Pulmonary Metabolism of Endogenous Prostaglandin E2 in Man

2015 ◽  
pp. 118-123
Author(s):  
H. J. Kramer ◽  
H. Mattern ◽  
A. B�cker ◽  
G. Fricke ◽  
R. D�sing
Keyword(s):  
Prostaglandin E2 ◽  
Endogenous Prostaglandin

Bronchoprotective role for endogenous prostaglandin E2

The Lancet ◽  
1995 ◽  
Vol 345 (8947) ◽  
pp. 436-438 ◽  
Author(s):  
I.D. Pavord ◽  
A.E. Tattersfield
Keyword(s):  
Prostaglandin E2 ◽  
Endogenous Prostaglandin

scholarly journals Misoprostol inhibits gastric mucosal release of endogenous prostaglandin E2 and thromboxane B2 in healthy volunteers.

Gut ◽  
1995 ◽  
Vol 36 (4) ◽  
pp. 511-515 ◽  
Author(s):  
A Mertz-Nielsen ◽  
O Eskerod ◽  
K Bukhave ◽  
J Rask-Madsen
Keyword(s):  
Prostaglandin E2 ◽  
Healthy Volunteers ◽  
Thromboxane B2 ◽  
Endogenous Prostaglandin

Tubular prostaglandin E2 production and its role in urinary hypotonicity after release of ureteral occlusion in the rat

1987 ◽  
Vol 73 (4) ◽  
pp. 395-399 ◽  
Author(s):  
Shozo Torikai
Keyword(s):  
Prostaglandin E2 ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Pge2 Production ◽  
Endogenous Prostaglandin ◽  
Collecting Ducts ◽  
Ureteral Occlusion

1. In order to explore the involvement of endogenous prostaglandin E2 (PGE2) in the urine concentration defect after ureteral occlusion, PGE2 production by isolated collecting ducts in vitro and effects of indomethacin on urine osmolality in vivo were examined. 2. Twenty-four hours ureter obstruction caused increased PGE2 production by the medullary collecting ducts, which was maintained at a high level on the day after release of obstruction (0.8 ± 0.2 pg/mm normal, 8.1 ± 0.9 pg/mm 24 h obstruction, and 6.6 ± 1.0 pg/mm post-obstruction, mean ± sem). An enhanced PGE2 production was also observed for papillary collecting duct on the day after release of 24 h ureteral occlusion (3.9 ± 0.5 pg/mm normal and 7.7 ± 1.2 pg/mm post-obstruction). 3. Administration of indomethacin to the unilateral post-obstructive rats slightly raised the urine osmolality of the post-obstructed kidney (from 339 ± 17 to 390 ± 22 mosmol/kg H2O), while it had a greater effect on the contralateral intact kidney (from 1569 ± 138 to 2567 ± 198 mosmol/kg H2O). 4. Our data may indicate that the urine concentration defect after 24 h ureteral occlusion is ascribable mainly to a mechanism other than increased endogenous PGE2.

Regulation of 25-Hydroxy-Vitamin D-1α-Hydroxylase in Chick Isolated Renal Tubules: Effects of Prostaglandin E2, Frusemide and Acetylsalicylic Acid

1981 ◽  
Vol 61 (1) ◽  
pp. 53-59 ◽  
Author(s):  
J. D. Wark ◽  
R. G. Larkins ◽  
J. A. Eisman ◽  
K. R. Wilson
Keyword(s):  
Vitamin D ◽  
Prostaglandin E2 ◽  
Acetylsalicylic Acid ◽  
Vitamin D3 ◽  
Incubation Medium ◽  
Prostaglandin E ◽  
Renal Tubules ◽  
Endogenous Prostaglandin ◽  
25 Hydroxy Vitamin D ◽  
1,25 Dihydroxy Vitamin D3

1. Isolated renal tubules were prepared from vitamin D-deficient chicks. The effects of added prostaglandin E2 (PGE2) and agents which modify prostaglandin metabolism on the metabolism of 25-hydroxy-vitamin D3 were studied. 2. Frusemide (0.1 mmol/l) raised the prostaglandin E (PGE) content of the tubule incubation medium; it significantly increased 1,25-dihydroxy-vitamin D3 [1,25-(OH)2D3] production from 25-hydroxy-vitamin D3 [25-(OH)D3] and significantly inhibited the net production of 24,25-dihydroxy-vitamin D3 [24,25-(OH)2D3]. 3. Acetylsalicylic acid (aspirin; 0.1 mmol/l) decreased the PGE content of the tubule incubation medium and significantly inhibited 1,25-(OH)2D3 production. 4. In the presence of 1,25-(OH)2D3, 4 h exposure of tubules from vitamin D-deficient chicks to concentrations of PGE2 between 2.8 × 10−6 and 2.8 × 10−8 mol/l significantly enhanced 1,25-(OH)2D3 production. 5. It is concluded that, in view of the effects of modulation of endogenous prostaglandin levels by frusemide in aspirin, and the stimulatory effect of exogenous PGE2, prostaglandins should be considered potential regulators of the renal 25-hydroxy-vitamin D-1α-hydroxylase [25-(OH)D-1α-hydroxylase] enzyme.

Vascular Actions of Frusemide and Bumetanide on the Rat Superior Mesenteric Vascular Bed: Interactions with Prostaglandins

1976 ◽  
Vol 51 (s3) ◽  
pp. 257s-258s
Author(s):  
D. F. Horrobin ◽  
M. S. Manku ◽  
J. P. Mtabaji
Keyword(s):  
Prostaglandin E2 ◽  
Inhibitory Effect ◽  
Prostaglandin Synthesis ◽  
Inhibitory Effects ◽  
Perfusion Fluid ◽  
Endogenous Prostaglandin ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed

1. The addition of frusemide or bumetanide to perfusion fluid inhibited the response of the isolated mesenteric vascular bed to noradrenaline. 2. Addition of prostaglandin E2 to the perfusion fluid completely restored the response to noradrenaline. 3. Inhibition of prostaglandin secretion by indomethacin with restoration of responses to noradrenaline by the addition of exogenous prostaglandin E2 prevented the inhibitory effect of frusemide or bumetanide on responses to noradrenaline. 4. The inhibitory effects of diuretics on responsiveness to noradrenaline is mediated by blockade of endogenous prostaglandin synthesis.

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