Disease relevance of PGF 1-alpha

• The present work studies the urinary excretion of PGE2 and PGI2 (6-keto PGF 1 alpha) in 11 insulin-dependent diabetic patients with chronic renal failure with a glomerular filtration rate of 33.9 +/- 9.03 ml/min who had hyporeninaemic hypoaldosteronism to evaluate the influence of these prostaglandins on the appearance of this latter process [1].
• The prostaglandins, PGE-1, PGE-2, PGF-1 alpha, PGF-2 alpha, 19-OH-PGE-(1 + 2), 19-OH-PGF-alpha were estimated by RIA in the semen of (a) normal men of proven fertility (total semen or split ejaculate); (b) men 1 year after vasectomy; and (c) men with agenesia of the vas deferens and seminal vesicles [2].
• Furthermore, size and number of liver metastases per animal were determined and concentration of PGF1alpha, PGE2 and leukotrienes was measured in hepatic and pancreatic tissue [3].
• Verapamil, administered before pancreatitis induction, prevented initial increases in 6-keto prostaglandin F1alpha (PGF1alpha) and thromboxane B2 (TXB2) but had no effect on PGF2alpha or PGE2 or on lipoperoxidative damage [4].
• A study was carried out on the effect of aspirin 175 mg/day on the plasma levels of 6 keto PGF 1 alpha and TXB2 in patients with acute myocardial infarction and in patients subjected to coronary artery bypass surgery [5].

High impact information on PGF 1-alpha

• Further studies showed that PGF1alpha, PGF2alpha, PGA1, and thromboxane B2 were high-affinity inhibitors (and therefore presumably substrates) of MRP4 [6].
• Glucagon, prostaglandin E1 (PGE1) and E2 (PG2), and epinephrine at concentrations of 10(-5)M also increased activity, whereas, no increased activity was seen with the additions of somatotrophin (10 mug/ml), PGF1alpha, PGF2alpha, or T3 at 10(-5)M [7].
• 2. Fever occurred when prostaglandin E1, E2, F1alpha or F2alpha (PGE1, PGE2, PGF1alpha, PGF2alpha) was injected into the cerebral ventricles in doses of 200 ng and 2 mug [8].
• PGF2alpha accelerated lysosomal enzyme release, had no effect on phagocytosis at high concentrations and inhibited both processes at low concentrations.. PGF1alpha was inactive [9].
• These data indicate that PGF1alpha and PGF2alpha increase pulmonary vascular resistance by constricting lobar veins and vessels upstream to small veins, presumed to be small arteries [10].

Biological context of PGF 1-alpha

• The increase in lobar arterial pressure in response to PGF1alpha and PGF2alpha was associated with a significant increase in lobar venous pressure but no change in left atrial pressure [10].
• In conclusion, in poorly controlled diabetes, there was no differential lack of aspirin sensitivity to platelet aggregation, or lack of aspirin suppression of urinary TxB2 or PGF1alpha, compared with controls on aspirin [11].

Anatomical context of PGF 1-alpha

• The changes with time in intrauterine tissue production and concentrations of PGE-2, PGF-2 alpha, 6-keto PGF-1 alpha and PGFM (13,14-dihydro-15-keto PGF-2 alpha) in maternal and fetal plasma and amniotic fluid were investigated during the first 72 h of pulsatile administration of ACTH1-24 to chronically catheterized fetal sheep [12].
• It is concluded that exogenous progesterone administered on dioestrus II inhibits granulosa PGE and 6-keto PGF-1 alpha accumulation in preovulatory follicles, probably by reducing serum LH concentrations, and that the granulosa cells, which are LH-dependent, are a major source of follicular PGE [13].
• 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 [14].
• PGF1alpha treatment increased the tonus of the smooth muscle cells in the wall of the tubules as indicated by a reduction in the diameter of the tubules [15].
• Significantly less PGF-1 alpha, PGF-2 alpha and 12-hydroxyheptadecatrienoic acid (HHT) were found in the capillaries of MFO treated animals, in comparison to the SFO group [16].

Associations of PGF 1-alpha with other chemical compounds

• Determination of thromboxane B2, (TXB2), leukotriene B4, (LTB4) and 6-keto prostaglandin F1 alpha, (PGF1a), revealed a decrease in their concentrations during ischaemia and a transient, marked increase on reperfusion [17].
• Renal malondialdehyde, 6 keto PGF 1 alpha, and TxB2 tissue levels were studied after reperfusion [18].
• A comparison of radioimmunoassay (R.I.A.) for 6-keto PGF 1 alpha, PGE2 and TXB2 using 125I-histamine ligands and tritiated tracers showed a 7 to 10 fold increase in sensitivity for the 125I derivative, with a resultant reduction in antisera requirements by 80% [19].

Analytical, diagnostic and therapeutic context of PGF 1-alpha

• The release of PGF1alpha and PGF2alpha from superfused blood platelets was studied by the combined use of two radioimmunoassay systems with different specificities [20].
• In the group of patients subjected to coronary bypass surgery but after treatment with aspirin 175 mg/day for a period of five days both 6 keto PGF 1 alpha and TXB2 levels fell significantly [5].
• Small rises in IOP and the concentrations of aqueous PGF1 alpha, TBB2, and protein were observed after Nd:YAG laser iridectomies [21].

References