RELACION ENTRE EL SISTEMA DE LAS QUININAS Y LAS ENFERMEDADES CARDIOVASCULARES




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RELACION ENTRE EL SISTEMA DE LAS QUININAS Y LAS ENFERMEDADES CARDIOVASCULARES

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El presente estudio describe el papel de los componentes del sistema calicreína-quinina en pacientes de Kuwait que padecen hipertensión, diabetes y otras alteraciones cardiovasculares.
sharma9.jpg Autor:
Jagdish N. Sharma
Columnista Experto de SIIC

Institución:
Department of Applied Therapeutics, Faculty of Pharmacy, Health Sciences Centre, Kuwait University


Artículos publicados por Jagdish N. Sharma
Recepción del artículo
9 de Marzo, 2006
Aprobación
20 de Marzo, 2006
Primera edición
18 de Agosto, 2006
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
Las enfermedades cardiovasculares son la causa más frecuente de muerte en todo el mundo. En Kuwait, la muerte relacionada a enfermedades cardiovasculares puede llegar al 40%. De este modo, será la mayor carga para el sistema de salud del siglo XXI. La hipertensión y la diabetes son los dos factores de riesgo mayores en la producción de hipertrofia cardíaca, cardiopatía isquémica, insuficiencia cardíaca, arritmias cardíacas e infarto de miocardio. Los componentes del sistema calicreína-quinina (quininógenos plasmáticos y urinarios, calicreínas, quininasas y quininas) regulan la PA y los niveles de glucosa sanguínea mediante estimulación de la vasodilatación, efectos natriuréticos y metabolismo de la glucosa. Esos componentes se localizan en el tejido cardíaco, riñón y células musculares lisas. El sistema quinina se encuentra deprimido anormalmente en varios modelos animales experimentales de hipertensión y diabetes que podrían ser responsables de la aparición de complicaciones cardíacas. Se ha señalado que el hallar un compuesto con actividad renal similar a la calicreína puede ser útil al propósito de excretar el exceso de sodio por el riñón en el tratamiento de la hipertensión. También se demostró que los ratones transgénicos que sobreexpresan calicreína por el tejido renal eran hipotensos y que la administración de aprotinina, un inhibidor de la calicreína tisular, restaura la PA de los ratones transgénicos. Esos hallazgos realzaron el papel de la calicreína tisular en la regulación de la PA. Se ha propuesto que el gen de la calicreína tisular entregado en varios modelos de hipertensión ejerce protección, como reducción de la PA aumentada, atenuación de la hipertrofia cardíaca, inhibición de la estenosis y del daño renal. Esto puede indicar la posibilidad de este tratamiento con gen de calicreína para trastronos cardiovasculares. Varios informes indican que la excreción urinaria de calicreína está disminuida en la hipertensión esencial en humanos y en modelos de hipertensión experimental. De este modo, la reducción de la calicreína urinaria puede reflejar una deficiencia en el sistema vasodilatador endógeno calicreína /quinina que contribuye a la patogénesis de la hipertensión. Algunos estudios previos realizados en la población blanca y negra en los EE.UU. demostraron que la excreción urinaria de calicreína está disminuida en miembros familiares con riesgo de hipertensión hereditaria (esencial) y que la calicreína urinaria es uno de los mayores marcadores genéticos asociado con historia familiar de hipertensión. También se informó la existencia de unión genética entre el locus de la calicreína y la presión sanguínea, en ratas. Algunos estudios sugirieron que la excreción urinaria disminuida de calicreína se asocia con sensibilidad de la presión sanguínea a la sal. La excreción de calicreína también está disminuida en afroamericanos y la deficiencia del sistema renal vasodilatador de calicreína-quinina puede explicar muchas de las características singulares de la hipertensión y de las enfermedades cardíacas en algunos sujetos de rarza negra.

Palabras clave
Calicreína, quinina, bradiquinina, hipertensión, diabetes, hipertrofia cardíaca, enfermedades cardiovasculares


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Abstract
Cardiovascular diseases are the most common cause of death worldwide. In Kuwait, death related to cardio vascular diseases may account for about 40%. Thus, it will be the greatest health care burden of the twenty-first century. Hypertension and diabetes are the two major risk factors in the development of cardiac hypertrophy, ischemic heart disease, cardiac failure, cardiac arrhythmias and myocardial infarction. The kallikrein-kinin components (plasma and urinary kininogens, kallikreins, kininases and kinins) are able to regulate BP and blood glucose levels via promoting; vasodilator, natriuretic effects and glucose metabolism. These components are located in the cardiac tissue, kidney and vascular smooth muscle. The kinin system is found to be abnormally depressed in various experimental animal models of hypertension and diabetes which might be responsible for inducing cardiac complications. It has been pointed out that the development of a compound having renal kallikrein-like activity may serve the purpose of excreting excessive sodium from the kidney in the treatment of hypertension. Also it has been demonstrated that transgenic mice over-expressing renal tissue kallikrein were hypotensive and that administration of aprotinin, a tissue kallikrein inhibitor, restored the BP of the transgenic mice. These findings highlight a role of tissue kallikrein in the regulation of BP. It has been proposed that tissue kallikrein gene delivery into various hypertensive models exhibits protection, such as reduction in high BP, attenuation of cardiac hypertrophy, inhibition of renal damage and stenosis. This may indicate the prospect of this kallikrein gene therapy for cardiovascular pathology. Several reports indicate that urinary kallikrein excretion is decreased in essential hypertension in humans and in models of experimental hypertension. Thus, reduced urinary kallikrein may reflect a deficiency in the endogenous kallikrein/kinin vasodilatory system that contributes to the pathogenesis of hypertension. Previous studies conducted in white and black population in the USA demonstrated that urinary kallikrein excretion is diminished in family members at risk for hereditary (essential) hypertension and that urinary kallikrein is one of the major genetic markers associated with family history of hypertension. Also evidence for genetic linkage between the kallikrein locus and blood pressure has been reported in the rat. Previous studies have suggested that diminished urinary kallikrein excretion is associated with salt sensitivity of blood pressure. Kallikrein excretion is also diminished in African-Americans and deficiency of the kallikrein-kinin renal vasodilatory system may explain many of the unique features of essential hypertension and heart diseases in some black subjects.

Key words
Kallikrein, kinin, bradykinin, hypertension, diabetes, cardiac hypertrophy, cardiac diseases


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Especialidades
Principal: Cardiología
Relacionadas: Bioquímica, Medicina Interna



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Jagdish N. Sharma, Department of Applied Therapeutics, Faculty of Pharmacy, Health Sciences Centre, Kuwait University, 13110, PO Box 24923, Safat, Kuwait
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Expertos del Mundo

Especialidad principal:
Cardiología


Relacionadas:
Bioquímica
Medicina Interna
 
 
 
 
 
 
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