Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The specific binding of 3H-labeled prostaglandin (PG) F2alpha to bovine corpus luteum cell membranes was a rapid (K1=1.1 X 10(4) M(-1)S(-1) and reversible (K(-1)=3.3 X 10(-4) S(-1)) process at 22 degrees C. The specific binding was also a saturable process exhibiting two classes of receptors with apparent dissociation constants (Kds) of 1.6 X 10(-9) M and 2.4 X 10(-8) M. The heterogenous nature of [3H]PGF2alpha binding does not appear to be due to negative cooperatively but merely to represent the existence of two independent groups of receptor sites with discrete affinities. Free energy changes of +11.9 and +10.3 Kcal/mol were calculated from the Kds of high and low affinity receptors, respectively. The binding of [3H]PGF2alpha to the membranes was not accompanied by any detectable changes in receptor-bound or free [3H]PGF2alpha. Addition of increasing amounts of unlabeled PGF2alpha resulted in a dose-dependent inhibition of [3H]PGF2alpha binding to the membranes, with complete inhibition occurring at 10(-6) M. Other unlabeled PGs such as PGF1alpha, PGE2 (5-fold), PGE1 (120-fold), PGA1 and PGB1 (about 10,000-fold) were less effective when compared to unlabeled PGF2alpha in inhibiting [3H] PGF2alpha binding to the membranes. The metabolites of PGF2alpha, 15-keto-PGF2alpha and 13,14-dihydro-15-keto-PGF2alpha had 100-fold less affinity for PGF2alpha receptors. 15(S)15-Methyl-PGF2alpha, an analogue of PGF2alpha, had a fairly high affinity but lower than its parent molecule. Various unsaturated fatty acids, indomethacin and 7-oxa-13-prostynoic acid had 3,000- to 10,000-fold less affinities for PGF2alpha receptors. Incubation of membranes with various enzymes revealed that PGF2alpha receptor molecules are protein in nature which require membrane lipids and specific phospholipids for binding function. Among the various phospholipids used, sphingomyelin was found to be very effective in restoring the loss of [3H]PGF2alpha binding in phospholipase C-treated membranes. N-Ethylmaleimide, but not other SH group alkylating agents inhibited binding. The binding was also inhibited by tetranitromethane, dinitrofluorobenzene and acetic anhydride. This suggested that tyrosyl, histidyl, tryptophan and amino (any one or all of them) but not SH groups were involved in binding interaction.
Mol Cell Endocrinol 1976 Nov
PMID:Properties of prostaglandin F2alpha receptors in bovine corpus luteum cell membranes. 1 62

Selected properties of [3H]prostaglandin (PG) E1 binding to collagenase dispersed bovine luteal cells were studied and compared with those observed in luteal plasma membranes. [3H]-PGE1 specific binding to a relatively homogeneous population of luteal cells was a rapid (K1 = 4.2 X 10(5) M-1 .sec-1), reversible (K-1 = 3.9 X 10(-3) sec-1), saturable and specific process at 38 degrees C. The binding was homogeneous with an apparent dissociation constant of 2.4 nM and 1.8 X 10(5) receptors per cell. The presence of increasing amounts of unlabeled PGs inhibited [3H]PGE1 binding in a dose-dependent manner. The potency order for this inhibition of binding was: PGE 2 greater than PGE1, (15S)-15-methyl-PGE2 methyl ester greater than PGF2alpha greater than PGF1alpha greater than other PGs, PGE, PGF metabolites and PGF analogs. Other than the homogeneous nature of [3H]PGE1 binding and the greater effectiveness of PGE2 compared to PGE1 in cells, the rest of the properties of [3H]PGE1 binding to cells were in excellent agreement with those observed in plasma membranes.
Mol Cell Endocrinol 1978 Jan
PMID:Selected properties of [3H]prostaglandin E1 binding to dispersed bovine luteal cells. 20 3

