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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma prostaglandins were determined by radioimmunoassay in 92 pregnant and 14 nonpregnant women. There was significant elevation of PGA-like material in the first trimester of pregnancy (1744 pg/ml) over that seen in nonpregnant women (576 pg/ml) with continuation of that elevation in the second and third trimesters. No significant difference existed among PGE levels of the nonpregnant group (251 pg/ml) and the first two trimesters of pregnancy (384 pg/ml and 294 pg/ml); the PGE level of the third trimester group (443 pg/ml) was significantly elevated over that of the nonpregnant group. PGF levels remained constant during all trimesters (135 pg/ml, 144 pg/ml, and 130 pg/ml) but exhibited plasma concentrations significantly higher than the nonpregnant group (78 pg/ml). Potential role (s) of prostaglandins as mediators of cardiovascular and renal changes of pregnancy are discussed.
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PMID:Plasma prostaglandins in pregnancy. 61 37

In addition to its well known prohypertensive role in various states of experimental and human hypertension, the kidney has also been shown to exert an antihypertensive "endocrine" function. According to this hypothesis, certain forms of experimental and human hypertension might not solely be the result of an excess in the activity of such renal pressor systems as the renin-angiotensin system and the sympathetic nervous system, but might also result from an absolute or relative deficiency of intra-renal vasodilator antihypertensive factors which might allow pressor systems to act unopposed to produce peripheral arteriolar vasoconstriction and sustained hypertension. At least four factors have been characterized in the kidney of various animal species and man which might be responsible for such an antihypertensive function. These are (1) the renomedullary prostaglandins (PGs), (2) the renomedullary antihypertensive neutral lipid, (3) antirenin phospholipid and (4) the renal kinins. This review is restricted to an examination of the possibility that the vasodepressor renomedullary prostaglandins (PGA and/or PGE) may, at least in part, mediate the so-called antihypertensive function of the kidney and participate in the regulation of renal blood flow and natriuresis by physiologic antagonism of various renal vasoconstrictor stimuli such as the renal renin-angiotensin and the sympathetic nervous systems.
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PMID:Renal prostaglandins and the regulation of blood pressure and sodium and water homeostasis. 79 89

Experimental data now strongly suggest that the PGs, by nature of their natural local occurrence and destruction, powerful effects on, and release from lung tissue are important in regulating both pulmonary homeostasis and dysfunction. Laboratory studies on their activity, potency, duration, preferred route of administration, mechanism and possible antiallergic effects, have been largely substantiated in humans. Structure activity studies on a large number of congeners of PGE, PGF, and PGA emphasize the critical importance of stereochemistry and various substituent groups on biologic activity in the lung.
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PMID:Actions of prostaglandins on the respiratory tract of animals. 82 48

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

Plasma prostaglandins were studied by radioimmunoassay on alternate days during the menstrual cycle in fourteen normal women. No cyclic patterns were found for A-like prostaglandins using an assay which measured 13,14-dihydro-PGA. Mean subject values of PGA-like prostaglandin ranged from 367 to 904 pg/ml and varied significantly among women. Prostaglandin E determinations showed an upward trend beginning 8 days before the LH peak. PGE subject means varied significantly and ranged from 182 to 362 pg/ml. Prostaglandin F did not exhibit a cyclic pattern. The average concentration of PGF for individual women ranged from 58 to 153 pg/ml, showing significant variance. The physiologic implications of the results are discussed as well as recommendations for the design of future studies.
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PMID:Plasma prostaglandins in the normal menstrual cycle. 92 52

Venous prostaglandins A, E, and F were determined by radioimmunoassay in 10 dogs before and one hour after administration of sodium pentobarbital (35 mg/Kg, iv). In the conscious state, PGA was 0.34 + 0.04 ng/ml (mean +/- SE), PGE 0.20 + 0.01 ng/ml, and PGF 0.25 + 0.03 ng/ml. During pentobarbital anesthesia, these levels were unchanged (p greater than 0.05). Thus, pentobarbital anesthesia had no effect on peripheral venous prostaglandin levels.
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PMID:Pentobarbital anesthesia: lack of effect on venous prostaglandins in dogs. 94 22

The relative stability of Prostaglandins (PGs) E1, E2 and F1alpha in cultures of BALB/c 3T3 and SV3T3 cells has been evaluated using 3 different approaches. First, total recovery of tritium in the ethyl acetate phase following incubation and extraction of PGF1alpha and PGE1 demonstrated greater stability for PGF1alpha (88.8%) than PGE1 (65.9%). Second, analysis of incubated, extracted, tritiated PGs by thin layer chromatography revealed decreases of up to 23% in the PGE zone following incubation of 3H-PGE1. With increasing time of incubation, decreases in the PGE zone were accompanied by increase in PGA-like compounds. 3H-PGF1alpha demonstrated greater stability, having greater than 90% recovery of the tritium in the PGF zone. A third approach to the assessment of PG stability in culture was the comparison of the production of individual PGs by radioimmunoassay (RIA). The data obtained by RIA indicated a lag in the increase of PGA and PGB, until an initial rise in PGE was noted, suggesting that PGA and PGB may be secondary products arising from PGE which exhibits only partial stability in culture. By employing two RIAs, one for total PGE and one for PGA and PGB, the composite determination PG [E + (A + B)] can be used to provide a more meaningful determination of PG production because of the instability of the PGs. On the other hand, individual determinations are helpful in assessing the stability of PGEs in cell cultures.
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PMID:The simultaneous use of two prostaglandin radioimmunoassays employing two antisera of differing specificity. II. Relative stability of prostaglandins E1, E2 and F1alpha in cell cultures of BALB/c 3T3 and SV3T3 mouse fibroblasts. 98 8

In experiments in which blood was cross-circulating in rats, the blood pressure of the recipient dropped while that of the donor rose, following the increase of the circulating blood volume, produced by infusion either of saline or blood. The phenomenon was almost imperceptible when binephrectomized animals were used. In experiments in which the blood-bathed organ technique was used, prostaglandin-like substances were detected, released during the rise of the blood pressure, produced by the same stimulus (the expansion), in anaesthetized rats. A significant difference was found between the prostaglandin-like substances detected using the blood-bathed organ technique, in normal rats (5.387 ng per ml of blood plus or minus 0.288 = SEM) and those detected in binephrectomized rats (3.202 ng per ml of blood plus or minus 0.330, p smaller than 0.025). The biologically active substances detected in 25 ml of blood collected during expansion, while the assay organs showed a prostaglandin-like activity, were found to have the chromatographic behaviour and the bioassay properties of PGA, PGE and PGF series. A great quantity of the biologically active substances, having the chromatographic behaviour and the bioassay properties of PGA, PGS and PGF was detected in the rat renal medulla. Sufficient quantities of the released prostaglandin-like substances could escape the pulmonary vascular bed in this species of animal. It was concluded that a great quantity of the released prostaglandin-like substances came from the kidney and their release by this particular mechanism suggested that they play an important homeostatic role on the blood pressure, blood volume, and sodium and water balance regulation.
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PMID:[Origin, nature, role and fate of prostaglandins liberated during the expansion of intravascular space in the anesthetized rat]. 109 32

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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