Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandins PGE-1 or PGA-1 (0.5 to 1 mug per min) were infused into the stenosed renal artery of anesthetized hypertensive dogs. Increased urine volume, sodium and potassium excretion, and p-aminohippurate clearance were found during the prostaglandin infusion period in the infused kidney as compared to the control periods before infusion. Creatinine clearance was increased during infusion of PGE-1. The noninfused, nonischemic kidney showed no effect at the time of infusion with PGE-1 but in the case of PGA-1, the p-aminohippurate and creatinine clearances and urine diuresis were decreased. As a result, the mean aortic blood pressure decreased. Both prostaglandins increased the renal vein renin in the infused kidney. PGA-1 did affect renin release of the noninfused kidney, but PGE-1, which is rapidly inactivated by the lung, did not have this effect. Renin release seems to be influenced by electrolyte diuresis operating through the macula densa mechanism. However, the lowering of blood pressure seen in this study cannot exclude the involvement of the stretch receptors (the juxtaglomerular cells) for renin release. The increased renin release after prostaglandin administration seems to be a protective renal mechanism against the drug-induced hypotension. It seems to be induced by the direct sodium and water diuretic effects of prostaglandins.
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PMID:Direct effect of prostaglandins in renal function and renin release in the presence of renal ischemia in the dog. 111 61

The role of prostaglandins in blood pressure regulation was studied in normal rats and in animals with renal artery constriction. The effects of chronic inhibition of prostaglandin (PG) synthesis on arterial pressure were observed, and renal medullary PG synthesis was measured in vitro. The prostaglandin synthetase inhibitor indomethacin was given in a dose of 2 mg/kg/day by mouth to one of two groups of male Wistar rats with a unilateral renal artery constriction and the other kidney untouched, and to one of two sham-clipped groups. Systolic blood pressures were higher in indomethacin-treated clipped rats than in non-indomethacin-treated clipped animals, and at 18 days averaged 188 mm Hg (plus or minus SEM 5.9, n = 36) and 162 mm Hg (plus or minus SEM 7.6, n = 34), respectively (P less than 0.005 for data pooled from two experiments). Indomethacin did not affect pressures of sham-clipped animals treated for 40 days. Analysis of PG synthesis by gas-liquid chromatography in renal medullary slices incubated for 30 minutes in Krebs-Henseleit buffer showed: (1) 40% suppression of PGE synthesis in hypertensive animals (P less than 0.001): (2) no differences between clipped and untouched kidneys; (3) chronic indomethacin treatment did not affect PGE synthesis in the in vitro buffer system; and (4) no PGA synthesis was detected. In a further experiment in which medullary slices were incubated in plasma of rats treated with equivalent doses of indomethacin, PGE synthesis was suppressed by 35%. The experiments support the concept that prostaglandins modulate pressor mechanisms which come into play when renal blood flow is drastically reduced. The effects could be mediated by PG synthesis in the kidney and/or in other systemic vascular beds.
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PMID:Renal prostaglandin synthesis in the Goldblatt hypertensive rat. 113 85

Immunoreactive (IR) plasma prostaglandin (PG) levels were measured in samples collected simultaneously through catheters placed in the right ventricle and the thoracic aorta in fasting anesthetized dogs. There were significantly greater levels of IRPGB (P less than .01) and IRPGA (P less than .05), but significantly less IRPGE (P less than .01) in the aorta than in the ventricle. During femoral vein infusion of PGE1, PGB1, and PGA1, respectively, PGE1 was approximately 87% metabolized, but PGB1 and PGA1 were not degraded by the lung. There was no measurable increase in IRPGB or IRPGA levels in the thoracic aorta during intravenous PGE1 infusion. It was concluded that in the resting state PGE is actively degraded by the lung; that the lung very effectively degrades PGE1 but does not degrade PGB1 or PGA1 during infusion of these prostaglandins; and that pulmonary metabolism of PGE1 probably does not result in formation and release of PGB or PGA into the arterial circulation. Additionally, the possibility exists that in the resting state PGB and/or PGA are actively secreted by the lung, but the immunoassay methodology used does not permit resolution of this point.
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PMID:Differential in vivo pulmonary degradation of prostaglandins E1, B1, and A1. 114 29

