Studies on Extraction, Separation and Estimation of Prostaglandins by Radioimmunoassay

Inagawa, Toshiwo; Ohki, Shiro; Sawada, Masafumi; Hirata, Fumio

doi:10.1248/yakushi1947.92.10_1187

Cited by 51 publications

(9 citation statements)

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“…containing 1 X 10-4 M sodium meclofenac (Parke-Davis) to prevent new formation of prostaglandins. After homogenization, each sample was processed for extraction and chromatography of pro staglandins, as described (8,9).…”

Section: Methodsmentioning

confidence: 99%

Pathogenic Mechanisms Involved in Mepirizole-lnduced Duodenal Damage in the Rat

Tanaka¹,

Ueki²,

Ohno³

et al. 1986

Japanese Journal of Pharmacology

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Abstract-Mepirizole(60 and 200 mg/kg) administered s.c. induced damage in the surface epithelial cells of the rat proximal duodenum as early as 2 hr after the treatment. 16,16-Dimethyl prostaglandin E2 (dmPGE2, 30 /cg/kg) administered s.c. significantly protected the duodenal mucosa against mepirizole-induced damage for up to 6 hr. Gastric acid secretion in acute fistula preparations was significantly reduced 1 hr after administration of mepirizole (60 and 200 mg/kg). The secretion reverted to the control level 2 hr later. In the 60 mg/kg-treated group, however, there was a significant increase in the acid output for up to 6 hr. Duodenal HC03 secretion stimulated with 10 mM HCI was significantly inhibited with mepirizole (60 and 200 mg/kg). Mepirizole (60 and 200 mg/kg) significantly increased the amount of acid in the duodenum for 2 to 6 hr after the treatment. dmPGE2 (30 irg/kg) significantly inhibited gastric acid secretion, stimulated duodenal HC03 secretion, and reduced the increased amount of acid in the duodenum in response to mepirizole. Endogenous prostaglandin E2 and 6-keto prostaglandin Fia in the duodenal mucosa were significantly reduced by mepirizole (200 mg/kg) 1 to 2 hr later. Mepirizole-induced duodenal damage appears to be caused by the increased amount of acid in the duodenum.

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Section: Methodsmentioning

confidence: 99%

Pathogenic Mechanisms Involved in Mepirizole-lnduced Duodenal Damage in the Rat

Tanaka¹,

Ueki²,

Ohno³

et al. 1986

Japanese Journal of Pharmacology

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“…After 30 min, 0.1 ml of the media were taken for measurement of 6-keto-PGF1a. The concentration of 6-keto-PGF1a, the stable hydrolysis product of prostacyclin, was measured by radioimmunoassay according to Inagawa's method (13), with the specific antibody to 6-keto-PGF1a. The cross reaction rates with the 6-keto-PGF1a antiserum were almost zero for thromboxane B2, 9.1% for PGE2, and 5.0% for PGF2a.…”

Section: Flow Methodsmentioning

confidence: 99%

Interaction between Flow-Induced Prostacyclin Production and Nitric Oxide Synthesis in Vascular Smooth Muscle Cells.

et al. 1994

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The interaction between flow-induced prostacyclin production and nitric oxide (NO) synthesis in vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) was studied. Flow was made by 3 cm-amplitude horizontal shaking at various frequencies at 37 °C under 5% CO 2 and 95% air. Basal prostacyclin and NO production rates did not differ between strains. Prostacyclm production during flow was significantly greater with increasing shear stress from shaking frequencies of 120/min to 180/min, and was greater in SHR than in WKY. In contrast, flow-induced NO production was greater in WKY than in SHR. The addition of N nitro-L-arginine further increased the flow-induced increase in the production of prostacyclin in WKY in a dose-dependent manner, but had no effects in SHR. Indomethacin did not affect flow-induced NO production in either strain. We conclude that increases in prostacyclin production in SHR-derived VSMC during shear stress may be due to decreases in the suppression by NO and may compensate for hypertension.(Hypertens Res 1994;17: 227-232) Key Words: spontaneously hypertensive rat, shear stress, prostacyclin, nitric oxide, vascular smooth muscle cell Prostacyclin, a potent vasodilator and the most potent endogenous inhibitor of platelet aggregation known, is synthesized from arachidonic acid (AA) in many types of cells. In vascular endothelial cells, mechanical forces associated with blood flow, such as shear stress and pressure-stretch, are known to stimulate prostacyclin production(1), and play an important role in the regulation of vascular tone (2), vascular remodeling (3), and the focal development of atherosclerotic lesions (4) . Shear stress also stimulates the production of nitric oxide (NO) via a shear-sensitive K current (5,6) in endothelial cells. Although previous studies of the effect of shear stress on prostacyclin or NO production were focused on vascular endothelial cells, vascular smooth muscle cells (VSMC) are also exposed to shear stress, such as blood flow when intima is exfoliated, and interstitial fluid flow during skeletal muscle contraction or relaxation. Moreover, previous evidence (7,8) has shown that shear stress caused by blood flow displaces the inner layers of the artery wall in the direction of flow as well as the endothelium, and that ion transport is more sensitive to shear in VSMC than in several other types of cells, including endothelial cells.Previous studies have shown that in VSMC shear stress opens nitrendipine-sensitive calcium channels (8), stimulates cell growth (9), and induces endocytosis of large amounts of extracellular sodium and cholesterol (9). Recent evidence (10) has shown that shear stress reduces the 24-hour incorporation of tritiated thymidine and cell proliferation. However, none of those studies addressed the effects of shear stress on production of prostacyclin and NO in VSMC. Because recent evidence (11) has shown that these compounds are also synthesized in VSMC and regulate the proliferation rates and ...

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“…The reaction was stopped by 10-5 M of indomethacin and cooled in ice. PGE2 and 6-keto-PGE2a in the medium were ex tracted by the method of Inagawa et al (13) and measured by radioimmunoassay (RIA). c) Histamine assay: The suspension of rat PMC (2-5x105 mast cells) was incubated at 37'C for 5 min before adding 300 fig/ml of DMP-Ascaris and then incubated for 20 min.…”

Section: Methodsmentioning

confidence: 99%