Tubular prostaglandin E2 production and its role in urinary hypotonicity after release of ureteral occlusion in the rat

1987 ◽  
Vol 73 (4) ◽  
pp. 395-399 ◽  
Author(s):  
Shozo Torikai
Keyword(s):  
Prostaglandin E2 ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Pge2 Production ◽  
Endogenous Prostaglandin ◽  
Collecting Ducts ◽  
Ureteral Occlusion

1. In order to explore the involvement of endogenous prostaglandin E2 (PGE2) in the urine concentration defect after ureteral occlusion, PGE2 production by isolated collecting ducts in vitro and effects of indomethacin on urine osmolality in vivo were examined. 2. Twenty-four hours ureter obstruction caused increased PGE2 production by the medullary collecting ducts, which was maintained at a high level on the day after release of obstruction (0.8 ± 0.2 pg/mm normal, 8.1 ± 0.9 pg/mm 24 h obstruction, and 6.6 ± 1.0 pg/mm post-obstruction, mean ± sem). An enhanced PGE2 production was also observed for papillary collecting duct on the day after release of 24 h ureteral occlusion (3.9 ± 0.5 pg/mm normal and 7.7 ± 1.2 pg/mm post-obstruction). 3. Administration of indomethacin to the unilateral post-obstructive rats slightly raised the urine osmolality of the post-obstructed kidney (from 339 ± 17 to 390 ± 22 mosmol/kg H2O), while it had a greater effect on the contralateral intact kidney (from 1569 ± 138 to 2567 ± 198 mosmol/kg H2O). 4. Our data may indicate that the urine concentration defect after 24 h ureteral occlusion is ascribable mainly to a mechanism other than increased endogenous PGE2.

Effect of calcitonin on urine concentration in the rat

1983 ◽  
Vol 244 (4) ◽  
pp. F432-F435 ◽  
Author(s):  
S. Carney ◽  
T. Morgan ◽  
C. Ray ◽  
L. Thompson
Keyword(s):  
Water Permeability ◽  
Partial Agonist ◽  
Collecting Duct ◽  
Free Water ◽  
Urine Concentration ◽  
Distal Nephron ◽  
Free Water Clearance ◽  
Normal Increase

Because mammalian distal nephron segments with both calcitonin- and antidiuretic hormone- (ADH) sensitive adenylate cyclase activity have been described, in vivo and in vitro experiments were performed to study the effect of calcitonin on rat distal nephron water permeability. Calcitonin 1 and 0.1 U/ml, but not 0.01 U/ml, significantly increased the diffusional water permeability in the isolated papillary collecting duct by 15 and 11%, respectively. However, this effect was small when compared with a 68% increase with a supramaximal concentration of ADH (from 4.0 +/- 0.3 to 6.7 +/- 0.9 microns/s; n = 6, P less than 0.01). The normal increase in water permeability with increasing concentration of ADH (0.02 and 0.2 mU/ml) was depressed by the previous addition of calcitonin (1 U/ml) to the bath but was unaltered with the supramaximal ADH concentration (2 mU/ml). Verapamil, a compound that antagonizes cellular calcium entry, did not alter the effect of calcitonin on diffusional water permeability. Calcitonin in concentrations of 0.05, 0.5, and 5 U/ml produced a significant reduction in urine flow and free water clearance. Pretreatment with calcitonin in these concentrations inhibited the antidiuretic action of ADH. These studies suggest that calcitonin acts as a partial agonist to ADH within the distal nephron. It is unclear whether such an action represents a physiological or a pharmacological effect.

scholarly journals Interaction between vasopressin and angiotensin II in vivo and in vitro: effect on aquaporins and urine concentration

2010 ◽  
Vol 299 (3) ◽  
pp. F577-F584 ◽  
Author(s):  
Weidong Wang ◽  
Chunling Li ◽  
Sandra Summer ◽  
Sandor Falk ◽  
Robert W. Schrier
Keyword(s):  
Angiotensin Ii ◽  
Collecting Duct ◽  
Receptor Activation ◽  
Urine Concentration ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Vitro Effect