A specific, sensitive and accurate radioimmunoassay (RIA) method for the measurement of prostaglandin A1 (PGA1) in either human whole blood or plasma is described. Whole blood is immediately lysed with distilled water containing tritiated indicator. When plasma is assayed, the blood samples are handled at 4 C and rapidly centrifuged. The lysate or plasma is adjusted to pH 5 with buffer and quickly extracted with 5% methanol in dichloromethane. The whole blood or plasma extract is then purified by Sephadex LH20 chromatography using the system methanol: methylene chloride (5:95) which separates the major groups of PGA, PGE and PGF. The RIA is then performed using an antiserum generated in rabbits from PGA1 coupled to bovine thyroglobulin. The antibody is highly specific, possessing very low cross reactivity to other prostaglandins (PGA2, PGE, PGB and PGF). Activated florisil or ammonium sulfate can be used to separate bound from free prostaglandin. This whole blood or plasma method yields blank values of only 2 +/- 2 pg per sample with a between assay precision determined by duplicate analysis of 8% and interassay precision of 3%. The mean whole blood PGA1 concentration in 27 subjects in 2.5 +/- 1.6 (SD) ng per 100 ml. No significant sex difference in PGA1 levels was noted and values were similar whether measured in whole blood or cooled plasma rapidly prepared and extracted. These values of PGA1 are much lower than those RIA values reported by others for "PGA" using antibodies with lower specificities.
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PMID:A radioimmunoassay for prostaglandin A1 in human peripheral blood. 115 43

A charcoal adsorption method was developed to measure specific prostaglandin binding in low speed supernates of hamster myometrial homogenates. This method was used to characterize and quantitate PGE-1-specific binding. The equilibrium binding constants and the concentration of specific PGE-1 binding sites were determined during the hamster estrous cycle. The apparent association constant for 12 different preparations was 1.16 plus or minus 0.08 times 10-9M-1. The concentration of PGE-1 specific binding sites was significantly higher on days 2 and 3 of the estrous cycle that it was on days 1 or 4. The competition for PGE-1 binding sites by PGE-2, PGF-2alpha, tpga-1 and various PGE-1 metabolites and derivatives was measured in hamster myometrial homogenates. Relative affinities of the natural prostaglandins for the PGE-1 binding sites, calculated by parallel line assay, were: PGE-2 greater than PGE-1 greater than PGA-1 greater than PGF-2alpha. For PGE-1 metabolites the relative affinities were: PGE-1 greater than 13,14-dihydro-PGE-1 greater than 13,14-dihydro-15-keto-PGE-1 greater than 15-keto-PGE-1. For the analogs and derivatives the compounds tested ranked as: 16,16-dimethyl-PGE-1 greater than PGE-1 methyl ester greater than 17-phenyl-18,19,20-trinor-PGE-1 greater than 15(S) 15-methyl-PGE-1 methyl ester. Arachidonic acid, bis-homo-gamma-linolenic acid and 7-oxa-13 prostynoic acid had relative affinities greater than 0.1 compared to PGE-1 equal 100. Indomethacin had a relative affinity of 0.4 compared to PGE-1.
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PMID:Prostaglandin specific binding in hamster myometrial low speed supernatant. 116

Levels of PGE in renal venous blood were found to be significantly elevated at the time RBF was increased by furosemide. Following indomethacin, a second dose of furosemide failed to increase RBF and levels of PGE in renal venous blood were not elevated. Levels of PGF and PGA were not affected by furosemide. The increase of PGE in renal venous blood at the time of renal dilation supports the hypothesis that furosemide increases RBF by releasing PGE. An intrarenal action of the released PGE is implied by this mechanism.
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PMID:Furosemide induced release of prostaglandin E to increase renal blood flow. 118 79

1. Renal venous prostaglandin concentrations (PGA, PGE and PGF) were determined, together with renal plasma flow, urinary output and blood pressure changes, before and after infusion of sodium chloride solution (saline) in four normotensive and three hypertensive subjects. 2. No changes in blood pressure and in glomerular filtration rate were observed. 3. Saline infusion induced a significant increase in renal venous PGA and PGE, and also in total and non-cortical renal plasma flow and urinary output. There was an insignificant increase in renal venous PGF. 4. These findings show that prostaglandin release after saline infusion is associated with changes in renal blood flow and suggest that the natriuretic and diuretic effect of saline could be the result of prostaglandin release.
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PMID:The release of renal prostaglandins during saline infusion in normal and hypertensive subjects. 119 3

