Effects of inhibitors of prostaglandin synthesis on renal sodium excretion in normal dogs and dogs with decreased renal mass

Altsheler, P.; Klahr, Saulo; Rosenbaum, Robert M.; Slatopolsky, E

doi:10.1152/ajprenal.1978.235.4.f338

Cited by 17 publications

(9 citation statements)

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“…These values for FENa are closely similar to those reported for conscious, trained, normal dogs undergoing sustained water diuresis, e.g. FEwa of 0.14 ± 0.03% at MRAP of 106 ± 7 mm Hg [39], Autoregulation of ERBF and of GFR were almost perfect. The near constancy of ERBF and of GFR is shown graphically in figure 3.…”

Section: Protocol Group Asupporting

confidence: 86%

Modest Pressure Natriuresis and Autoregulation during Water Diuresis in Dogs

Waugh

1991

J Vasc Res

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The effects of renal arterial pressure change on renal output of sodium and volume were measured during water diuresis in 25 chloralose-anesthetized dogs. Conditions included a minimal invasive stress, limited sodium administration, and mean renal arterial pressures varied suprarenally, by aortic balloon inflation to lowermost levels of 82–106 mm Hg. Group A dogs received no aldosterone; group B, C and D dogs were given aldosterone. Dogs of group C also received (1-Sar, 8-Ile)-angiotensin II. Group D dogs received phenylephrine which elevated arterial and right atrial pressures moderately without decrease in renal blood flow. In groups A, B and C, mean changes in sodium output, volume output, fractional excretions and free water clearances were not detectable with mean renal arterial pressure reductions, which averaged 29 ± 2.9, 22 ± 2.8 and 27 ± 5.2 mm Hg, respectively. Right atrial pressures, effective renal blood flows and glomerular filtration rates did not change with the renal arterial pressure changes in these groups. In the group D dogs, during the larger pressure reductions of 54 ± 6.6 mm Hg from higher values of 158 ± 7.0 mm Hg, mean urine flow and effective renal blood flow remained constant while glomerular filtration rate and sodium output decreased only slightly. Output efficiency ratios related to perfusion pressure were calculated. With no more than modest pressure-induced excretory changes, it is concluded that excretory sodium and urinary volume autoregulation in concert with nearly perfect circulatory autoregulation were demonstrated with regionally varied mean renal arterial pressure. The same preglomerular myogenic responses to transvascular pressure, which restrict glomerular and transcapillary pressures, are viewed dominantly responsible for both circulatory and excretory autoregulation under normal conditions of minimal stress and low fractional sodium excretions. Homeostatic implications are discussed concerning likely relevance to the Guyton-Coleman theory for the long-term control of arterial blood pressure.

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Section: Protocol Group Asupporting

confidence: 86%

Modest Pressure Natriuresis and Autoregulation during Water Diuresis in Dogs

Waugh

1991

J Vasc Res

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“…Ear lier studies have documented this finding in normovolemic, conscious animals [7,10.19, 20. 37], while experiments utilizing a water diuresis, and therefore severely reduced plasma ADH levels, show little or no anti diuretic effect prostaglandin inhibition [1,10,16,23,31]. However, the fact that a slight antidiuresis has been observed upon prosta glandin inhibition even during a water di uresis suggests that other mechanisms may be involved in reducing urine flow.…”

Section: Discussionmentioning

confidence: 99%

“…Earlier studies on conscious, waterdiuresing dogs administered prostaglandin synthesis inhibitors have shown a natriuretic effect [23], no effect [1,16] or an antinatri uretic effect [10], so that no definite conclu sions as to a role of endogenous prostaglan dins on sodium excretion could be made. [1,16] have shown no effect of prostaglandin inhi bition on sodium excretion. Additionally, in two experiments conducted in our laborato ry, meclofenamate caused no change in so dium excretion in dogs undergoing a water diuresis, although the same animals de creased sodium excretion when hydropenic.…”

Section: Discussionmentioning

confidence: 99%

Antidiuresis and Decreased Sodium Excretion during Cyclo-Oxygenase Inhibition in the Conscious Dog

Walker¹

1983

Kidney Blood Press Res

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Studies were undertaken to further elucidate the role of endogenous prostaglandins in normal renal function in the awake dog. Meclofenamate (2 mg/kg and 2 mg/kg/h, i.v.) was administered after control measurements. Parallel time control experiments were also performed. Inhibition of renal prostaglandin synthesis was documented by significant reduction in urinary prostaglandin E₂ excretion rate. Urine flow and sodium excretion were reduced by meclofenamate infusion. In addition, fractional excretion of sodium was reduced, implying enhanced sodium reabsorption during prostaglandin synthesis inhibition. Renal hemodynamics, glomerular filtration and systemic hemodynamics were unaffected. It is concluded that endogenous prostaglandin release is important in influencing sodium and water excretion in the conscious dog.

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“…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). In addition, Ganguli et al (40) demonstrated an increase in medullary NaCl content following prostaglandin synthesis inhibition even in the absence of any discernible change in papillary blood flow.…”

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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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Effects of inhibitors of prostaglandin synthesis on renal sodium excretion in normal dogs and dogs with decreased renal mass

Cited by 17 publications

References 0 publications

Modest Pressure Natriuresis and Autoregulation during Water Diuresis in Dogs

Modest Pressure Natriuresis and Autoregulation during Water Diuresis in Dogs

Antidiuresis and Decreased Sodium Excretion during Cyclo-Oxygenase Inhibition in the Conscious Dog

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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