Purpose of review: We review the known mechanisms of sodium-sensitive hypertension in the metabolic syndrome with a focus on preclinical models, differences between these models, and methodological limitations. We also identify future directions for a better understanding and treatment of this common condition.
Recent findings: Rigorous methodologies to measure blood pressure in preclinical models may clarify some of the inconsistencies in the literature. Renal, neural, hormonal, and cardiovascular systems are dysregulated and contribute to elevated blood pressure. Local renin-angiotensin systems enhance systemic hormone signaling to increase blood pressure. Since the original description of metabolic syndrome, investigators from many fields have contributed to an increasingly complex and mechanistic understanding of this common condition. These systems integrate to regulate sodium transport in the kidney leading to hypertension and enhanced sodium sensitivity. An array of non-uniform preclinical models are used and support clinical studies to inform which models are pathophysiologically relevant for further mechanistic studies to guide targeted therapy.
Keywords: High fat diet; Insulin resistance; Mineralocorticoid receptor; Obesity; Sodium sensitivity.