Synthesis of prostaglandin E2 in different segments of isolated collecting tubules from adult and neonatal rabbits

1985 ◽  
Vol 248 (1) ◽  
pp. F134-F144 ◽  
Author(s):  
D. Schlondorff ◽  
J. A. Satriano ◽  
G. J. Schwartz
Keyword(s):  
Arachidonic Acid ◽  
Prostaglandin E2 ◽  
Feedback Loop ◽  
Pge2 Production ◽  
Large Variability ◽  
Pge2 Synthesis ◽  
Collecting Tubule ◽  
Concentrate Urine ◽  
Collecting Tubules

Prostaglandin E2 (PGE2) inhibits the action of the antidiuretic hormone (ADH) in isolated collecting tubules. A negative feedback loop has been postulated whereby ADH stimulates PGE2 synthesis. Furthermore, lysyl-bradykinin (LBK) inhibits the antidiuretic effect of ADH, probably via PGE2. Enhanced PGE2 synthesis has also been implicated as contributing to the inability to maximally concentrate urine during the neonatal period. We investigated PGE2 synthesis in microdissected cortical (CCT), medullary (MCT), and branched cortical (BCT) collecting tubules from adult and in corticomedullary collecting tubules (CT) from newborn rabbits. Isolated BCT produced significantly less PGE2 (12 +/- 2 pg X mm-1 X 20 min-1) than CCT (65 +/- 9) or MCT (76 +/- 8) from kidneys of adult rabbits. CT from newborn rabbits produced only 19 +/- 3 pg/mm, significantly less than either CCT or MCT from adults. A large variability in basal PGE2 production and hormonal response was observed from tubule to tubule. Under either basal conditions or in the presence of 2 microM arachidonic acid, LBK enhanced PGE2 synthesis in CCT and MCT from adults. ADH enhanced PGE2 production in MCT under basal conditions and in CCT in the presence of arachidonic acid. Neither LBK nor ADH stimulated PGE2 synthesis in neonatal CT. A23187 consistently stimulated PGE2 synthesis in CCT and MCT from adults and, to a lesser extent, in CT from newborn rabbits. Our results support the hypothesis that ADH and LBK enhance PGE2 synthesis in the collecting tubule. This response is, however, subject to large variations from tubule to tubule and depends on the in vitro incubation conditions.

Effects of atrial natriuretic peptide on renal medullary prostaglandin E2 production

1989 ◽  
Vol 257 (3) ◽  
pp. F336-F340
Author(s):  
R. J. Bolterman ◽  
M. D. Bentley ◽  
S. M. Sandberg ◽  
M. J. Fiksen-Olsen ◽  
J. C. Romero
Keyword(s):  
Arachidonic Acid ◽  
Atrial Natriuretic Peptide ◽  
Prostaglandin E2 ◽  
Natriuretic Peptide ◽  
Inhibitory Effect ◽  
Pge2 Production ◽  
In Vitro Effects ◽  
Different Doses ◽  
Atrial Natriuretic

Like arachidonic acid (AA) and bradykinin (BK), the intrarenal administration of atrial natriuretic peptide (ANP) has been shown to increase the urinary excretion of prostaglandin E2 (PGE2). In the present study, the direct in vitro effects of ANP on PGE2 production were compared with those of AA and BK. Canine renal inner medullary slices were preincubated for 30 min and washed in aerated Krebs-Ringer buffer (37 degrees C). During the final incubation period, with the use of varied concentrations of AA, BK, or ANP in Krebs-Ringer buffer, samples were obtained at 0 and 30 min to be used for radioimmunoassay of PGE2. Although the rate of PGE2 production was significantly increased 11-fold with AA and threefold with BK, it was unaffected by four different doses of ANP (10(-5) to 10(-11) M). Furthermore, the production of PGE2 during basal and stimulated (BK or AA) conditions was significantly blocked by indomethacin but not by ANP. These results indicate that ANP had no direct stimulatory or inhibitory effect on the medullary production of PGE2.

