Changes in Renal Concentrating Ability Produced by Parathyroid Extract*

Epstein, Franklin H.; Beck, David; Carone, Frank A.; Levitin, Howard; Manitius, A

doi:10.1172/jci103896

Cited by 89 publications

(32 citation statements)

References 15 publications

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“…Thus, more osmotically active solute accumulated in the hypertonic medulla to produce greater net movement of water into the medulla from the large volume of isotonic collecting duct urine. Similar to observations by other investigators (14,(16)(17)(18) (27,28).…”

Section: III B a Typical Study Is Illustrated Insupporting

confidence: 92%

“…Obviously, quantitative comparison of our data with rat micropuncture data is not possible. The rise in potassium, titratable acid, and ammonium excretion following ethacrynic acid suggests that sodium reabsorption occurred distal to the loop of Henle (24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36). Hence, a portion of sodium rejected proximal to the distal tubule and collecting duct would not have been excreted.…”

Section: III B a Typical Study Is Illustrated Inmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Ethacrynic Acid (a New Saluretic Agent) on Renal Diluting and Concentrating Mechanisms: Evidence for Site of Action in the Loop of Henle*

Goldberg¹,

McCurdy²,

Foltz³

et al. 1964

J. Clin. Invest.

156

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Section: III B a Typical Study Is Illustrated Insupporting

confidence: 92%

Section: III B a Typical Study Is Illustrated Inmentioning

confidence: 99%

Effects of Ethacrynic Acid (a New Saluretic Agent) on Renal Diluting and Concentrating Mechanisms: Evidence for Site of Action in the Loop of Henle*

Goldberg¹,

McCurdy²,

Foltz³

et al. 1964

J. Clin. Invest.

156

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“…To determine the significance of All in the control of RBF and GFR in hypercalcemia, inhibitors of the synthesis or action of All were administered to normocalcemic control and hypercalcemic rats. In the first group of studies (group 3 A), following 4 d of on either control (n = 5) or vitamin D-supplemented diet (n = 8), animals were given the converting enzyme inhibitor, captopril (SQ 14,225, E. R. Squibb & Sous, Inc., Princeton, NJ) (13.33 mg/kg, orally, every 8 h for 4 d). This dose of captopril completely prevented the pressor response to 50 ng of exogenous AI in every animal studied.…”

Section: Pg In Chronic Hypercalcemiamentioning

confidence: 99%

“…The association of acute and chronic hypercalcemia with decrements in renal blood flow (RBF)' and glomerular filtration rate (GFR) has been widely recognized in both man and experimental animals (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). While the mechanisms responsible for the decrement in RBF and GFR have been studied in anesthetized, acutely hypercalcemic animals, there have been no such studies in the setting of chronic hypercalcemia.…”

mentioning

confidence: 99%

Control of Renal Hemodynamics and Glomerular Filtration Rate in Chronic Hypercalcemia

Levi¹,

Ellis²,

Berl³

1983

J. Clin. Invest.

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A B S T R A C T The role of prostaglandins (PG), reninangiotensin system (RAS) and calcium (Ca) in the control of renal hemodynamics and glomerular filtration rate (GFR) in chronic hypercalcemia (serum Ca 12.8 mg%) was studied. Renal blood flow (RBF, 6.39 ml/ min per gram kidney weight [gkw]) and GFR (0.52 ml/min per gkw) were significantly decreased in hypercalcemic rats when compared with normocalcemic rats (7.15, P < 0.001 and 0.74, P < 0.05, respectively). These changes in RBF and GFR occurred independent of any significant alterations in systemic hemodynamics, blood and plasma volume. Inhibition of the renal PG with indomethacin resulted in marked decrements in both RBF (6.39-4.12 ml/min per gkw, P < 0.01) and GFR (0.52-0.19 ml/min per gkw, P < 0.01) in hypercalcemic rats, whereas there was no significant alterations in normocalcemic rats. Inhibition of the RAS with captopril resulted in marked increments in both RBF (6.39-7.35 ml/min per gkw, P < 0.05) and GFR (0.52-0.74 ml/min per gkw, P < 0.05) in hypercalcemic rats. In fact, there was no significant difference from the RBF and GFR of similarly treated normocalcemic rats. Similar results were also obtained with the competitive angiotensin II (AII) antagonist (sarcosyll-isoleucyl5-glycyl8) AII. Since both the renal PG and the RAS are involved in the control of RBF and GFR in hypercalcemia, the role of each is best revealed in the absence of the other. Hence, comparison of the RBF and GFR in the PG-inhibited hypercalcemic rats in the presence of AII (4.12 and 0.19 ml/ min per gkw, respectively) and absence of AII (5.99 and 0.53 ml/min per gkw, P < 0.01 for both) reveals the vasoconstrictive role for All in hypercalcemia. On the other hand, comparison of the RBF and GFR in the AII-inhibited hypercalcemic rats in the presence of PG (7.35 and 0.74 ml/min per gkw, respectively) and absence of PG (5.99 and 0.53 ml/min per gkw, P < 0.01 and P < 0.05, respectively) reveals the vasodilatory role for PG in hypercalcemia. Finally, comparison of the RBF and GFR in both PG-and Allinhibited hypercalcemic rats (5.99 and 0.53 ml/min per gkw, respectively) with similarly treated normocalcemic rats (7.30 and 0.94 ml/min per gkw, P < 0.001 and P < 0.005, respectively) reveals the vasoconstrictive role for Ca in chronic hypercalcemia. Our study therefore demonstrates that in chronic hypercalcemia the RBF and GFR are controlled by an active interplay of the vasoconstrictive effect of AII, the vasodilatory effect of renal PG, and the direct vasoconstrictive effect of Ca, independent of either AII or PG. The sum total of these forces produces a modest but significant decrease in RBF and GFR. INTRODUCTIONThe association of acute and chronic hypercalcemia with decrements in renal blood flow (RBF)' and glomerular filtration rate (GFR) has been widely recognized in both man and experimental animals (1-15). While the mechanisms responsible for the decrement in RBF and GFR have been studied in anesthetized, acutely hypercalcemic animals, there have been no such studies in the setting...

