Since the atrial receptor was suggested to be involved in the control of extracellular fluid volume, it has been shown that the granularity of atrial cardiocytes can be changed by water and salt depletion, and that an extract of atrial tissue, when injected intravenously into anesthetized rats, causes a large and rapid increase in renal excretions of sodium and water. The immunoreactive atrial natriuretic peptide (ANP) has been found in the plasma of patients suffering from various cardiovascular diseases. A high level of ANP in the plasma has been reported in essential hypertension. Several studies on the effects of ANP on renal function and arterial blood pressure have presented contradictory results showing attenuated or accentuated responses. Thus, involvement of the ANP in the development of hypertension remains unresolved. Present study was undertaken to investigate whether the ANP is involved in the development of hypertension in two-kidney one-clip Goldblatt hypertensive rats. The plasma concentration of immunoreactive ANP appeared to be significantly elevated in hypertensive rats as compared with normotensive Goldblatt operated and sham-operated rats. Plasma renin concentration was higher in hypertensive rats than in normotensive rats, as observed in earlier experiments. Intravenous infusions of ANP resulted in increases of urine flow and urinary excretions of sodium and potassium in both hypertensive and normotensive rats. The renal response to ANP was markedly accentuated in Goldblatt hypertensive rats. The plasma concentration of ANP showed a linear relationship with the arterial blood pressure. Infusions of ANP reduced blood pressure both in hypertensive and normotensive rats. These results suggest that in Goldblatt hypertensive rats an elevation of ANP level in the plasma may not be a cause, but instead a consequence of hypertension, and that the renal responsiveness to the ANP is accentuated by some unknown mechanisms.