The study was undertaken to examine the potential cross talk between vasopressin and angiotensin II (ANG II) intracellular signaling pathways. We investigated in vivo and in vitro whether vasopressin-induced water reabsorption could be attenuated by ANG II AT1 receptor blockade (losartan). On a low-sodium diet (0.5 meq/day) dDAVP-treated animals with or without losartan exhibited comparable renal function [creatinine clearance 1.2 ± 0.1 in dDAVP+losartan (LSDL) vs. 1.1 ± 0.1 ml·100 g−1·day−1 in dDAVP alone (LSD), P > 0.05] and renal blood flow (6.3 ± 0.5 in LSDL vs. 6.8 ± 0.5 ml/min in LSD, P > 0.05). The urine output, however, was significantly increased in LSDL (2.5 ± 0.2 vs. 1.8 ± 0.2 ml·100 g−1·day−1, P < 0.05) in association with decreased urine osmolality (2,600 ± 83 vs. 3,256 ± 110 mosmol/kgH2O, P < 0.001) compared with rats in LSD. Immunoblotting revealed significantly decreased expression of medullary AQP2 (146 ± 6 vs. 176 ± 10% in LSD, P < 0.01), p-AQP2 (177 ± 13 vs. 214 ± 12% in LSD, P < 0.05), and AQP3 (134 ± 14 vs. 177 ± 11% in LSD, P < 0.05) in LSDL compared with LSD. The expressions of AQP1, the α1- and γ-subunits of Na-K-ATPase, and the Na-K-2Cl cotransporter were not different among groups. In vitro studies showed that ANG II or dDAVP treatment was associated with increased AQP2 expression and cAMP levels, which were potentiated by cotreatment with ANG II and dDAVP and were inhibited by AT1 blockade. In conclusion, ANG II AT1 receptor blockade in dDAVP-treated rats on a low-salt diet was associated with decreased urine concentration and decreased inner medullary AQP2, p-AQP2, and AQP3 expression, suggesting that AT1 receptor activation plays a significant role in regulating aquaporin expression and modulating urine concentration in vivo. Studies in collecting duct cells were confirmatory.

Luminal prostaglandin E2 modulates sodium and water transport in rabbit cortical collecting ducts

1995 ◽  
Vol 268 (6) ◽  
pp. F1093-F1101 ◽  
Author(s):  
Y. Ando ◽  
Y. Asano
Keyword(s):  
Prostaglandin E2 ◽  
Collecting Duct ◽  
Dependent Manner ◽  
Cortical Collecting Duct ◽  
Osmotic Water ◽  
Basolateral Side ◽  
Luminal Side ◽  
Transepithelial Voltage

We have previously found that arginine vasopressin (AVP) acts not only from the basolateral side but also from the luminal side of the rabbit cortical collecting duct (CCD). In the present study, we examined whether prostaglandin E2 (PGE2), another classic and potent modulator of the collecting duct functions, exerts luminal actions in the rabbit CCD perfused in vitro. Although luminal prostaglandin I2 was inert, luminal PGE2 (> 1 nM) induced transient hyperpolarization of transepithelial voltage followed by sustained depolarization in a dose-dependent manner. This action was preserved in the presence of basolateral PGE2, luminal AVP, or luminal BaCl2, but abolished by basolateral ouabain or luminal amiloride. Furthermore, unlike luminal AVP, luminal PGE2 suppressed Na transport and increased osmotic water permeability. The present study suggests that PGE2, similar to AVP but in a different fashion, modulates transepithelial transports from both luminal and basolateral sites in the CCD in vivo.

Net acid transport by isolated perfused inner medullary collecting ducts

1990 ◽  
Vol 258 (1) ◽  
pp. F75-F84 ◽  
Author(s):  
S. M. Wall ◽  
J. M. Sands ◽  
M. F. Flessner ◽  
H. Nonoguchi ◽  
K. R. Spring ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Intercalated Cells ◽  
Acid Transport ◽  
Concentration Gradients ◽  
Collecting Ducts ◽  
Acidic Form ◽  
Medullary Collecting Duct ◽  
Stop Flow

The isolated perfused tubule technique was used to study net acid transport in rat terminal inner medullary collecting duct (IMCD) segments. The stop-flow luminal pH [measured fluorometrically with the acidic form of the pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein in the lumen] fell 0.35 units below the bath pH in tubules from control rats and 0.53 units below the bath in tubules from deoxycorticosterone-treated rats. Tubules from control rats absorbed bicarbonate and secreted ammonium against concentration gradients, although at low rates. In control rats, 10(-8) M vasopressin added to the bath increased bicarbonate absorption almost threefold. Treatment of rats in vivo with deoxycorticosterone significantly increased the rate of bicarbonate absorption in vitro. In vivo NH4Cl loading also significantly increased bicarbonate absorption. Staining microdissected tubules with acridine orange confirmed that the perfused segments lacked intercalated cells. We conclude that the terminal IMCD spontaneously acidifies the lumen despite an absence of intercalated cells. Bicarbonate absorption appears to be regulated by the same factors that affect net acidification in other collecting duct segments.