ADH-PGE2 interactions in cortical collecting tubule. II. inhibition of Ca and P reabsorption

1981 ◽  
Vol 241 (4) ◽  
pp. F461-F467 ◽  
Author(s):  
W. F. Holt ◽  
C. Lechene
Keyword(s):  
Prostaglandin E2 ◽  
Arginine Vasopressin ◽  
Inhibitory Action ◽  
Prolonged Incubation ◽  
Collecting Tubule ◽  
Calcium And Phosphorus ◽  
Collecting Tubules ◽  
Endogenous Synthesis ◽  
Cortical Collecting Tubule

In the absence of ADH, microperfused cortical collecting tubules of rabbits reabsorb calcium and phosphorus. Antidiuretic hormone (ADH) (200 microunits/ml Pitressin or synthetic arginine vasopressin) inhibits the reabsorption and may promote the secretion of calcium and phosphorus. At 5 min after incubation with ADH, there was a transitory increase in the potential difference and the reabsorption of sodium. The fluxes of calcium and phosphorus, however, showed no significant change from the control values. At 30-50 min after treatment with ADH, the reabsorption of calcium and phosphorus was inhibited and in some tubules calcium and phosphorus were secreted. The removal of vasopressin from the bath or the addition of 10(-5) M meclofenamate in vitro prevented ADH from inhibiting the reabsorption of calcium and phosphorus. Treatment of tubules with 10(-5) M prostaglandin E2 (PGE2) subsequent to incubation in a medium containing ADH and meclofenamate inhibited the reabsorption or even promoted the secretin of calcium and phosphorus, as did the prolonged incubation with ADH alone. We conclude that cortical collecting tubules reabsorb calcium and phosphorus in the absence of vasopressin and that ADH inhibits calcium and phosphorus reabsorption. Endogenous synthesis of PGE2 may mediate the inhibitory action of ADH, since meclofenamate (an inhibitor of the synthesis of prostaglandins) opposes and exogenous PGE2 mimics ADH.

PGE2, PGF2 alpha, 6-keto-PGF1 alpha, and TxB2 synthesis along the rabbit nephron

1987 ◽  
Vol 252 (1) ◽  
pp. F53-F59 ◽  
Author(s):  
N. Farman ◽  
P. Pradelles ◽  
J. P. Bonvalet
Keyword(s):  
Arachidonic Acid ◽  
Prostaglandin E2 ◽  
Proximal Tubule ◽  
Enzyme Immunoassay ◽  
Thick Ascending Limb ◽  
Pge2 Synthesis ◽  
Nephron Segments ◽  
Prostaglandin F2 Alpha ◽  
Collecting Tubule ◽  
Cortical Collecting Tubule

The capacity of synthesis of prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), 6-keto-PGF1 alpha, and thromboxane (TxB2) along the rabbit nephron was determined. A sensitive enzyme immunoassay was applied to isolated nephron segments, from the glomerulus to the terminal collecting tubule. The three prostaglandins and thromboxane (PG) were measured on the same samples after incubation in the presence of arachidonic acid. In the glomerulus, PGE2 synthesis (29.4 +/- 3.3 pg X glomerulus-1 X 30 min-1) represented 60% of the sum of the four PGs. PGF2 alpha and 6-keto-PGF1 alpha represented 22 and 17%, respectively, and TxB2 1.4%. The contribution of each PG to tubular synthesis was different, since at least 90% of PG synthesis consisted of PGE2. In the medullary collecting tubule (MCT), by far the major tubular site of PG synthesis, it was 809.6 +/- 140.8 pg X mm-1 X 30 min-1 for PGE2, 17.7 +/- 7.2 for PGF2 alpha, 8.3 +/- 1.9 for 6-keto-PGF1 alpha and 0.24 +/- 0.08 for TxB2. These relative proportions were roughly respected all along the tubule. Values were much lower in the convoluted and straight portions of the proximal tubule (proximal convoluted tubule: PGE2 8.2 +/- 2.0, PGF2 alpha 0.4 +/- 0.06, 6-keto-PGF1 alpha 0.26 +/- 0.04, TxB2 0.017) and the medullary and cortical thick ascending limb of the loop. They increased regularly along the distal structures of the tubule (light portion of the cortical collecting tubule (CCT1): PGE2 228.3 +/- 20.4, PGF2 alpha 4.34 +/- 0.6, 6-keto-PGF1 alpha 1.8 +/- 0.3, TxB2 0.22 +/- 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Involvement of prostaglandin E2, cAMP, and vasopressin in lithium-induced polyuria

