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Los mediadores proinflamatorios desregulan crónicamente la formación del factor hiperpolarizante derivado del

P Kessler¹, R Popp, R Busse

¹Institut für Kardiovaskuläre Physiologie und Institut für Anaesthesiologie, Klinikum der J.W.G.-Universität, Frankfurt/Main, Germany.

|April 13, 1999

Resumen

Los mediadores proinflamatorios perjudican la formación del factor hiperpolarizante derivado del endotelio (EDHF) en las arterias mediante la inducción de la óxido nítrico sintasa II (NOS II). Esta reducción en el EDHF contribuye a la disfunción endotelial en condiciones como la arteriosclerosis y la sepsis.

Área de la Ciencia:

Biología Vascular Biología Vascular
La función endotelial es la función endotelial.
La inflamación es la inflamación.

Sus antecedentes:

Las respuestas del dilatador dependientes del endotelio involucran óxido nítrico (NO) y EDHF.
Estas respuestas se ven alteradas en la arteriosclerosis y la sepsis.
Los mediadores proinflamatorios pueden afectar la generación de EDHF a través de la NO sintasa inducible (NOS II).

Objetivo del estudio:

Investigar el efecto de los mediadores proinflamatorios en la generación de EDHF en arterias aisladas.
Para determinar si la expresión NOS II influye en la formación de EDHF.

Principales métodos:

Las arterias carótidas aisladas de conejo y las arterias coronarias de cerdo fueron expuestas a citoquinas y lipopolisacáridos.
La síntesis de óxido nítrico (NOS) y la ciclooxigenasa fueron bloqueadas.
Se evaluó la expresión NOS II y la relajación mediada por EDHF.
Se midió la hiperpolarización de las células del músculo liso vascular.

Principales resultados:

Los mediadores proinflamatorios atenuaron significativamente la relajación mediada por EDHF, coincidiendo con la expresión de NOS II.
La inhibición de NOS II o la síntesis de proteínas impidió esta relajación embotada.
Los donantes NO imitaron el efecto de los mediadores proinflamatorios.
Los mediadores proinflamatorios redujeron la síntesis de EDHF y disminuyeron la expresión de las enzimas del citocromo P450.

Conclusiones:

Los mediadores proinflamatorios inhiben la formación de EDHF en las arterias aisladas.
Esta inhibición está vinculada a la expresión de NOS II y probablemente está mediada por la generación inducida de NO.
La disminución de la formación de EDHF puede contribuir a la disfunción endotelial en la arteriosclerosis y la sepsis.

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