1. Biosynthesis of PGE2 from [14C]arachidonic acid has been found to be lower and PGF2alpha higher in the renal medulla of spontaneously hypertensive (SH) rats than in normal Wistar (NW) rats. 2. Biosynthesis of prostacyclin (PGF1alpha) from [14C]arachidonic acid was decreased in lungs, aorta and heart of SH rats. 3. Metabolism of [3H]PGF1alpha was decreased in renal cortex and lungs and PGE2 increased in SH rats in comparison with NW rats. Thus the lungs of SH rats let more PGF and less PGE enter the systemic circulation. 4. Emotional stress decreased the metabolism of [3H]PGF1alpha in lungs of SH and NW rats, the effect being less in SH rats.
Clin Sci Mol Med Suppl 1978 Dec
PMID:The role of prostaglandins in the pathogenesis of hypertension. 36 32

Prostaglandins (PGA1, PGE2, PGF2 alpha) were found to increase cholesterol side-chain clevage activity in isolated bovine adrenal cortex mitochondria, provided calcium was present in the incubation medium. Optimal stimulation was observed at low PG concentrations (10-7 to 10-9 M), with malate or malate-NADPH supported side-chain cleavage. Under the same conditions, two endoperoxide analogs and several fatty acids were ineffective. The PG action was not observed with a mitochondrial acetone powder preparation. These observations suggest that primary PG may act by interfering with calcium distribution at the mitochondrial level, leading to the activation of cholesterol side-chain cleavage. Thus, an intracellular action of endogenous PG may be considered in the regulation of adrenal cortex steroidogenic functions.
Mol Cell Endocrinol 1977 Jun
PMID:Effect of prostaglandins on steroidogenesis by bovine adrenal cortex mitochondria. 40 12

The PGE2, PGF2 alpha and 6-keto-PGF1 alpha contents of the incubation medium of glomeruli isolated from rat kidney were measured at different times with or without addition of arachidonic acid. These prostaglandins accumulated progressively with time and reached equilibrium after 60--120 min incubation. Synthesis of the 3 prostaglandins was inhibited when indomethacin was added whereas it was markedly enhanced, mainly for PGE2, at increasing doses of arachidonic acid. Plateaus were reached above 5 micrograms/ml and concentrations corresponding to 50% of the maximum values were 2 micrograms/ml for PGE2 and PGF2 alpha, and 0.8 microgram/ml for 6-keto-PGF1 alpha. There were strictly linear relationships between PGE2 or PGF2 alpha productions and the concentration of glomerular protein. PGE2 and PGF2 alpha synthesis with or without arachidonic acid were maximum at 30--37 degrees C. PGE2 glomerular content was almost undetectable initially and increased with time. These data demonstrate that PGE2, PGF2 alpha and PGI2, in order of decreasing abundance, are synthesized by the glomerular cells and suggest that PGE2 and PGI2-sensitive glomerular adenylate cyclase activities and PGE2-sensitive renin synthesis may be stimulated by prostaglandins formed in the glomeruli themselves.
Mol Cell Endocrinol 1979 Oct
PMID:Prostaglandin synthesis by isolated rat renal glomeruli. 49 53

1. The daily urine excretion has been studied of prostaglandins (PG) E2 and F2alpha, as measured by radioimmunoassay, in eight children and seven adults with Bartter's syndrome. 2. Excretion of both PGE2 and PGF2alpha was significantly higher in the patients with Bartter's syndrome than in 17 normal children. 3. Twelve normal adults excreted significantly more PGE2 and PGF2alpha than did the normal children. In contrast, adults with Bartter's syndrome did not show an increase in prostaglandin excretion.
Clin Sci Mol Med 1978 Jan
PMID:Bartter's syndrome: contrasting patterns of prostaglandin excretion in children and adults. 62 Apr 89

