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Am J Physiol Renal Physiol (November 13, 2001). doi:10.1152/ajprenal.00194.2001
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Articles in PresS, published online ahead of print November 13, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00194.2001
Submitted on June 26, 2001
Accepted on October 24, 2001

Angiotensin II Stimulates Cyclooxygenase-2 mRNA Expression in Renal Tissue From Rats With Kidney Failure

Jose A Hernandez1, Horacio Astudillo2, and Bruno Escalante3*

1 Dept of Pharmacology, Centro de Investigacion y de Estudios Avanzados del I.P.N., Mexico City, Mexico D.F., Mexico; Dept of Physiology and Pharmacology, Escuela Superior de Medicina I.P.N, Mexico City, Mexico D.F., Mexico
2 Unidad de Investigacion Medica en Enfermedades Oncologicas, Centro Medico Nacional Siglo XXI, Mexico City, Mexico D.F., Mexico
3 Dept of Molecular Bimedicine, Centro de Investigacion y de Estudios Avanzados del I.P.N., Mexico City, Mexico D.F., Mexico

* To whom correspondence should be addressed. E-mail: bescalan{at}mail.cinvestav.mx.

We have shown increased cyclooxygenase-2 expression in kidney failure rats. Increased angiotensin II concentration, hypertension and renal mass reduction have been described during development of kidney failure. Thus, we explored each of these mechanisms, as any one of them could be responsible for cyclooxygenase-2 induction. Kidney failure increased systolic blood pressure from 104±5 to 138±2mmHg, urinary PGE2 from 74±17to 185±25 ng/24h and cyclooxygenase-2 expression from 0.06±0.04 to 0.17±0.03 A.U. Treatment of the rats with Ramipril or Losartan, prevented the increase in the blood pressure, urinary PGE2 and cyclooxygenase-2 expression of the kidney failure rats. Infusion of angiotensin II increased blood pressure from 101±6 to132±6 mmHg, urinary PGE2 excretion from 62±15 to 155±17 ng/24h and cyclooxygenase-2 expression from 0.23±0.01 to 1.6±0.3 A.U. when the angiotensin II-infused rats were treated with nitrendipine, blood pressure decreased from 132±6 to 115±2 mmHg and urinary PGE2 excretion decreased from 152±18 to 97±12 ng/24h whereas cycloxygenase-2 expression was 1.6±0.7and 1.7±0.5 A.U. for rats with and without nitrendipine. Blood pressure of the rats with renal poles resection was similar to sham rats (97±7 and 91±4 mmHg respectively) whereas cyclooxygenase-2 expression was increased in rats with renal poles resection from 0.06±0.04 to 0.12±0.03 A.U. We suggest that in kidney failure the increase in Angiotensin II concentration regulates cyclooxygenase-2 expression, thereby increasing prostaglandin synthesis that contributes to development of kidney failure.




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