Evidence from animal, clinical and epidemiological studies suggests that high blood pressure is associated with abnormalities of calcium metabolism, leading to increased calcium loss, secondary activation of the parathyroid gland, increased movement of calcium from bone and increased risk of urinary tract stones. Some of these abnormalities are detectable in children and young people and continue throughout adult life. The cluster of abnormalities may be due either to a primary renal tubular defect ('renal calcium leak' hypothesis) or to the effect of central volume expansion seen in hypertension ('central blood volume' hypothesis). A high salt intake is known to aggravate these abnormalities and their consequences. If substantial calcium loss related to high blood pressure is sustained over many decades, increased excretion of calcium in the urine may result in an increased risk of urinary tract stones, and the increased movement of calcium from bone may result in higher rates of bone mineral loss, thereby increasing the risk of osteoporosis. The present review summarises the evidence, suggests a unifying hypothesis and discusses clinical and public health implications.