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

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 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

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

Using the Fell technique of organ culture of 8-day chick embryo femoral and tibial rudiments, the effects of indomethacin, dihomo-gamma-linolenic acid and arachidonic acid on limb rudiment linear growth and differentiation were investigated. Indomethacin (50 and 100 mumol/l) elicited a statistically significant decrease in rudiment linear growth without affecting differentiation or cell structure. Dihomo-gamma-linolenic acid and arachidonic acid, both at 100 mumol/l, exerted no effect on limb rudiment linear growth or differentiation. From previous work, it has been shown that PGA1 and PGB1 caused a marked inhibition of linear growth, PGA1 being cytotoxic. The failure of the prostaglandin (PG) precursors to reproduce these effects suggests that PGA or PGB biosynthesis in embryonic chondrocytes plays no significant role in cartilage growth regulatory mechanisms. Moreover, the growth inhibitory effect of the PG cyclooxygenase inhibitor, indomethacin, suggests that a product of arachidonic acid metabolism via the cyclooxygenase pathway may promote cartilage growth.
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PMID:Effects of prostanoid precursors and indomethacin on chick embryonic cartilage growth in organ culture. 640 86