The cardiovascular system participates in both blood pressure (BP) and temperature regulation. As a result, salt ingestion creates conflict between BP and temperature homeostasis, as vasodilatation that would promptly lower the BP would simultaneously increase cutaneous blood flow, thereby accelerating heat loss. If temperature homeostasis has precedence over blood pressure homeostasis, as postulated by the thermoregulatory-vascular remodeling (TVR) hypothesis, then in order to minimize heat loss, BP remains elevated following salt ingestion until the kidneys excrete the excess salt. A case of amlodipine overdose offered an opportunity to test a corollary of the TVR hypothesis: vasodilators should cause a drop in body temperature and/or an increase in the metabolic rate. Following the ingestion of 1000 mg of amlodipine, the temperature and BP of a single patient were monitored during the initial 36 hours and during the 13th day of hospitalization. The BP dropped markedly between the fifth and seventh hours postingestion, but then rose steadily and normalized by 28 hours postingestion. The temperature was normal at 7 hours postingestion, declined gradually between the seventh and 26th hours postingestion, stabilized between the 26th and 31st hours postingestion, then began to rise. During this case of amlodipine overdose, a modest temperature decline lagged behind a marked BP decline. As the BP rose, the temperature also rose, but lagged behind the BP increases. These findings suggest that there is a relationship between BP and temperature and are consistent with the TVR hypothesis.