Variability in the renal clearance of cephalexin in experimental renal failure

1993 ◽  
Vol 21 (1) ◽  
pp. 19-30 ◽  
Author(s):  
Amor Maïza ◽  
Peter T. Daley-Yates
Author(s):  
HERVÉ P. LEFEBVRE ◽  
VALÉRIE LAROUTE ◽  
MICHEL ALVINERIE ◽  
MARC SCHNEIDER ◽  
PATRICK VINCLAIR ◽  
...  

1993 ◽  
Vol 92 (6) ◽  
pp. 2934-2940 ◽  
Author(s):  
A E Raine ◽  
A M Seymour ◽  
A F Roberts ◽  
G K Radda ◽  
J G Ledingham

1974 ◽  
Vol 47 (1) ◽  
pp. 80-86 ◽  
Author(s):  
Raymond G. Slavin ◽  
Neil I. Gallagher

2010 ◽  
Vol 26 (3) ◽  
pp. 832-838 ◽  
Author(s):  
S. Bernardi ◽  
R. Candido ◽  
B. Toffoli ◽  
R. Carretta ◽  
B. Fabris

Radiology ◽  
1970 ◽  
Vol 97 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Patrick C. Walsh ◽  
Ruben F. Gittes ◽  
James W. Lecky

1999 ◽  
Vol 277 (4) ◽  
pp. H1622-H1629 ◽  
Author(s):  
Jarkko Kalliovalkama ◽  
Pasi Jolma ◽  
Jari-Petteri Tolvanen ◽  
Mika Kähönen ◽  
Nina Hutri-Kähönen ◽  
...  

Chronic renal failure is associated with increased cardiovascular morbidity and abnormal arterial tone, but the underlying pathophysiological mechanisms are poorly understood. Therefore, we studied the responses of isolated mesenteric arterial rings from Wistar-Kyoto rats in standard organ chambers 6 wk after subtotal (5/6) nephrectomy or sham operation. Subtotal nephrectomy resulted in a 1.7-fold elevation of plasma urea nitrogen, whereas blood pressure was not significantly affected. Endothelium-mediated relaxations of norepinephrine-precontracted rings to ACh were impaired in renal failure rats. The nitric oxide (NO) synthase inhibitor N G-nitro-l-arginine methyl ester inhibited relaxations to ACh more effectively in the renal failure group, whereas the cyclooxygenase inhibitor diclofenac did not significantly affect the response in either group. Inhibition of Ca2+-activated K+ channels by charybdotoxin and apamin attenuated NO synthase- and cyclooxygenase-resistant relaxations to ACh in control but not renal failure rats and abolished the difference between these groups. Endothelium-independent relaxations to isoproterenol and cromakalim, vasodilators acting via β-adrenoceptors and ATP-sensitive K+ channels, respectively, were impaired in the renal failure group, whereas relaxations to the NO donor nitroprusside were similar in both groups. In conclusion, endothelium-mediated relaxation in renal failure rats was impaired in the absence and presence of NO synthase and cyclooxygenase inhibition but not with prevented smooth muscle hyperpolarization. Endothelium-independent relaxations to isoproterenol and cromakalim were also attenuated after 5/6 nephrectomy. These results suggest that impaired vasodilatation in experimental renal failure could be attributed to reduced relaxation via arterial K+ channels.


Nephron ◽  
1977 ◽  
Vol 18 (1) ◽  
pp. 26-34 ◽  
Author(s):  
Steven E. Weisbrode ◽  
Charles C. Capen

Biotherapy ◽  
1990 ◽  
Vol 2 (1) ◽  
pp. 77-85 ◽  
Author(s):  
Akinori Kawamura ◽  
Masato Higuchi ◽  
Nobuo Imai ◽  
Tsutomu Kawaguchi ◽  
Yohsuke Ogura

1986 ◽  
Vol 30 (5) ◽  
pp. 687-693 ◽  
Author(s):  
Claire Kleinknecht ◽  
Denise Laouari ◽  
Nicole Hinglais ◽  
Renée Habib ◽  
Catherine Dodu ◽  
...  

2010 ◽  
Vol 87 (1) ◽  
pp. 60-67 ◽  
Author(s):  
Daniella G. Batista ◽  
Kátia R. Neves ◽  
Fabiana G. Graciolli ◽  
Luciene M. dos Reis ◽  
Rafael G. Graciolli ◽  
...  

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