In the isolated perfused rat kidney, the superimposition of a number of calcium entry blockers (CEB) upon norepinephrine vasoconstriction prompts an increase in the glomerular filtration rate (GFR) to a level substantially greater than the original value. A similar acute GFR response to CEB is manifested in the intact anesthetized rat with the renal perfusion pressure remaining constant. This glomerular response to CEB is accentuated in isolated perfused kidneys from Dahl salt-sensitive (DS) rats as compared with kidneys from Dahl salt-resistant (DR) rats. The disparities between DS and DR kidney responses are further amplified in the DS rat kidney after a high NaCl intake and the development of hypertension by the DS rat. In addition, vasoconstrictor responses to BAY-K 8644, a calcium entry facilitator, are accentuated in DS rat kidneys, and even more so following a high NaCl intake or ‘chemical sympathectomy’ with 6-hydroxydopamine. These results suggest that subtle changes in vascular and glomerular calcium entry modulation may be the key determinants of altered renal hemodynamics in salt-dependent hypertens