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)

Testicular interstitial cells were utilized to study the effects of prostaglandins (PG) on in vitro testosterone production and to examine the role of cyclic adenosine-3',5'-monophosphate (cAMP) in this process. Testosterone production was assessed after 3 hour incubations while cAMP accumulation was examined after a 0.5 hour incubation period. Testosterone and cAMP were measured by radioimmunoassay. None of the PGs tested (PGA, PGA2, PGB1, PGE1, PGE2, PGF1alpha PGF2alpha) altered basal testosterone production when present in incubates at concentrations of 1.3 X 10(-8) M to 1.3 X 10(-4). However, at concentrations of 1.3 X 10(-4) M all of these PGs were capable of decreasing Luteinizing Hormone (LH; 100ng)-induced testosterone production. The inhibition of LH-induced testosterone production by the B, E and F series PGs was less pronounced than that for the A series. PGA1 and PGA2 exhibited 80% and 95% inhibition, respectively, at 1.3 X 10(4) M. The inhibitory action of 4 X 10(5) M PGA1 or PGA2 was evident within 30 minutes. Preincubation of interstitial cells with indomethacin (10(-5) or 10(-6) M) for 30 minutes did not alter subsequent basal or LH (100ng)-induced testosterone production. Accumulation of cAMP was stimulated by LH (10 microgram) or by PGs (1.3 X 10(-4) M PGA1, PGA2, PGB1, PGE1 or PGF2alpha). The PG-induced cAMP accumulation thus occurred at concentrations where LH-stimulated testosterone production was inhibited. Furthermore, PGA1 and PGA2 (1.3 X 10(-4) M) inhibited testosterone production induced by either 3-isobutyl-1-methyl xanthine (MIX; 10(-4) M or 10(-3) M) or dibutyryl cAMP (dbcAMP; 10(-4) M or 10(-3) M). These results indicate that PGs can block testosterone production by a direct effect on testicular interstitial cells and suggest that PGs exert their inhibitory action distal to stimulation of cAMP formation. PGs do not appear to play a role in the mechanism of LH action.
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PMID:Prostaglandin inhibition of testosterone production induced by luteinizing hormone, dibutyryl cyclic AMP or 3-isobutyl-1-methyl xanthine in dispersed rat testicular interstitial cells. 8 81

Prostaglandins (PG) A1, B1, E2, F2 alpha and plasma renin activity (PRA) were measured by radioimmunoassay in 8 patients with unilateral artery stenosis, 7 hypertensive patients with unilateral renal atrophy without stenosis ans 20 controls. The measurement of the PG and PRA in the hypertensive group was performed in the infra-renal inferior vena cava and in the two renal veins. PRA and PGA1 were significantly raised in the renovascular hypertensive patients but no significant change was observed in the group with unilateral renal atrophy. On the other hand, the PGE2 and PGF2 alpha were raised in both groups, especially in the renal veins on the stenosed or atrophic side. There was a positive significant correlation between PRA and PGA1 and PGB, but none with PGE2 or PGF2 alpha. This study suggests that the increase in PGA1 and PGE2 represents a secondary hypertensive mechanism which is diuretic and natiuretic. The increase of PGF2 alpha represents a direct mechanism of hypertension. Simultaneous measurement of the vasopressor (PRA and PGF2 alpha) and vasodepressor (PGA and PGE) systems may give a better diagnostic and prognostic approach to renovascular hypertension.
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PMID:[Prostaglandins in renovascular arterial hypertension]. 11 9

Prostaglandins A1, B1, E2, Falpha and PRA have been measured by radioimmunoassay in peripheral or renal venous blood of different groups of hypertensive and control subjects. PGA1 and PGE2 were significantly increased in renal, renovascular, labile and essential hypertension. PGFalpha was significantly increased only in patients with unilateral renal atrophy and in some patients with renovascular and essential hypertension. There was a significant positive correlation between PRA and PGA1 or B1, but not with PGE2 or Falpha. The increase of PGA and PGE represents a secondary antihypertensive, diuretic and natriuretic mechanism, the increase of PGF a direct hypertensive mechanism.
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PMID:Prostaglandins and high blood pressure. 35 39

