The supposition that temperature homeostasis has precedence over blood pressure homeostasis, that vascular remodeling ensues, that hypertension is the consequence and that sodium chloride ingestion sets the sequence in motion, constitutes the thermoregulatory-vascular remodeling hypothesis. Because the cardiovascular system plays a role in both temperature and blood pressure regulation, the ingestion of sodium chloride creates conflict between temperature homeostasis and blood pressure homeostasis. Vasodilatation would lower the blood pressure following the ingestion of sodium chloride, but increased blood flow to the cutaneous circulation would increase heat loss and decrease core body temperature. Regional vasodilatation that does not involve the cutaneous circulation could lower the blood pressure without lowering the core temperature, but if temperature homeostasis has precedence over blood pressure homeostasis, and if regional vasodilatation incompletely restores blood pressure homeostasis, then elevations in blood pressure may persist following the ingestion of sodium chloride. The kidneys gradually excrete the excess sodium chloride, thereby normalizing the blood pressure, but prolonged elevations in blood pressure lead to vascular remodeling, sustained increases in peripheral resistance, and a higher baseline blood pressure. Following countless sodium chloride ingestions, essential hypertension develops. The thermoregulatory-vascular remodeling hypothesis predicts that antihypertensive medications that are vasodilators will accelerate heat loss due to increased blood flow to the cutaneous circulation. As a result, either core body temperature will decrease or there will be a compensatory increase in the metabolic rate. This prediction could be tested experimentally. The main clinical implication of the thermoregulatory-vascular remodeling hypothesis is that avoiding the ingestion of sodium chloride is the key to preventing essential hypertension.