1988 ◽  
Vol 254 (6) ◽  
pp. R863-R869 ◽  
Author(s):  
M. Sugawara ◽  
K. Hashimoto ◽  
Z. Ota
Keyword(s):  
Prostaglandin E2 ◽  
Rat Kidney ◽  
Urine Volume ◽  
Renal Medulla ◽  
Pge2 Production ◽  
Camp Production ◽  
Vasopressin Release ◽  
Pge2 Synthesis ◽  
Plasma Vasopressin

The involvement of prostaglandin E2 (PGE2), adenosine 3',5'-cyclic monophosphate (cAMP), and vasopressin in lithium-induced polyuria was investigated in rats. Administration of LiCl (4 mmol/kg body wt) for 7 days induced a marked polyuria with a significant excretion of urinary PGE2. Administration of indomethacin (IND, 5 mg/kg body wt) for 4 days to lithium-induced diabetes insipidus (LiDI) rats diminished urine volume by 80% and urinary PGE2 by 85%. The in vitro data of the intact rat kidney showed that lithium stimulated arginine vasopressin (AVP)-induced PGE2 production and suggested that PGE2 suppressed cAMP synthesis in rat renal medulla. The AVP-induced PGE2 synthesis was greater and the AVP-stimulated cAMP production lower in the LiDI rat kidney in vitro. Interference of the vasopressin-associated cAMP system and the increased PGE2 synthesis in the kidney may be involved in the development of LiDI. The reduced cAMP production in the LiDI rat kidney might be partly due to the increased PGE2 synthesis. In LiDI rats plasma vasopressin increased, whereas AVP concentration in the hypothalamus and the neurohypophysis significantly decreased. It is postulated that lithium stimulates vasopressin release from the central nervous system and that elevated plasma vasopressin potentiates PGE2 production in the kidney synergistically with lithium.

ADH-PGE2 interactions in cortical collecting tubule. I. Depression of sodium transport

1981 ◽  
Vol 241 (4) ◽  
pp. F452-F460 ◽  
Author(s):  
W. F. Holt ◽  
C. Lechene
Keyword(s):  
Prostaglandin E2 ◽  
Inhibitory Action ◽  
Inhibitory Effect ◽  
Bathing Medium ◽  
Ionic Fluxes ◽  
Collecting Tubule ◽  
Collecting Tubules ◽  
Net Fluxes ◽  
Cortical Collecting Tubule

Antidiuretic hormone (ADH) (200 microunits/ml Pitressin or synthetic arginine vasopressin) causes a transitory increase followed by a sustained decrease in the potential difference (PD) and in the net fluxes of sodium and chloride across rabbit cortical collecting tubules perfused in vitro. The inhibitory action of vasopressin is reversible; removal of the hormone from the bath promotes recovery in the PD and in the transport of sodium and chloride to the level of the controls. After 70 min of incubation with ADH, 10(-5) M meclofenamate, an inhibitor of the synthesis of prostaglandins, was added to the bath of some tubules. Despite the presence of ADH, the PD and ionic fluxes increased to control levels. The introduction of exogenous prostaglandin E2 (10(-5) M PGE2) to the bathing medium containing ADH and meclofenamate mimicked the inhibitory action of ADH, decreasing the PD and the reabsorption of sodium and chloride. Pretreatment of collecting tubules with meclofenamate prevented the inhibitory effect of ADH. These findings show that vasopressin exerts a prolonged inhibitory action on PD and on net reabsorption of Na and Cl and that this action may be exerted through stimulating the biosynthesis of prostaglandin E2 by the cortical collecting tubule.

Prostaglandin E2 and muscle proteolysis: effect of burn injury and cycloheximide

1986 ◽  
Vol 250 (2) ◽  
pp. R207-R210
Author(s):  
C. J. McKinley ◽  
J. Turinsky
Keyword(s):  
Protein Synthesis ◽  
Arachidonic Acid ◽  
Prostaglandin E2 ◽  
Burn Injury ◽  
Pge2 Production ◽  
Limb Muscle ◽  
Tissue Protein ◽  
Pge2 Release ◽  
Tissue Protein Synthesis