These studies were directed toward determining effects of selected vasoactive compounds on oxygenated erythrocytes. Considering the major circulatory effects that small changes in blood flow might initiate in sickle cell anemia patients, erythrocytes from individuals with this disease and from one person with the trait condition were included. PGA1, PGE1, and PGE2 significantly increase filtration times in normal erythrocytes (AA-type hemoglobin) at 10(-11) M by this method. From studies of the effects of L-epinephrine, D,L-isoproterenol, PGA1, PGA2, PGE1, PGE2, PGF1alpha and PGF2alpha on red blood cell filterabilities, the following observations and conclusions appear to hold: (1) Erythrocytes from different individuals (or from the same individual at different times) vary greatly in responses to these compounds. Effects of vasoactive compounds upon red cell filterability may be positive, negligible or negative. Decreased filterability (positive effect) was seen more frequently than increased. (2) Effects are observed with all compounds on some erythrocyte preparation at every concentration tested (10(-5), 10(-7), 10(-9), 10(-11) M). (3) Where epinephrine showed significant positive effect, PGA2 and PGE2 did also when tested. The reverse was not always true. (4) For PGA and PGE analogs, the subscript 2 analogs affected filterability more frequently. (5) When significant average effects for a group of donors were produced by a given compound at a particular concentration, these effects were positive for the donors studied.
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PMID:Examination of the filterability of oxygenated erythrocytes (containing normal, trait or sickle cell disease type hemoglobins) in the presence of L-epinephrine, D,L-isoproterenol or prostaglandins (PG) A1, A2, E1, E2, F1alpha or F2alpha. 84 33

It is recognized that the lung extracts norepinephrine and 5-hydroxytryptamine from the pulmonary circulation and that this process is affected by cardiopulmonary bypass. Since alterations in the lung's processing of vasoactive substances may be a mechanism of pulmonary injury sustained during operation, we investigated the lung's ability to extract or metabolize prostaglandin A1 (ga1) and prostaglandin E1 (PGE 1). Sixteen patients undergoing cardiac surgery were studied. In five patients, just before going on bypass, a 10 ml of blood was withdrawn at a constant rate, simultaneously from the pulmonary artery and left atrium. In 11 patients, 3H-PGE1 was injected just prior to bypass and, in five of these, again after coming off bypass. Extraction was calculated from tritium activity in the samples. Metabolites were quantitated by thin-layer chromatography after being identified by marker compounds run simultaneously in each chromatogram. The pulmonary extraction of PGA1 was 11.3 +/- 2.3% and there were no detectable metabolites in left atrial blood. Before bypass the extraction of PGE1 was 42.3 +/- 14.3% and after bypass 24.8 +/- 10.0% (P less than 0.005; Student's paired t test). PGE1 was extensively metabolized with 79.7 +/- 7.1% of total radioactivity appearing in the left atrium as metabolites before bypass and 89.1 +/- 2.0% appearing after bypass. This study indicates that PGA(1) is not metabolized by the lung and is only slightly extracted. On the other hand, PGE(1) is extensively extracted and metabolized. While the rate of metabolism is not significantly affected by cardiopulmonary bypass, the extractiom before bypass was significantly greater than after bypass.
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PMID:Fate of prostaglandins E(1) and A(1) in the human pulmonary circulation. 87 Oct 15

We have investigated the uptake and subsequent metabolism of the prostaglandins (PGs) PGE1, PGA1, and PGB1 by rat, guinea pig and rabbit isolated perfused lungs (IPL). Significant species differences were not observed in the uptake or metabolism of any PG on passage through the IPL. However, differences in the uptake of PGA1 and PGB1 and in the metabolism of PGA1 were observed with a given species when the composition of the perfusion medium was varied. The IPL removed minimal amounts (less than 20% of the supply rate) of PGA1, and PGB1 from the circulation when the perfusate contained 4.5% bovine serum albumin (BSA). In the absence of BSA, however, both PGA1 and PGB1 were substantially removed from circulation (approximately 53% of the supply rate) and PGA1 was also metabolized. The composition of the perfusate had no effect on the uptake and metabolism of PGE1 which was always taken up and metabolized to a greater extent than was PGA1 and PGB1. Thus, the apparent species differences previously reported for the pulmonary biotransformation of PGA can result from differences in the perfusion medium used. Our data suggest that both plasma protein binding and a transport system play important roles in determining the selectively of the uptake of PGs by the lung.
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PMID:Uptake and metabolism of prostaglandins by isolated perfused lung: species comparisons and the role of plasma protein binding. 89 17