The effects of intrarenal infusion of prostaglandins (PGs) of the E, A and F series on renal vascular resistance and on vasoconstrictor responses to renal nerve stimulation (RNS), norepinephrine (NE) and angiotensin (A) were determined in the in situ feline kidney under conditions of controlled blood flow. Infusion of PGE2 (3 and 0.3 mug/min) and PGE1 (3 mug/min) resulted in a marked decrease in renal perfusion pressure and a reduction in responses to all vasoconstrictor stimuli. PGE2 (0.03 mug/min) did not alter perfusion pressure. However, responses to RNS and A but not to NE were attenuated. PGA2 (3 and 0.3 mug/min) had no significant effect on perfusion pressure. PGA1 (3 mug/min) resulted in a transient decrease in renal vascular resistance which was not maintained during the infusion period. PGA2 (3 mug/min) reduced the response to RNS at 10 and 30 cps and reduced the response to A, whereas responses to NE were not affected. PGA2 (0.3 mug/min) had no effect on responses to either of the pressor stimuli. PGA1 infusion resulted in an enhanced response to RNS at the highest stimulus frequency and decreased the response elicited by A. PGF2alpha (3 mug/min) had no significant effect on renal vascular resistance or on responses to NE and nerve stimulation. However, the response to angiotensin was decreased and responses to RNS at 10 and 30 cps were decreased 30 minutes after the PGF2alpha infusion. The present data demonstrate that, of the natural renal PGs, PGE2 and PGA2 possess the capacity to modulate the effects of the sympathetic nervous system on the feline kidney. In addition, the effects of PGE and PGA on responses to adrenergic stimuli and on vascular resistance could be separated.
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PMID:Influence of prostaglandins E, A and F on vasoconstrictor responses to norepinephrine, renal nerve stimulation and angiotensin in the feline kidney. 124 15

The measurement of 13,14-dihydro-15-keto prostaglandin E2 [PGEM] is complicated by the artefactual formation of compounds of the corresponding A series which are reactive towards protein. Existing methods of assay depend on the deliberate dehydration to the 'A' form followed by cyclization in alkaline solution to a bicyclic derivative which is stable and can be measured by radioimmunoassay. We report an alternative approach using methyl oximation of the 9- and 15-keto groups which confer stability on the molecule. This derivatization is simple and does not involve an active intermediate such as those of the PGA series. The antiserum for radioimmunoassay is raised against the methyl oxime form. The label is the methyl oxime of PGEM coupled to a tripeptide Pro-gly-tyr through the nitrogen in the proline ring. This is a linkage distinct from that used to raise the antiserum and thus is not preferentially recognized over the endogenous analyte; this results in a high sensitivity assay. The results correlated well with those from the bicyclic assay when both assays were used to measure the same samples of peripheral blood from women receiving a sustained release PGE pessary for ripening the cervix. The technique provides a rapid and reliable method for determining prostaglandin E metabolites.
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PMID:The measurement of the main PGE metabolite, 13,14-dihydro-15-keto prostaglandin E by radioimmunoassay using methyl oxime stabilization. 158 44

A luteotropic role for prostaglandins (PGs) during the luteal phase of the menstrual cycle of rhesus monkeys was suggested by the observation that intraluteal infusion of a PG synthesis inhibitor caused premature luteolysis. This study was designed to identify PGs that promote luteal function in primates. First, the effects of various PGs on progesterone (P) production by macaque luteal cells were examined in vitro. Collagenase-dispersed luteal cells from midluteal phase of the menstrual cycle (Day 6-7 after the estimated surge of LH, n = 3) were incubated with 0-5,000 ng/ml PGE2, PGD, 6 beta PGI1 (a stable analogue of PGI2), PGA2, or PGF2 alpha alone or with hCG (100 ng/ml). PGE2, PGD2, and 6 beta PGI1 alone stimulated (p less than 0.05) P production to a similar extent (2- to 3-fold over basal) as hCG alone, whereas PGA2 and PGF2 alpha alone had no effect on P production. Stimulation (p less than 0.05) of P synthesis by PGE2, PGD2, and 6 beta PGI1 in combination with hCG was similar to that of hCG alone. Whereas PGA2 inhibited gonadotropin-induced P production (p less than 0.05), that in the presence of PGF2 alpha plus hCG tended (p = 0.05) to remain elevated. Second, the effects of various PGs on P production during chronic infusion into the CL were studied in vivo. Saline with or without 0.1% BSA (n = 12), PGE2 (300 ng/h; n = 4), PGD2 (300 ng/h; n = 4), 6 beta PGI1 (500 ng/h; n = 3), PGA2 (300 ng/h; n = 4), or PGF2 alpha (10 ng/h; n = 8) was infused via osmotic minipump beginning at midluteal phase (Days 5-8 after the estimated LH surge) until menses. In addition, the same dose of PGE, PGD, PGI, or PGA was infused in combination with PGF2 alpha (n = 3-4/group) for 7 days. P levels over 5 days preceding treatment were not different among groups. In 5 of 8 monkeys receiving PGF2 alpha alone, P declined to less than 0.5 ng/ml within 72 h after initiation of infusion and was lower (p less than 0.05) than controls. The length of the luteal phase in PGF2 alpha-infused monkeys was shortened (12.3 +/- 0.9 days; mean +/- SEM, n = 8; p less than 0.05) compared to controls (15.8 +/- 0.5). Intraluteal infusion of PGE, PGD, PGI, or PGA alone did not affect patterns of circulating P or luteal phase length.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intraluteal infusions of prostaglandins of the E, D, I, and A series prevent PGF2 alpha-induced, but not spontaneous, luteal regression in rhesus monkeys. 227 32


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