Biochemical characterization and osmolytes in papillary collecting ducts from pig and dog kidneys

1988 ◽  
Vol 66 (10) ◽  
pp. 1282-1290 ◽  
Author(s):  
Yvan Boulanger ◽  
Pascale Legault ◽  
Alberto Tejedor ◽  
Patrick Vinay ◽  
Yves Theriault
Keyword(s):  
Oxidative Phosphorylation ◽  
Biochemical Characterization ◽  
Collecting Duct ◽  
Proton Nuclear Magnetic Resonance ◽  
Collecting Ducts ◽  
Papillary Collecting Duct ◽  
Biochemical Measurements ◽  
Sugar Phosphates

Papillary collecting duct tubules were prepared in gram quantities from the papillae of dog and pig kidneys. Measurements of substrate and oxygen utilizations by these tubules under both aerobic and anaerobic conditions showed the potential for both glycolysis and oxidative phosphorylation. Oxygen is not necessary to maintain a normal adenosine 5′-triphosphate concentration, but oxidative phosphorylation contributes to more than 65% of the metabolism under aerobic conditions in the two species. Both phosphorus-31 and proton nuclear magnetic resonance spectra recorded from extracts of dog cortex, red medulla, and papilla showed a clear gradient from cortex to papilla for osmolytes, such as glycerophosphorylcholine, sorbitol, inositol, betaine, and sugar phosphates. Other molecules identified in the spectra included glucose, sorbitol, mannitol, lactate, glutamine, alanine, threonine, and adenosine 5′-triphosphate. Conventional biochemical measurements supported these findings. An increase in osmolality from 300 to 600 mosmol/kg H2O for 120 min did not increase the glycerophosphorylcholine and sorbitol concentrations of dog papillary collecting ducts in vitro, but a small effect of a 24-h dehydration was detected in vivo.

Effect of oxybenzone on PGE2-production in vitro and on plaque and gingivitis in vivo

2004 ◽  
Vol 31 (2) ◽  
pp. 91-94 ◽  
Author(s):  
Lillemor Jannesson ◽  
Dowen Birkhed ◽  
Dale Scherl ◽  
Abdul Gaffar ◽  
Stefan Renvert
Keyword(s):  
Pge2 Production

Is the function of the renal papilla coupled exclusively to an anaerobic pattern of metabolism?

1979 ◽  
Vol 236 (5) ◽  
pp. F423-F433 ◽  
Author(s):  
J. J. Cohen
Keyword(s):  
Oxidative Metabolism ◽  
Aerobic Glycolysis ◽  
Collecting Duct ◽  
High Rate ◽  
O2 Uptake ◽  
Duct Cells ◽  
Collecting Duct Cells ◽  
Mitochondrial Oxidative Metabolism

It is widely accepted that in vivo the function of the papilla of the mammalian kidney is supported primarily by anaerobic metabolism. As a result, the major source of energy for support of function in the papilla is considered to be derived from glycolysis. This orientation originates from two concepts: 1) that in vivo the gaseous environment of the papilla has such a low PO2 that O2 availability limits O2 consumption, and 2) that papillary tissue has a high rate of glycolysis when compared with either cortical tissue or extrarenal tissues. It has also been tacitly assumed that papillary tissue has a "low" O2 uptake. Review of the measurements of PO2 of papillary tissue and of urine PO2 indicates that the PO2 of papillary tissue should not limit its aerobic mitochondrial oxidative metabolism. While the rate of aerobic glycolysis in papillary tissue is high, simultaneously papillary tissue has a rate of O2 uptake similar to that of liver and higher than that of muscle. The major (two-thirds) source of energy for papillary tissue in vitro is from O2 uptake. That papillary tissue is not exclusively dependent on glucose for its energy requirements is indicated by the greater stimulation of papillary tissue QO2 by succinate than by glucose. Thus, papillary tissue has both a high aerobic mitochondrial oxidative metabolism and a high aerobic glycolytic metabolism. It is suggested that the mechanism for the high rate of aerobic glycolysis in the presence of an adequate O2 supply is due to the relatively small mass of mitochondria in papillary tissue in relation to the amount of work done by the tissue. As a result of the limited rate of ATP production by the mitochondrial electron transport chain, the phosphorylation state ([ATP]/[ADP][Pi]) is reduced and the cytoplasmic redox state ([NAD+]/[NADH]) of the papillary collecting duct cells also becomes more reduced; changes in both ratios enhance the rate of glycolysis. This limited metabolic capacity of the collecting duct cells may permit an excess volume of solute and water to be excreted during volume expansion diuresis. The metabolic characteristics of the papilla, when compared to cortex, also provide a basis for the observed differences in substrate selectivity of cortex and medulla with respect to utilization of glucose and lactate. The experimental approaches that may provide information bearing on the suggested mechanisms for regulation of papillary metabolism in relation to tubular work functions are indicated.

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