Fluid Balance in the Urological Patient: Disturbances in the Renal Regulation of the Excretion of Water and Sodium Salts Following Decompression of the Urinary Bladder

Wilson, B.; Reisman, David D.; Moyer, Carl A.

doi:10.1016/s0022-5347(17)74418-7

Cited by 62 publications

(19 citation statements)

References 3 publications

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“…DISCUSSION A characteristic set of renal functional defects has been observed in the rat after release of bilateral ureteral obstruction, namely, diuresis, natriuresis, and impairment of gloxnerular filtration. Identical findings have been described in patients after relief of urinary obstruction (7,(11)(12)(13)(14). While a number of recent studies have been directed to the renal functional changes associated witlh unilateral obstruction (15,16) and acute (17,18) and chronic (18) elevation of ureteral pressure, data obtained after release of total obstruction have been sparse and related primarily to the defects in sodium and water excretion in this lesion (8).…”

Section: Methodsmentioning

confidence: 91%

“…It is well established that enhanced sodiumi excretion occurs after release of urinary obstruction in man (7,(11)(12)(13)(14). The clinical reports of postobstructive natriuresis include only patients in whom there is either bilateral obstruction or unilateral obstruction with absence of the contralateral kidney (7,(11)(12)(13)(14).…”

Section: Methodsmentioning

confidence: 99%

“…The clinical reports of postobstructive natriuresis include only patients in whom there is either bilateral obstruction or unilateral obstruction with absence of the contralateral kidney (7,(11)(12)(13)(14). This phenomenon does not appear to occur after release of unilateral obstruction when the opposite kidney is functionally intact.…”

Section: Methodsmentioning

confidence: 99%

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The Renal Functional Defect of Postobstructive Nephropathy

Jaenike¹

1972

J. Clin. Invest.

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A B S T R A C T This study was designed to examine the pathogenesis of the excretory defect produced by bilateral ureteral' obstruction in the rat. After release of obstruction of 24 hr duration glomerular filtration rate was reduced to 20% of normal. Free flow proximal tubular pressure was normal, excluding residual obstruction as a cause of depressed filtration, and indicating that an intrarenal hemodynamic abnormality was primarily responsible for the excretory defect. Total renal blood flow and cortical distribution of flow were normal. Clearance and micropuncture studies indicated the presence of marked heterogeneity of nephron function with residual excretory function residing primarily in vasodilated nephrons in which decreased postglomerular arteriolar resistance effected a reduction in glomerular filtration pressure. Heterogeneity of nephron function was evidenced by a wide scatter of values for single nephron filtration rate and from direct intratubular injection of dye which revealed that at least 28% of surface nephrons were either nonfiltering or had filtration rates too-low to measure. The observed decrease in Hippuran extraction and increased ratio of Hippuran to inulin clearance ratio is characteristic of the vasodilated kidney. Further evidence of the vasodilated nature of residual functioning nephrons was demonstrated by the failure of intrarenal papaverine infusion to increase filtration rate in this lesion.The hemodynamic defect produced by bilateral obstruction is contrasted with that seen after release of unilateral ureteral ligation in which depression of filtration rate appears to result primarily from preglomerular vasoconstriction. This difference raises the possibility that a vasodilating substance accumulates during total suppression of renal excretory function.

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Section: Methodsmentioning

confidence: 91%

Section: Methodsmentioning

confidence: 99%

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The Renal Functional Defect of Postobstructive Nephropathy

Jaenike¹

1972

J. Clin. Invest.

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“…Partial urinary tract obstruction is known to produce, in addition to a nonspecific depression in renal function, certain characteristic derangements, especially profound polyuria (1)(2)(3)(4)(5); release of the obstruction may result in a transient salt-wasting state (6,7). Three hypotheses may be advanced to explain the altered function of the hydronephrotic kidney.…”

mentioning

confidence: 99%

Patterns of nephron perfusion in acute and chronic hydronephrosis.

