<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>1405-9940</journal-id>
<journal-title><![CDATA[Archivos de cardiología de México]]></journal-title>
<abbrev-journal-title><![CDATA[Arch. Cardiol. Méx.]]></abbrev-journal-title>
<issn>1405-9940</issn>
<publisher>
<publisher-name><![CDATA[Instituto Nacional de Cardiología Ignacio Chávez]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1405-99402024000400488</article-id>
<article-id pub-id-type="doi">10.24875/acm.23000245</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Nuevos conceptos en la fisiopatología de la hipertensión arterial. Receptores purinérgicos]]></article-title>
<article-title xml:lang="en"><![CDATA[New concepts in the physiopathology of hypertension. Purinergic receptors]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Bautista-Pérez]]></surname>
<given-names><![CDATA[Rocío]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pérez-Méndez]]></surname>
<given-names><![CDATA[Óscar]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Franco]]></surname>
<given-names><![CDATA[Martha]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Instituto Nacional de Cardiología Ignacio Chávez Departamento de Biología Molecular ]]></institution>
<addr-line><![CDATA[ Ciudad de México]]></addr-line>
<country>México</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Instituto Nacional de Cardiología Ignacio Chávez Departamento de Fisiopatología Cardio-Renal ]]></institution>
<addr-line><![CDATA[ Ciudad de México]]></addr-line>
<country>México</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2024</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2024</year>
</pub-date>
<volume>94</volume>
<numero>4</numero>
<fpage>488</fpage>
<lpage>494</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1405-99402024000400488&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1405-99402024000400488&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1405-99402024000400488&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La hipertensión arterial descontrolada es un factor de riesgo muy relevante para el desarrollo de complicaciones cardiovasculares graves. A pesar de los recursos disponibles en la actualidad, el control de la hipertensión arterial y sus complicaciones dista mucho de lograrse. Por ello, sus secuelas continúan siendo catastróficas, como la insuficiencia renal crónica. De ahí la relevancia de reconocer factores que pudieran modificarse para evitar esta complicación. Recientemente se ha propuesto que los receptores purinérgicos contribuyen en forma importante en las alteraciones renales que ocurren en la hipertensión arterial; en esta revisión se resume brevemente su papel. En varios estudios se ha demostrado que cuando existen concentraciones elevadas de ATP en el intersticio renal, la activación de los receptores purinérgicos constituye una vía fundamental en la generación y la persistencia de hipertensión arterial. Las concentraciones elevadas de ATP alteran mecanismos fundamentales asociados en el control de la presión arterial, como el mecanismo de natriuresis de presión, la autorregulación del flujo renal y la filtración glomerular, así como el aumento en la sensibilidad del mecanismo de retroalimentación tubuloglomerular. La alteración de estos mecanismos contribuye a la disminución de la excreción urinaria de sodio. Además, se modifica la expresión de receptores de ATP (purinérgicos). Bajo la influencia de alteraciones genéticas, el ATP estimula la producción de compuestos vasoactivos y en conjunto producen una disminución de la función renal y lesión tubulointersticial antes de que se lesione el glomérulo. Al mismo tiempo, la interacción de la angiotensina II y los receptores purinérgicos favorece la progresión del daño renal.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Hypertension is a major risk of morbidity and mortality in patients when it is uncontrolled. In spite of improved therapies currently available for blood pressure control, their complications are far away from being accomplished. Therefore, chronic renal failure is frequently observed in hypertensive patients. Thus, insights on mechanisms that may contribute to arterial pressure control should be studied to prevent life-threatening cardiovascular disorders. Purinergic receptors have been recognized in the physiopathology of hypertension; this review summarizes their participation in the renal abnormalities of the kidney in hypertension. Several studies have suggested the activation of renal purinergic receptors under an elevated interstitial ATP milieu as a fundamental pathway that leads to generation and maintained hypertension. Elevated ATP concentration alters fundamental mechanisms involved in the long-term control of blood pressure such as pressure natriuresis, autoregulation of glomerular filtration rate and renal blood flow, as well as increased tubule-glomerular feedback responses, overall, these alterations decrease sodium excretion; in addition, the expression of ATP receptors is modified. Under a genetical background, ATP induces the production of vasoactive compounds, decreases renal function and induces tubulointerstitial injury before glomerular damage. Simultaneously, a deleterious interaction between angiotensin II and purinergic receptors lead to the progression of renal damage.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Hipertensión arterial]]></kwd>
<kwd lng="es"><![CDATA[Angiotensina II]]></kwd>
<kwd lng="es"><![CDATA[ATP]]></kwd>
<kwd lng="es"><![CDATA[Receptores purinérgicos]]></kwd>
<kwd lng="en"><![CDATA[Hypertension]]></kwd>
<kwd lng="en"><![CDATA[Angiotensin II]]></kwd>
<kwd lng="en"><![CDATA[ATP]]></kwd>
<kwd lng="en"><![CDATA[Purinergic receptors]]></kwd>
</kwd-group>
</article-meta>
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