Metabolic alterations in the endogenous formation of 6 keto-prostaglandin F1.ALPHA., thromboxane B2 and prostaglandin E2 in the brain-stem of stroke-resistant spontaneously hypertensive rats.

Abstract

SummaryEndogenous biosynthetic capacities for prostaglandin (PG)E2, thromboxane (TX)B2 (a stable degradation product of TXA2) and 6 keto-PGF1a (a stable degradation product of PGI2) in the brain stem fractions of stroke-resistant spontaneously hypertensive rats (SHRSR) and control Wistar-Kyoto rats (WKR) were determined with novel methods and presented in an original report. In comparison with WKR, it is characteristically found that TXB2 synthesis is increased in excess of threefold in the pons-medulla oblongata of SHRSR, while being decreased by 75% in the hypothalamic region of SHRSR (0.01<p<0.05).On the other hand, the biosynthesis of PGE2 is adaptively elevated in both hypothalamus and pons-medulla oblongata regions of each animal, although the PGI2/PGE2 ratio was lowered in both these regions of SHRSR. Keywords prostaglandins, thromboxane, brain-stem, stroke-resistant spontaneously hypertensive rats, gas chromatography-mass spectrometry Horton (1) has implied that the natural prostanoids are involved in at least two mechanisms which possibly contribute to the normal control of arterial blood pressure: 1) The first mechanism (neurotransmitter control) stands on the fact that if PGE2 is administered during nerve stimulation, responses to the nerve stimulation diminish and the amount of noradrenaline released is reduced (2). 2) The second mechanism (vasodilator control) relates to the fact that the vasodilator prostaglandins (PGE, PGA and PGI) will lower systemic arterial pressure (3). Here we propose the data which support both mechanisms mentioned above, by analyzing the metabolic alterations of the endogenous PG and TX biosyntheses in the brain-stem regions between SHRSR, established by Okamoto et al. (4), and

Endogenous formation of prostanoids and the levels of long‐chain fatty acyl CoA derivatives in suspensive and adhesive cells from in vitro embryoid bodies of teratoma OTT 6050

“…This might be reflected on a relatively smaller amount of PGEz formation in differentiated adhesive cells. It was already confirmed that a neuroblastoma clone N 18, whose differentiated revertants formed more PGEz than TXB2, made conspicuous neurite extensions when 0.2-0.5 mM of N6, Oz'-dibutyryl 3', 5'-monophosphate or 20-50 pg/ml of PGE2 coexisted with 2 x lo3 -2 x lo4 cells from day 4 to day 6 (during the logarithmic phase) [14].…”

“…This might be reflected on a relatively smaller amount of PGEz formation in differentiated adhesive cells. It was already confirmed that a neuroblastoma clone N 18, whose differentiated revertants formed more PGEz than TXB2, made conspicuous neurite extensions when 0.2-0.5 mM of N6, Oz'-dibutyryl 3', 5'-monophosphate or 20-50 pg/ml of PGE2 coexisted with 2 x lo3 -2 x lo4 cells from day 4 to day 6 (during the logarithmic phase) [14]. tion from multipotential cells in our cultures, but attachment per se is not necessarily the critical condition, as Mintz's group [ l l ] already pointed out, since the effect may be mediated by a deposit of some other cellular product(s) such as glycoprotein or collagen [21].…”

Central nervous system effects of arachidonic acid, PGE2, PGF2α, PGD2 and PGI2 on gastric secretion in the rat

“…An endogenous l O formation of the order PGD2 > PGF2, > PGE2 is found when rat hypothalamic or median eminence tissue in incubated in vitro (Wolfe, 1982). Furthermore, thromboxane B2 (TxB2) and 6-keto-PGF1, is formed in the hypothalamus indicating synthesis of PGI2 and the presence of the thromboxane pathway in this brain region (Ohtsu & Matsuzawa, 1980). Taken together, these reports indicate that PGD2, PGF,A, PGE2 and PGI2 are formed in the brain areas which are implicated in the physiological regulation of gastric secretion, viz.…”