Suki¹,

Eknoyan²,

Rector³

et al. 1966

J. Clin. Invest.

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“…prostaglandin E2; AQP2; vasopressin; ureteral obstruction THE POSTOBSTRUCTED KIDNEY exhibits a markedly reduced urinary concentrating capacity due to decreased abundance of major renal transport proteins (15,22,27,28). Importantly, the vasopressin type 2 receptor (V2R) and vasopressin-regulated transport proteins are downregulated, causing vasopressinresistant polyuria (20,51,55). A number of hormone/signaling systems contribute to postobstructive kidney disease, including the prostanoid system (13,26,32,36) and the renin-angiotensin-system (RAS) (21,40,56).…”

mentioning

confidence: 99%

Cyclooxygenase 2 inhibition exacerbates AQP2 and pAQP2 downregulation independently of V2 receptor abundance in the postobstructed kidney

Jensen

Bae

Nørregaard³

et al. 2010

American Journal of Physiology-Renal Physiology

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Previously we demonstrated that ANG II receptor (AT1R) blockade attenuates V2 receptor (V2R), AQP2, and pS256-AQP2 downregulation in the postobstructed kidney and partially reverses obstruction-induced inhibition of cAMP generation and cyclooxygenase 2 (COX-2) induction. Therefore, we speculated whether the effects of AT1R blockade on V2R and the vasopressin-regulated pathway are attributable to attenuated COX-2 induction. To examine this, rats were subjected to 24-h bilateral ureteral obstruction (BUO) followed by 48-h release and treated with the COX-2 inhibitor parecoxib or saline. Control rats were sham-operated. Parecoxib treatment significantly reduced urine output 24 h after release of BUO whereas urine osmolality and solute-free water reabsorption was comparable between saline-and parecoxib-treated BUO rats. Immunoblotting revealed a significant decrease in AQP2 and pS256-AQP2 abundance to 20 and 23% of sham levels in parecoxib-treated BUO rats compared with 40 and 55% of sham levels in saline-treated BUO rats. Immunohistochemistry confirmed the exacerbated AQP2 and pS256-AQP2 downregulation in parecoxib-treated BUO rats. Finally, parecoxib treatment had no effect on V2R downregulation and the inhibited, vasopressin-stimulated cAMP generation in inner medullary membrane fractions from the postobstructed kidney. In conclusion, COX-2 inhibition exacerbates AQP2 and pS256-AQP2 downregulation 48 h after release of 24-h BUO independently of V2R abundance and vasopressin-stimulated cAMP generation. The results indicate that COX-2 inhibition does not mimic AT1R blockade-mediated effects and that AT1R-mediated AQP2 regulation in the postobstructed kidney collecting duct is independent of COX-2 induction. prostaglandin E2; AQP2; vasopressin; ureteral obstruction THE POSTOBSTRUCTED KIDNEY exhibits a markedly reduced urinary concentrating capacity due to decreased abundance of major renal transport proteins (15,22,27,28). Importantly, the vasopressin type 2 receptor (V2R) and vasopressin-regulated transport proteins are downregulated, causing vasopressinresistant polyuria (20,51,55). A number of hormone/signaling systems contribute to postobstructive kidney disease, including the prostanoid system (13,26,32,36) and the renin-angiotensin-system (RAS) (21,40,56).The most abundant prostaglandin in the kidney, prostaglandin E 2 (PGE 2 ), is involved in the regulation of kidney water and salt handling. In the medullary thick ascending limb (TAL), PGE 2 acutely blunts vasopressin-stimulated NaCl transport and cAMP generation (9, 46, 49) and the long-term effect of PGE 2 is downregulation of the vasopressin-regulated Na-K-2Cl cotransporter (NKCC2) (12). Similar PGE 2 -mediated effects are observed in the isolated rabbit cortical collecting duct (CD) (3,19,45,49), but parallel studies in rat collecting ducts have not yet been able to confirm an inhibitory effect of PGE 2 on cAMP generation (3, 4, 31, 49). However, PGE 2 does inhibit vasopressin-stimulated water permeability in rat inner medullary collecting duct (IMCD) ind...

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Fluid Balance in the Urological Patient: Disturbances in the Renal Regulation of the Excretion of Water and Sodium Salts Following Decompression of the Urinary Bladder

Cited by 62 publications

References 3 publications

The Renal Functional Defect of Postobstructive Nephropathy

The Renal Functional Defect of Postobstructive Nephropathy

Patterns of nephron perfusion in acute and chronic hydronephrosis.

Cyclooxygenase 2 inhibition exacerbates AQP2 and pAQP2 downregulation independently of V2 receptor abundance in the postobstructed kidney

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