After nephrectomy, the level of arterial pressure is determined by the permitted degree of fluid volume expansion. With kidneys present, the fundamental requirement for fluid volume homeostasis is met by maintaining the balance between sodium and water intake and output. When one-kidney, one-clip (1-K,1-C) hypertension develops on a free diet, early sodium retention occurs with transient increase in extracellular (ECFV) and plasma (PV) volumes, which may persist into the chronic stage. In sodium deprivation, hypertension is not inhibited and ECFV and PV are not significantly raised. Thus, when sodium is available, sodium retention may contribute to the hypertensive mechanism, but when unavailable, other mechanisms must be largely, if not wholly, responsible. When hypertension is reversed by unclipping, the immediate fall in blood pressure is attributable to reduction first in cardiac output and second in peripheral resistance, accompanied by diuresis and contraction of PV: but if external fluid balance is maintained, cardiac output and blood pressure still fall, although at a slower rate, indicating that factors other than volume are implicated. In the development of hypertension, the hemodynamic changes are the reverse of those on unclipping, with transient increase in cardiac output associated with increased myocardial contractility and decreased venous capacity which, when coupled with fluid retention, raise mean circulatory filling pressure. In conclusion, the kidney possesses many mechanisms for raising pressure and reestablishing sodium homeostasis including not only sodium retention, but also release of pressor hormones, renin and possibly others, enhanced afferent sympathetic activity and suppression of the release of medullary hypotensive factors.