Epigenetics of the blood pressure reactivity to salt: Is the salt sensitive phenotype correctable?

Abstract

Salt sensitivity defines a state characterized by a highly reactive blood pressure to changes in salt intake. The salt-sensitive phenotype is strongly associated with hypertension, visceral adiposity/metabolic syndrome, and ageing. Obesity accounts for around 70% of hypertension in young adults, and 30% to 50% of adult hypertensives carry the salt-sensitive phenotype. It is estimated that the salt-sensitive phenotype is responsible for high blood pressure in over 600 million adults. But is the salt-sensitive phenotype correctable? Interventional, controlled, clinical trials in obese adolescents and young obese adults, demonstrated that weight-reducing lifestyle modifications revert the salt-sensitive to the salt-resistant phenotype, and restored the faulty production of nitric oxide. Correction of the salt-sensitive phenotype lowers the blood pressure by reducing its reactivity to dietary salt. In a random sample of obese adults subjected to lifestyle modifications, those who were salt-resistant at baseline, were also normotensive and failed to further lower their blood pressure despite a 12% drop in body weight. The salt-resistant phenotype protects the metabolically healthy obese from hypertension, even if their salt consumption is comparable to that of salt-sensitive obese. In summary, at early stages, the elevated blood pressure of obesity, is determined by epigenetic changes leading to a state of salt-sensitivity.