info:eu-repo/semantics/article
Hypertension linked to allostatic load: From psychosocial stress to inflammation and mitochondrial dysfunction
Fecha
2019-03Registro en:
Mocayar Maron, Feres Jose; Ferder, Leon Fernando; Saraví, Fernando Daniel; Manucha, Walter Ariel Fernando; Hypertension linked to allostatic load: From psychosocial stress to inflammation and mitochondrial dysfunction; Taylor & Francis Ltd; Stress; 22; 2; 3-2019; 169-181
1025-3890
CONICET Digital
CONICET
Autor
Mocayar Maron, Feres Jose
Ferder, Leon Fernando
Saraví, Fernando Daniel
Manucha, Walter Ariel Fernando
Resumen
Although a large number of available treatments and strategies, the prevalence of cardiovascular diseases continues to grow worldwide.émergingévidence supports the notion of counteracting stress as a critical component of a comprehensive therapeutic strategy for cardiovascular disease. Indeed, an unhealthy lifestyle is a burden to biological variables such as plasma glucose, lipid profile, and blood pressure control. Recent findings identify allostatic load as a new paradigm for an integrated understanding of the importance of psychosocial stress and its impact on the development and maintenance of cardiovascular disease. Allostasis complement homeostasis and integrates behavioral and physiological mechanisms by which genes,éarlyéxperiences,énvironment, lifestyle, diet, sleep, and physicaléxercise can modulate and adapt biological responses at the cellular level. Foréxample, variability is a physiological characteristic of blood pressure necessary for survival and the allostatic load in hypertension can contribute to its related cardiovascular morbidity and mortality. Therefore, the current review will focus on the mechanisms that link hypertension to allostatic load, which includes psychosocial stress, inflammation, and mitochondrial dysfunction. We will describe and discuss new insights on neuroendocrine-immuneéffects linked to allostatic load and its impact on the cellular and molecular responses; the links between allostatic load, inflammation, andéndothelial dysfunction; theépidemiologicalévidence supporting the pathophysiological origins of hypertension; and the biologicalémbedding of allostatic load and hypertension with anémphasis on mitochondrial dysfunction.