmotic water flow (10). The present studies were deisgned, therefore, to examine directly the effect of prostaglandin E2 (PGE2), the renal prostaglandin occurring in greatest quantity, on sodium transport across the in vitro-perfused rabbit collecting tubule.…”

Section: Introductionmentioning

confidence: 99%

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

Stokes¹,

Kokko²

1977

J. Clin. Invest.

348

151

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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.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Stokes¹,

Kokko²

1977

J. Clin. Invest.

348

151

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“…Studies conducted in vivo have demonstrated increased sodium excretion following infusions of prostaglandins of the E series (33-35), and, in hydropenic dogs, decreased absorption of free water (34,35). Inhibition of endogenous renal prostaglandin synthesis, either with indomethacin or with meclofenamate, has resulted in antinatriuresis (36,37) and in an enhanced urinary concentrating ability in response to administration of vasopressin (36,38,39 Kaukker (42), using micropuncture techniques, and by Stokes (43), using the isolated, perfused rabbit mTALH, have also been consistent with the notion that PGE2 inhibits NaCl absorption by the TALH.…”

mentioning

confidence: 99%

Interactions among prostaglandin E2, antidiuretic hormone, and cyclic adenosine monophosphate in modulating Cl- absorption in single mouse medullary thick ascending limbs of Henle.

Culpepper¹,

Andreoli²

1983

J. Clin. Invest.

109

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A B S T R A C T This paper describes the inhibitory effect of prostaglandin E2 (PGE2) on antidiuretic hormone (ADH)-stimulated net Cl-absorption and spontaneous transepithelial voltage (Ve) in single medullary thick ascending limbs of Henle (TALH, thick ascending limb; mTALH, medullary segment; cTALH, cortical segment) obtained from mouse kidney. The experimental data indicate that PGE2 reduced the ADHdependent values of net Cl-absorption (Je,', eq cm-2 s-') and Ve (mV) in a dose-dependent manner; that increasing concentrations of peritubular ADH reversed the PGE2-mediated reductions in the ADH-dependent moiety of Ve in the mouse mTALH; that PGE2 had no effect on cyclic AMP-stimulated increments in Ve in the mouse mTALH; and that PGE2 had no In the renal medulla, this process enriches medullary osmolality, thereby contributing to urinary concentrating power (13,14). In certain species, like the mouse, salt absorption (11) and adenyl cyclase activity (15,16) in the water permeability of mammalian collecting ducts.In the isolated mouse mTALH, NaCl absorption involves the coupled entry of Cl-, and possibly K+ (17, 18), to Na+ entry across apical plasma membranes. In other words, Cl-transport in this nephron segment is a secondary active transport process, driven in part by the Na+ gradient between luminal fluid and cell interior (11,17). Conservative NaCl absorption in this nephron segment is enhanced considerably, and in a dose-dependent manner, by ADH, operating through the second messenger cyclic (c)AMP (11). Conversely, conservative NaCl absorption in the mouse mTALH is suppressed significantly by increases in peritubular osmolality independently of transepithelial osmotic pressure gradients (19).The mouse mTALH, like the rabbit cTALH (6, 20) and mTALH (7), behaves as a hybrid epithelium: the mouse mTALH is electrically leaky (11, 17) and rather permeable to Na+ and to 17), yet is virtually water impermeable either in the presence or absence of ADH (9-11). Consequently, as medullary peritubular salt concentrations vary, there occur varying degrees of dissipative NaCl backleak from interstitium to lumen through the paracellular pathway. Thus, for the mouse mTALH, maintenance of diluting power in the presence of varying NaCl concentrations in peritubular media depends, at least in part, on the interplay between ADH and peritubular osmolality in modifying conservative NaCl transport (11, 19). We will argue in this paper that PGE2 represents yet another factor that modulates the latter in the mouse mTALH.In the amphibian urinary bladder, Orloff et al. (21) found that prostaglandins inhibited the hydro6smotic effect of ADH but did not change the response of the epithelium to cAMP. They inferred that prostaglandins had acted at a locus proximal to hormone-dependent accumulation of cAMP within the cell, with little or no discernible prostaglandin action on transport events beyond cAMP accumulation. Based on in vitro studies in the isolated rabbit collecting duct, Grantham and Orloff (22) also suggested that prosta...

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“…Pulmonary vasodilatation by histamine has been attributed to release of adrenaline from the adrenal gland (Colebatch, 1970 (Gross & Bartter, 1973). Phenylbutazone causes salt and water retention in man through an action on the kidney (see Goodman & Gilman, 1975).…”

Section: P Physiological Society April 1976mentioning

confidence: 99%

Communications

1976

The Journal of Physiology

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Effects of prostaglandins E 1 , A 1 , and F 2 on renal handling of salt and water

Cited by 112 publications

References 0 publications

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

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

Interactions among prostaglandin E2, antidiuretic hormone, and cyclic adenosine monophosphate in modulating Cl- absorption in single mouse medullary thick ascending limbs of Henle.

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