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“…The association of hypercalcemia with disturbances in renal concentrating ability, water intake, and loop of Henle function has been widely recognized in both humans (1,2) and experimental animals (3,4). Studies in rats show that chronic hypercalcemia is associated with inhibition of thick ascending limb NaCl reabsorption (5).…”

Section: Introductionmentioning

confidence: 99%

Hypercalcemia stimulates expression of intrarenal phospholipase A2 and prostaglandin H synthase-2 in rats. Role of angiotensin II AT1 receptors.

Mangat¹,

Peterson²,

Burns³

1997

J. Clin. Invest.

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In chronic hypercalcemia, inhibition of thick ascending limb sodium chloride reabsorption is mediated by elevated intrarenal PGE 2 . The mechanisms and source of elevated PGE 2 in hypercalcemia are not known. We determined the effect of hypercalcemia on intrarenal expression of cytosolic phospholipase A 2 (cPLA 2 ), prostaglandin H synthase-1 (PGHS-1), and prostaglandin H synthase-2 (PGHS-2), enzymes important in prostaglandin production. In rats fed dihydrotachysterol to induce hypercalcemia, Western blot analysis revealed significant upregulation of both cPLA 2 and PGHS-2 in the kidney cortex and the inner and outer medulla. Immunofluorescence localized intrarenal cPLA 2 and PGHS-2 to interstitial cells of the inner and outer medulla, and to macula densa and cortical thick ascending limbs in both control and hypercalcemic rats. Hypercalcemia had no effect on intrarenal expression of PGHS-1. To determine if AT 1 angiotensin II receptor activation was involved in the stimulation of cPLA 2 and PGHS-2 in hypercalcemia, we treated rats with the AT 1 receptor antagonist, losartan. Losartan abolished the polydipsia associated with hypercalcemia, prevented the increase in cPLA 2 protein in all regions of the kidney, and diminished PGHS-2 expression in the inner medulla. In addition, losartan completely prevented the increase in urinary PGE 2 excretion in hypercalcemic rats. Intrarenal levels of angiotensin II were unchanged in hypercalcemia. These data indicate that hypercalcemia stimulates intrarenal cPLA 2 and PGHS-2 protein expression. Our results further support a role for angiotensin II, acting on AT 1 receptors, in mediating this stimulation. (

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Changes in Renal Concentrating Ability Produced by Parathyroid Extract*

Cited by 89 publications

References 15 publications

Effects of Ethacrynic Acid (a New Saluretic Agent) on Renal Diluting and Concentrating Mechanisms: Evidence for Site of Action in the Loop of Henle*

Effects of Ethacrynic Acid (a New Saluretic Agent) on Renal Diluting and Concentrating Mechanisms: Evidence for Site of Action in the Loop of Henle*

Control of Renal Hemodynamics and Glomerular Filtration Rate in Chronic Hypercalcemia

Hypercalcemia stimulates expression of intrarenal phospholipase A2 and prostaglandin H synthase-2 in rats. Role of angiotensin II AT1 receptors.

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