Rats were subjected to a single hindlimb scald, and 3 days later soleus muscles from the burned and contralateral unburned hindlimbs were studied in vitro. Burned limb muscle released 354% more prostaglandin E2 (PGE2) and 119% more tyrosine than the contralateral uninjured counterpart. Neither the rate of net proteolysis in the uninjured muscle nor the stimulated net proteolysis in the burned limb muscle could be reduced by 90% inhibition of PGE2 production with aspirin or indomethacin. Inhibition of tissue protein synthesis with 5 X 10(-5) M cycloheximide stimulated tyrosine release by soleus muscles of both hindlimbs, but the increment in the burned limb muscle was 167% greater than in the contralateral uninjured counterpart. Concomitantly, cycloheximide decreased PGE2 releases by injured and uninjured muscles 90 and 73%, respectively. This previously unrecognized action of cycloheximide was investigated in soleus muscles of normal uninjured rats. It was found that 1 X 10(-6) M cycloheximide produces a 70% inhibition of muscle PGE2 release and increasing the concentration of inhibitor up to 500-fold does not further decrease PGE2 production. Cycloheximide acts by reducing the availability of endogenous arachidonic acid for PGE2 synthesis.

Determination of prostaglandin E2 synthesis along rabbit nephron by enzyme immunoassay

1986 ◽  
Vol 251 (2) ◽  
pp. F238-F244 ◽  
Author(s):  
N. Farman ◽  
P. Pradelles ◽  
J. P. Bonvalet
Keyword(s):  
Arachidonic Acid ◽  
Prostaglandin E2 ◽  
Enzyme Immunoassay ◽  
Collecting Duct ◽  
Distal Tubule ◽  
Rabbit Kidney ◽  
Thick Ascending Limb ◽  
Pge2 Synthesis ◽  
Collecting Tubule ◽  
Cortical Collecting Tubule

Prostaglandin E2 (PGE2) content and synthesis have been measured in microdissected segments from the entire nephron of rabbit kidney. PGE2 was determined by an enzyme immunoassay on glomeruli or tubular segments (0.5-5 mm) either immediately after microdissection (PGE2 content) or after incubation for 15 min at 37 degrees C in the presence of arachidonic acid (PGE2 synthesis). We confirmed that collagenase used for microdissection did not modify PGE2 synthesis. A linear correlation was found between the length of tubule used in the assay and PGE2 synthesis, as well as between incubation time with arachidonic acid and PGE2 synthesis. PGE2 synthesis, expressed in picograms per millimeter tubular length per 15 min, was maximum in medullary collecting duct (517 +/- 73). High values were also found in the granular portion of distal tubule (134 +/- 22) and granular or light portion of cortical collecting tubule (199 +/- 24 and 146 +/- 10, respectively). Synthesis was lower in all other segments: 17 +/- 6 and 24 +/- 12, respectively, in convoluted and straight proximal tubule, 67 +/- 12 and 71 +/- 5, respectively, in thin descending and ascending limb, 51 +/- 9 and 23 +/- 4, respectively, in medullary and cortical thick ascending limb of Henle's loop, and 25 +/- 7 in initial distal tubule. Synthesis per glomerulus was 24 +/- 3. When the protein content of each nephron segment is taken into account, this profile was not modified, except for the thin limbs of the loop, which reached values per nanogram protein slightly higher than those of the cortical collecting tubule.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of ADH on Rat Renal Papilla, an Ultrastructural and Cytochemical Study

1973 ◽  
Vol 31 ◽  
pp. 410-411
Author(s):  
C. N. Sun ◽  
H. J. White ◽  
E. J. Towbin
Keyword(s):  
Electron Microscopy ◽  
Diabetes Insipidus ◽  
Renal Papilla ◽  
Milk Diet ◽  
Intercellular Spaces ◽  
Cytochemical Study ◽  
Collecting Tubule ◽  
Concentrate Urine ◽  
Staining Techniques ◽  
Collecting Tubules

Diabetes insipidus and compulsive water drinking are representative of two categories of antidiuretic hormone (ADH) lack. We studied a strain of rats with congenital diabetes insipidus homozygote (DI) and normal rats on an isocaloric fortified dilute milk diet. In both cases, the collecting tubules could not concentrate urine. Special staining techniques, Alcian Blue-PAS for light microscopy and lanthanum nitrate for electron microscopy were used to demonstrate the changes in interstitial mucopolysaccharides (MPS). The lanthanum staining was done according to the method of Khan and Overton.Electron microscopy shows cytoplasmic lesions, vacules, swelling and degenerating mitochondria and intercellular spaces (IS) in the collecting tubule cells in DI and rats on milk diet.

