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)

We examined the hypothesis that the vascular abnormalities of Bartter's syndrome are due to excess production of prostaglandin. Balance studies and vascular reactivity studies were performed before and after indomethacin (200 mg/day) in a patient with well-documented Bartter's syndrome. During indomethacin, potassium balance became positive, serum potassium rose from 2.1--3 mEq/1 in the absence of potassium supplementation, plasma renin activity decreased from 55--3.2 ng/day and peripheral plasma PGA-like activity fell from 1460 +/- 220 to 456 +/- 71 pg/ml. Before indomethacin, forearm vasoconstrictor responses to brachial arterial infusions of angiotensin II, norepinephrine and to neurogenic reflex stimulation elicited by lower body suction were greatly depressed compared to those of normal subjects. During indomethacin these responses were restored to normal. The dose of intravenous angiotensin II required to increase diastolic blood pressure 20 mm Hg decreased from 160--30 ng/kg/min. These data support the hypothesis that the vascular insensitivity to exogenous angiotensin II, norepinephrine and to neurogenic reflex stimulation observed in this patient with Bartter's syndrome is due to excess prostaglandin. Moreover, stimulation of the renin-angiotensin-aldosterone system in this syndrome appears to be a compensatory adaptation to excess prostaglandin production.
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PMID:Effects of indomethacin on the vascular abnormalities of Bartter's syndrome. 67 46

Prostaglandins E(1) and E(2) significantly stimulated the synthesis of aldosterone, corticosterone, and to a lesser degree, cortisol in the outer slices of beef adrenal tissue. PGA, PGF(1a), and PGF(2a) were ineffective.PGE(1) was found to stimulate steroidogenesis in a manner similar to that of adrenocorticotropin (ACTH) in (a) needing calcium, (b) being inhibited by puromycin but not actinomycin D, (c) increasing the levels of cyclic AMP, and (d) not having an additive effect to exogenous cyclic AMP. PGE(1) did not produce an additive effect with either submaximal or maximal amounts of ACTH but did have an additive effect with angiotensin. These results are in keeping with the hypothesis that PGE(1) shares a receptor site on the plasma membrane with ACTH.
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PMID:Adrenocortical steroidogenesis: the effects of prostaglandins. 434 27

Cortisol, insulin, somatotropin, thyreotropin, thyroxine, triiodothyronine, testosterone, aldosterone, c-AMP, c-GMP, prostaglandins (PGF1-x, PGF2-x, PGA + E), and renin concentrations in serum or plasma of the venous blood of the third international crew of the scientific orbital complex of "Soyuz 29 - Salyut 6 - Soyuz 31" were determined following the 7-day space flight. The increased activity of the renin-angiotensin-aldosterone system before the flight as well as variations in the pressor/depressor prostaglandin ratios indicate an increased strain during the pre-flight period. During the first stage of the post-flight period some parameters were changed due to the landing process and the returning to earth gravity. The associated physical load and the onset of reactions for enhancement of the orthostatic tolerance resulted in an increase of cyclic nucleotid and thyroxine concentrations. The relatively higher levels of the pressor PGs of group F in comparison with the prostaglandins A + E could be evaluated as a compensatory reaction for enhancement of the orthostatic tolerance. The cortisol and STH concentrations increased with growing motor activity. The variations seen after the 7-day space flight were essentially within the reference areas. It may be assumed that the readaptation was not yet totally accomplished by the 8th day after landing.
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PMID:[Results of endocrinolgic studies of the 3rd international crew of the scientific orbital station complex; Soyuz 29 - Salyut 6 - Soyuz 31 (joint space flight enterprise of the USSR - GDR). 2. Hormones and biologically active substances in blood]. 675

Urinary immunoreactive PGA and PGE, plasma and urinary aldosterone, and plasma renin activity (PRA) were determined in eleven control subjects and four patients with diabetic hyporeninaemic hypoaldosteronism (HH) before and during 4 days of sodium chloride restriction and frusemide administration. Aldosterone and PRA increased steadily in control subjects, but not in patients with HH. Increases in urinary PGA and PGE were observed during volume depletion. The basal levels and increases observed were comparable in both groups. The apparently normal stimulation of PGA and PGE in subjects with diabetic HH suggests that this syndrome is not associated with abnormal prostaglandin metabolism, despite the fact that drug-induced abnormalities of the latter may precipitate or aggravate the clinical syndrome in susceptible individuals. The increase in PGA and PGE following frusemide treatment and salt depletion supports the possibility of a relationship between renal prostaglandin metabolism, frusemide-induced natriuresis and/or renin secretion. While the nature of this relationship remains obscure, the increases in PGA and PGE in the absence of increases in renin-angiotensin levels in subjects with HH suggests that these changes are not due to activation of the renin-angiotensin system.
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PMID:Urinary prostaglandins following frusemide treatment and salt depletion in normal subjects and subjects with diabetic hyporeninaemic hypoaldosteronism. 701 40