The binding of tritiated prostaglandins (PGA1, PGE1, PGF2alpha, and PGE2) to human and bovine serum albumins was studied by equilibrium dialysis and batchwise gel equilibration with Sephadex G-25. During equilibrium dialysis (36 hours, 4 degrees C), about half of the PGEs, but not PGA and PGF2alpha, were transformed into dehydration products; by contrast, equilibration of the prostaglandins was attained in less than a half-hour by the batchwise use of Sephadex G-25 at 25 degrees C, with no detectable ligand instability. The values of the apparent association constants for albumin-prostaglandin interactions were inversely related to the protein concentration in the assay systems. "True" apparent association constants (NKo) were measured by extrapolation to zero protein concentration. The NKo values were estimated to be 9.4 X 10(4), 2.7 X 10(4), 9 X 10(3) and 6 X 10(3) M-1 for the interaction of human serum albumin with PGA1, PGE1, PGF2alpha and PGE2, respectively. Very similar values were found for the corresponding bovine serum albumin-Prostaglandin interactions. When comparable, the data obtained by both methods were in excellent agreement. Our results were also in agreement with published values for PGA1 and PGF2alpha, both of which are relatively stable in neutral aqueous phase. Batchwise gel equilibration appears to be a useful method, if thermodynamically valid data are desired in the presence of possible ligand and/or "receptor" instability. We conclude that albumin binding probably affords circulating PGA1 a modest protection from its clearance mechanisms.
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PMID:Prostaglandin-macromolecule interactions. I. Noncovalent binding of prostaglandins A1, E1, F2alpha, and E2 by human and bovine serum albumins. 94 73

The effects of PGA1, PGA2 and PGB1 on the vasculature of the liver and small intestine were studied in 73 dogs. Infusions were made into a branch of the superior mesenteric artery, the hepatic artery, portal vein or femoral vein. They decreased systemic arterial pressure and dilated the hepatic arterial and prehepatic splanchnic (small intestinal) vascular beds, PGA being most active. Dilator response was not decreased by beta-adrenergic blockade. Compounds appear to be inactivated by liver and decreased systemic pressure less when infused directly into liver circulation. Dilator response was transient, particulary in small intestine, and abated or even converted to constriction when infusion was continued for a period of time. Intrahepatic portal venous vasculature appeared to be constricted by PGA.
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PMID:Splanchnic vascular responses to the infusion of prostaglandins A1, A2 and B1. 95 18

A highly sensitive radioimmunoassay for the measurement of plasma prostaglandins A and B, expressed in equivalents of PGA1, is described. This method was used for the measurement of prostaglandins A and B (PGA/B) in 23 healthy volunteers and 25 hypertensive patients. The PGA/B concentration in peripheral venous plasma of 23 healthy normotensive subjects is 115 +/- 15 pg/ml. The repeated measurement of the same plasma samples kept frozen for 60 days at -20 degrees C shows mean 194% increase of PGA/B concentration. The major site of synthesis of PGA/B seems to be the kidney. However in two patients PGA/B concentration in arterial blood was greater than in venous blood suggesting the possibility of cardio-pulmonary synthesis. The major site of inactivation is the hepatic circulation, as PGA/B concentration in hepatal venous blood is by 30% lower than in vena caval blood. The arterial concentration is 3% lower than venous PGA/B demonstrating very low pulmonary inactivation. Therefore the prostaglandins of the A and B series may represent a "circulating hormone". The plasmatic PGA/B is significantly increased in reno-vascular and essential hypertension.
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PMID:Radioimmunoassay of prostaglandins A and B in human blood. 96 52

The renal prostaglandins PGS2 and PGE2 possess potent antihypertensive and vasodepressor activity. The mechanism of blood pressure lowering effect is through peripheral arteriolar dilation with a fall in total peripheral resistance. PGA unlike PGE escape degradation by the lung and thus could circulate as antihypertensive hormones. Since plasma PGA levels rise in humans on a low sodium intake, it has been postulated that the beneficial effects of a low sodium diet in some hypertensives may be the result of an increase in peripheral vasodilating PGA. Support that plasma PGA may be a regulator of systemic blood pressure is also derived from the fact a PGA-secreting renal tumor was associated with a fall in blood pressure and a rise in plasma PGA in a previously hypertensive woman. The removal of the tumor resulted in a return of blood pressure to elevated levels and a concomitant fall in PGA. Recently, a number of human patients with essential hypertension have been infused with PGA1 and PGA2. It was observed that there was an initial increase in renal blood flow, sodium and water excretion which was associated with no change in the elevated blood pressure. When blood pressure ultimately fell, there was a return of renal blood flow, sodium and water excretion to preinfusion levels. It would appear that PGA compounds act as 'ideal' antihypertensive agents since they favorably effect renal resistance, sodium and water homeostasis, plasma volume, total peripheral resistance, blood pressure and indirectly cardiac output through baroreceptor stimulation, all factors known to be important in etiology in human hypertension.
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PMID:Renal prostaglandins. 110 Oct 92


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