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Nova metodologia de avaliação da sensibilidade ao sódio : implicações clínicas
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A hipertensão arterial (HTA) constitui, mundialmente, o principal fator de risco modificável para doenças cardiovasculares, morbilidade e mortalidade. Afeta 1,28 biliões de pessoas.
Associa-se a inúmeras complicações, doença cardíaca isquémica, insuficiência cardíaca, acidente vascular cerebral, demência e doença renal crónica. Em 2015 causou 10,7 milhões de mortes.
Estabeleceu-se causalidade entre o consumo de sal, a disrupção da homeostasia de sódio e HTA. A HTA sal sensível (≈50% dos doentes) carateriza-se pela elevação concomitante do consumo de sal e valores tensionais, constituindo um fator de risco para morbilidade e mortalidade cardiovascular tão importante como os fatores de risco tradicionais. Polimorfismos dos genes envolvidos no sistema renina-angiotensina-aldosterona, hiperativação do SNS e disfunção renal constituem fatores etiológicos importantes.
Segundo o modelo clássico de homeostasia, o sódio distribui-se equitativamente nos compartimentos intravascular e intersticial, existindo relação direta entre a composição do organismo em sódio, volume extracelular e pressão arterial. Foi criticado após constatação de dissociação entre o consumo e excreção diárias de sódio. Verificou-se acumulação de sódio em compartimentos, que o acumulam e libertam ciclicamente, sob regulação de eixos neuroendócrinos, incluindo endotélio, pele, cartilagem, músculo e osso.
A exposição endotelial a excesso de sal compromete a sua integridade estrutural e funcional. Observa-se disrupção do glicocálice e aumento da rigidez endotelial, desencadeando disfunção endotelial e vasoconstrição.
Na pele, a acumulação de sódio causa hiperplasia capilar linfática. A sua disrupção provoca aumento da resistência vascular epitelial.
Em indivíduos sal sensíveis, há alteração dos mecanismos centrais de regulação da pressão arterial, desencadeando hiperativação simpática, e consequente elevação tensional.
Tendo em conta a importância da avaliação da sensibilidade ao sódio, propõe-se um novo método, desenvolvido por Oberleithner et al., através da avaliação doglicocálice eritocitário. A sua aplicação permite a demarcação de um fenótipo distinto, do ponto de vista fisiopatológico e abordagem terapêutica, podendo requerer atualização das guidelines.
Systemic arterial hypertension (SAT) is, worldwide, the main avoidable risk factor for the establishment of cardiovascular disease, as well as morbidity and mortality risk. It affects 1.28 billion people. It is associated with serious long term health consequences, including ischemic heart disease, heart failure, stroke, dementia as well as chronic kidney disease. In 2015, SAT was directly responsible for 10.7 million deaths globally. One can establish a causal direct association between increased salt intake, the disruption of sodium homeostasis and SAT. Salt sensitive SAT is characterized by paralleled salt intake and blood pressure elevation. It is thought that this form of SAT encompasses 30 to 50% of patients. Regarding etiologic factors, genetic polymorphisms affecting genes that encode components of the renin-angiotensin-aldosterone system have been established as important contributors to salt sensitive SAT, as well as sympathetic nervous system hyperactivity and renal dysfunction. Salt sensitivity constitutes a risk factor for increased morbidity and mortality, considered as relevant and important as the other traditional cardiovascular risk factors. The traditional model of sodium balance considers the existence of two compartments, intravascular and interstitial, where sodium distributes equally. It postulates the existence of a linear association between total body sodium, extracellular volume and blood pressure. The model received criticism after it was recently detected that sodium intake doesn’t match excretion in 24 hours. Moreover, sodium storage in body was detected in the endothelium, skin, cartilage muscle and bone. It is generally accepted that these compartments store and release sodium rhythmically, under the influence of neuroendocrine cyclic axis. Salt loading compromises the structural and functional integrity of the endothelium. It triggers glycocalyx disruption, endothelial rigidity and, ultimately, endothelial dysfunction.Sodium storage was observed in the skin interstitium. This event drives capillary hyperplasia. When this process fails, it can be noticed increased resistance of capillary arterioles. In salt sensitive individuals, the central mechanisms that regulate blood pressure are abnormal, triggering sympathetic nervous system hyperactivation, leading to blood pressure elevation. Considering the importance of sodium sensitivity evaluation, a new method, developed by Oberleithner et al., that analyses changes in the glycocalyx of erythrocytes, is proposed. Its application allows the demarcation of a distinct phenotype, regarding physiopathologic mechanisms and therapeutic approach. Advances in the body of knowledge acquired through application of this new method might require adjustments in hypertension guidelines. The application of this new method enables the definition of a distinct hypertensive phenotype, encompassing specific pathophysiological mechanisms and, therefore, the need for a tailored therapeutic approach. These specificities might require a review of current arterial hypertension guidelines.
Systemic arterial hypertension (SAT) is, worldwide, the main avoidable risk factor for the establishment of cardiovascular disease, as well as morbidity and mortality risk. It affects 1.28 billion people. It is associated with serious long term health consequences, including ischemic heart disease, heart failure, stroke, dementia as well as chronic kidney disease. In 2015, SAT was directly responsible for 10.7 million deaths globally. One can establish a causal direct association between increased salt intake, the disruption of sodium homeostasis and SAT. Salt sensitive SAT is characterized by paralleled salt intake and blood pressure elevation. It is thought that this form of SAT encompasses 30 to 50% of patients. Regarding etiologic factors, genetic polymorphisms affecting genes that encode components of the renin-angiotensin-aldosterone system have been established as important contributors to salt sensitive SAT, as well as sympathetic nervous system hyperactivity and renal dysfunction. Salt sensitivity constitutes a risk factor for increased morbidity and mortality, considered as relevant and important as the other traditional cardiovascular risk factors. The traditional model of sodium balance considers the existence of two compartments, intravascular and interstitial, where sodium distributes equally. It postulates the existence of a linear association between total body sodium, extracellular volume and blood pressure. The model received criticism after it was recently detected that sodium intake doesn’t match excretion in 24 hours. Moreover, sodium storage in body was detected in the endothelium, skin, cartilage muscle and bone. It is generally accepted that these compartments store and release sodium rhythmically, under the influence of neuroendocrine cyclic axis. Salt loading compromises the structural and functional integrity of the endothelium. It triggers glycocalyx disruption, endothelial rigidity and, ultimately, endothelial dysfunction.Sodium storage was observed in the skin interstitium. This event drives capillary hyperplasia. When this process fails, it can be noticed increased resistance of capillary arterioles. In salt sensitive individuals, the central mechanisms that regulate blood pressure are abnormal, triggering sympathetic nervous system hyperactivation, leading to blood pressure elevation. Considering the importance of sodium sensitivity evaluation, a new method, developed by Oberleithner et al., that analyses changes in the glycocalyx of erythrocytes, is proposed. Its application allows the demarcation of a distinct phenotype, regarding physiopathologic mechanisms and therapeutic approach. Advances in the body of knowledge acquired through application of this new method might require adjustments in hypertension guidelines. The application of this new method enables the definition of a distinct hypertensive phenotype, encompassing specific pathophysiological mechanisms and, therefore, the need for a tailored therapeutic approach. These specificities might require a review of current arterial hypertension guidelines.
Descrição
Trabalho Final do Curso de Mestrado Integrado em Medicina, Faculdade de Medicina, Universidade de Lisboa, 2022
Palavras-chave
Hipertensão arterial Sensibilidade ao sódio Endotélio vascular Sistema renina-angiotensina-aldosterona