scholarly journals INVOLVEMENT OF RAF-1/MEK/ERK1/2 SIGNALING PATHWAY IN ZINC-INDUCED INJURY IN RAT RENAL CORTICAL SLICES

2006 ◽  
Vol 31 (3) ◽  
pp. 207-217 ◽  
Author(s):  
Yuka KOHDA ◽  
Yoshiko MATSUNAGA ◽  
Ryugo SHIOTA ◽  
Tomohiko SATOH ◽  
Yuko KISHI ◽  
...  
1976 ◽  
Vol 231 (1) ◽  
pp. 14-19 ◽  
Author(s):  
M Barac-Nieto

Rat renal cortical slices were incubated with [1-(14)C]palmitate bound to 2.5% albumin. The following effects were found: a)1 mM palmitate utilization or oxidation to CO(2) varied according to the concentration of lactate in the media, it increased at 0.8 and 3.2 mM, was unchanged at 8 mM, and decreased at 16 mM. Esterification was stimulated at 3.2 mM lactate. b) Addition of glutamine (0.1 mM) instead of lactate stimulated incomplete and complete oxidation of palmitate (1 mM), whereas high medium glutamine (10 mM) inhibited palmitate (1 mM) utilization, esterification, and oxidation to CO(2) but increased its incomplete oxidation. The low rate of exogenous palmitate oxidation observed in this study and the finding that exogenous palmitate oxidation is only partially inhibited at very high concentrations of exogenous lactate or glutamine are consistent with the view that these exogenous substrates contribute little to the oxidative metabolism of rat renal cortex in vitro, which probably depends on the supply of substrates endogenous to the tissue.


1990 ◽  
Vol 258 (5) ◽  
pp. F1363-F1371
Author(s):  
W. H. Beierwaltes

Studies were run to determine whether the renal microvascular endothelium influences renin release. Blood-free rat renal cortical slices were incubated in a bicarbonate buffer for 60 min and sampled at 30 and 60 min to determine renin concentration and at 60 min for prostaglandin (PG) E2 and I2 (6-keto-PGF1 alpha) synthesis. Stimulation by 10(-6) M melittin of endogenous PGs simultaneously increased renin release, PGE2, and PGI2 synthesis, and all were inhibited by 1.6 x 10(-6) M meclofenamate. Renin release was stimulated with isoproterenol [26.2 +/- 2.4 ng angiotensin I (ANG I) .h-1.mg-1.30 min-1; P less than 0.001], PGI2 (32.3 +/- 7.4 ng ANG I.h-1.mg-1.mg-1.30 min-1; P less than 0.005), and PGE2 (25.7 +/- 2.8 ng ANG I.h-1.mg-1.30 min-1, P less than 0.001). Acetylcholine did not affect basal renin but potentiated the response to PGE2 by 80% (46.0 +/- 5.8 ng ANG I.h-1.mg-1.30 min-1; P less than 0.001). Atropine (10(-7) M) reversed this potentiation. Deendothelialization of renal microvessels with H2O2 eliminated PGI2, but neither PGE2 nor renin release, and reversed acetylcholine-potentiation of PGE2-stimulated renin release as did meclofenamate. Hemoglobin increased PGE2-stimulated renin similarly to acetylcholine. These studies suggest that stimulating the endothelium with acetylcholine results in selective potentiation of PGE2-stimulated renin release, which may be mediated through some cyclooxygenase product and is independent of endothelium-derived relaxing factor. Thus the renal endothelium may influence or modulate renin release.


2005 ◽  
Vol 525 (1-3) ◽  
pp. 128-134 ◽  
Author(s):  
Junya Nagai ◽  
Reishi Nasu ◽  
Teruo Murakami ◽  
Mikihisa Takano

1995 ◽  
Vol 18 (3) ◽  
pp. 236-238
Author(s):  
Y. WANG ◽  
R. GRIGG ◽  
H. SYMONDS ◽  
C.J. BOWMER

1981 ◽  
Vol 166 (4) ◽  
pp. 484-488 ◽  
Author(s):  
S. Suzuki ◽  
R. Franco-Saenz ◽  
S. Y. Tan ◽  
P. J. Mulrow

2003 ◽  
Vol 143 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Kyoko Soejima ◽  
Jiro Uozumi ◽  
Takehiro Kanou ◽  
Chisato Fujiyama ◽  
Zenjiro Masaki

Sign in / Sign up

Export Citation Format

Share Document