1. Acute renal failure was induced in female Sprague-Dawley rats by the subcutaneous injection of glycerol. 2. Four groups of rats were studied; all animals received a glycerol challenge. Group A (control) were sham-operated only, group B received an infusion of sodium chloride solution (150 mmol/l; saline) for 24 h, group C received an infusion containing prostaglandin E2 (PGE2, 1.7 micronmol/l) in saline and group D a solution containing PGE2 (3.4 micronmol/l) in saline. 3. All rats were killed 48 h after glycerol challenge. The degree of renal impairment was assessed by serum creatinine concentration, which did not differ in sham-operated animals and the group receiving saline alone. The group of rats receiving the lower dose dose of PGE2 has a significantly lower mean serum creatinine concentration than the saline-infused control rats (P less than 0.0025). Creatinine concentration was further lowered by the higher dose of PGE2 but there was not a significant difference in the number of rats showing severe tubular necrosis histologically. 4. The study demonstrates that intravenous infusion of prostaglandin E2 has a protective influence on glycerol-induced renal failure in the rat; the protection afforded may be due to the vasodilator effect of PGE2 and/or an effect on glomerular permeability.
Clin Sci Mol Med 1978 Nov
PMID:Protective effect of prostaglandin [PGE2] and in glycerol-induced acute renal failure in rats. 72 5

1. Hypertension produced in two-kidney Goldblatt dogs was accompanied by a transient fluid retention, reaching a maximum 4 days after clamping. 2. Prostaglandin E and F concentrations in venous blood from the intact kidney also rose transiently, showing a maximum by the fifth day. 3. The rise in prostaglandin release from the intact kidney may be related to the fluid retention.
Clin Sci Mol Med 1978 May
PMID:Renal prostaglandins in renal hypertensive dogs. 75 Jan 58

1. The prostaglandin precursor arachidonic acid (C20:4) increases plasma renin activity in the rabbit and rat when it is infused into the renal arteries. 2. The increase in plasma renin activity after C20:4 in rats is not changed by volume expansion. 3. The inhibitor of prostaglandin synthesis indomethacin decreases plasma renin activity in the rabbit. 4. The increase plasma in renin activity after total renal ischaemia is abolished by pretreatment with indomethacin. 5. C20:4 increases dose- and time-dependent renin release from slices of rabbit kidney cortex. 6. Indomethacin or 5,8,11,14-eicosatetraynoic acid pretreatment in vivo, and addition to the incubation medium, reduces basal as well as C20:4-stimulated renin release in vitro. 7. The stimulating effect of C20:4 on renin release is assumed to be caused directly by formation of prostaglandin endoperoxides in the kidney cortex and not by prostaglandins since in vitro a natural prostaglandin endoperoxide (PGG2) and two stable synthetic prostaglandin endoperoxide analogues (EPA I and EPA II) do increase the release of renin, but PGE2 has no effect and PGF2alpha inhibits renin release.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Effects of stimulation and inhibition of the renal prostaglandin synthetase system on renin release in vivo and in vitro. 82 72

1. In the perfused rat mesenteric vascular bed, the effects of angiotensin II, cortisol and prostaglandin E2 on the vascular responses to noradrenaline or potassium chloride were studied. 2. Angiotensin II in subpressor concentrations potentiated the vasoconstrictor response to noradrenaline and potassium chloride. This effect of angiotensin II was inhibited in the presence of indomethacin and prostaglandin E2. 3. Cortisol in physiological concentrations inhibited the potentiating effect of angiotensin II. 4. Prostaglandin E2 enhanced the vasoconstrictor response to noradrenaline. This effect was not abolished by cortisol. 5. These results suggest that some actions of angiotensin II and cortisol in vivo are mediated by the regulation of prostaglandin synthesis or release.
Clin Sci Mol Med 1977 Sep
PMID:Potentiation of pressor effects of noradrenaline and potassium ions in the rat mesenteric arteries by physiological concentrations of angiotensin II: effects of prostaglandin E2 and cortisol. 91 46


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