Collecting tubule adaptation to respiratory acidosis induced in vivo

1990 ◽  
Vol 258 (1) ◽  
pp. F15-F20 ◽  
Author(s):  
M. E. Laski ◽  
N. A. Kurtzman
Keyword(s):  
Respiratory Acidosis ◽  
In Vitro Study ◽  
Co2 Flux ◽  
Urine Ph ◽  
Collecting Tubule ◽  
Bicarbonate Solutions ◽  
Animal Exposure ◽  
Collecting Tubules

To examine the effects of respiratory acidosis in vivo on the adaptation of acidification in the collecting tubule, New Zealand White rabbits were exposed to a 6.7% CO2-93.3% O2 gas mixture in an environmental chamber for 0, 6, 24, or 48 h before obtaining collecting tubules for in vitro study. These collecting tubules were then perfused and bathed in vitro in identical Krebs-Ringer bicarbonate solutions. After 1 h equilibration total CO2 flux (JtCO2) was measured. The urine pH of the rabbits fell, whereas the blood bicarbonate rose as CO2 exposure time increased. In cortical collecting tubules, JtCO2 in vitro correlated with length of animal exposure to hypercarbia (y = 1.14174 + 0.1437x, r = 0.57, P = 0.002), and with the blood bicarbonate of the animal (y = 26.8471 + 0.0858x, r = 0.59, P less than 0.05). In vitro JtCO2 in medullary collecting tubules from rabbits that had been in hypercarbic atmosphere for 48 h (23.2 +/- 4.9 pmol.mm-1.min-1) did not differ from JtCO2 in control tubules (25.0 +/- 3.2 pmol.mm-1.min-1, not significant). Thus the cortical collecting tubule exhibits an adaptive increase in JtCO2 in response to hypercarbia, whereas the medullary collecting tubule does not.

Phospholipids, prostaglandin E2, and proteolysis in denervated muscle

1986 ◽  
Vol 251 (1) ◽  
pp. R165-R173 ◽  
Author(s):  
J. Turinsky
Keyword(s):  
Protein Synthesis ◽  
Prostaglandin E2 ◽  
Pge2 Production ◽  
Nerve Transection ◽  
Denervated Muscle ◽  
Sciatic Nerve Transection ◽  
Tissue Protein ◽  
Pge2 Release ◽  
Denervated Muscles

Soleus muscles of rats were studied up to 16 days after sciatic nerve transection. At the end of this period the denervated soleus muscles exhibited decreased content of diphosphatidylglycerol (-44%), normal level of phosphatidylethanolamine, and increased contents of phosphatidylcholine (+24%), sphingomyelin (+48%), lysophosphatidylcholine (+110%), phosphatidylinositol (+37%), and phosphatidylserine (+40%) per milligram of tissue protein. In studies in vitro, prostaglandin E2 (PGE2) release and tyrosine release by denervated soleus muscles were 319 and 141%, respectively, greater than those of sham muscles. An almost complete inhibition of PGE2 release with 5 X 10(-4) M aspirin or 2.8 X 10(-6) M indomethacin had no effect on tyrosine release of sham muscles or the stimulated tyrosine release of the denervated muscles. Addition of 5 X 10(-5) M cycloheximide in the medium resulted in 63% inhibition of PGE2 release by both groups of muscles; concomitant absolute increments in tyrosine releases by denervated and sham muscles did not statistically differ. In the presence of both 5 X 10(-5) M cycloheximide and 5 X 10(-4) M aspirin in the medium, PGE2 production by denervated and sham muscles was inhibited 87% while tyrosine release of denervated muscles was 108% higher than that of sham animals. It is concluded that 1) atrophy of denervated soleus muscle is associated with stimulated activity of tissue phospholipase A2, increased production of prostaglandin E2, increased total proteolytic rate, and unchanged rate of protein synthesis; 2) acute inhibition of PGE2 production does not inhibit the stimulated proteolysis in denervated muscle; and 3) cycloheximide inhibits PGE2 production by muscle.

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