Role of Renal Prostaglandin E2 in Chronic Renal Disease Hypertension

Nephron ◽  
1982 ◽  
Vol 32 (3) ◽  
pp. 202-206 ◽  
Author(s):  
L. Ruilope ◽  
Garcia Robles ◽  
C. Bernis ◽  
A. Barrientos ◽  
J. Alcazar ◽  
...  
Nephron ◽  
1975 ◽  
Vol 15 (1) ◽  
pp. 35-49 ◽  
Author(s):  
P. Weidmann ◽  
M.H. Maxwell ◽  
P. Rowe ◽  
R. Winer ◽  
S.G. Massry

1992 ◽  
Vol 2 (7) ◽  
pp. 1163-1170
Author(s):  
L G Fine ◽  
M R Hammerman ◽  
H E Abboud

The roles of growth factors in the pathogenesis of various forms of acute and chronic renal disease are largely putative. Nevertheless, there is a growing body of information that links specific growth factors to particular forms of renal injury. In all instances, it is supposed that such associations are not necessarily unique and that multiple cytokines probably interact to determine the pattern of injury or the regenerative response to such injury. Regeneration of tubular epithelium after acute tubular necrosis involves upregulation of the epidermal growth factor (EGF) receptor. Early studies of exogenously administered EGF indicate that the severity and duration of renal failure may be attenuated by this growth factor. Thus far, the observed responses have been limited and the role of EGF as a therapeutic agent requires more study. The mechanism of generation of tubulointerstitial injury in most forms of renal disease is difficult to understand. Early in vitro studies of growth factor production by tubular cells (in the absence of any infiltrating cells) indicate that platelet-derived growth factor produced by the medullary collecting duct is mitogenic for renal medullary fibroblasts, suggesting a paracrine growth system in this region of the kidney. Insulin-like growth factor I has also been shown to be produced by collecting duct cells. Its production is increased by EGF, and its association with certain forms of renal hypertrophy, i.e., diabetes and hypersomatotrophic states, implies its participation in the hypertrophic growth response. Platelet-derived growth factor is a potent mitogen for glomerular mesangial cells, and its production is regulated by a variety of cytokines.(ABSTRACT TRUNCATED AT 250 WORDS)


1981 ◽  
Vol 61 (s7) ◽  
pp. 327s-330s ◽  
Author(s):  
Keishi Abe ◽  
Yutaka Imai ◽  
Makito Sato ◽  
Toshiaki Haruyama ◽  
KO Sato ◽  
...  

1. The role of renal prostaglandin E (PGE) and kallikrein in the mechanism of the exaggerated fractional sodium excretion in hypertensive patients with advanced renal disease was investigated. 2. Urinary excretion of PGE and kallikrein was significantly decreased in patients with sustained hypertension. 3. Four times higher values for fractional sodium excretion and four or five times higher values for the urinary excretion of PGE corrected for creatinine clearance were found in patients with sustained hypertension. There was a significant positive correlation (r = 0.677) between the two, suggesting that PGE in the renal tubular compartment may be involved in the mechanism of the exaggerated fractional Na excretion in patients with advanced renal disease. 4. The urinary excretion rate of kallikrein corrected for creatinine clearance was three times greater in patients with borderline hypertension, but not significantly increased in those with sustained hypertension, compared with that in healthy volunteers.


1983 ◽  
Vol 24 (5) ◽  
pp. 579-587 ◽  
Author(s):  
Saulo Klahr ◽  
John Buerkert ◽  
Mabel L. Purkerson

Cytokine ◽  
2000 ◽  
Vol 12 (8) ◽  
pp. 1248-1252 ◽  
Author(s):  
Julio Martı́n ◽  
Patricia de Sequera ◽  
Juan Antonio Quiroga ◽  
Miguel Rico ◽  
Mario Fernández ◽  
...  

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