The regulations of renal function and renin release are influenced by neural, humoral and physical factors. During the last decade, considerable progress has been made in the identification and characterization of these extrinsic renal control systems. Mechanisms intrinsic to the kidney are also important for renal function. These include the autoregulation of blood flow, and the local control of renin secretion. Fundamental questions regarding the mechanism of these intrinsic controls remain unanswered. Recently, endogenous renal adenosine has been claimed to influence the tubuloglomerular feedback control and renin release. Two subclasses of adenosine receptors A₁ and A₂ have been described. The present experiment was carried out to evaluate the effects of N₆-cyclohexyladenosine (CHA, A₁ selective) and 5 -N-ethylcarbox-amide adenosine (NECA, A₂ selective) on the renal function and renin release in the unanesthetized rabbit. Intra-renal arterial infusion of NECA (0.3 ~ 10.0n mole/min/rabbit) or CHA (0.03 ~ 10.0n mole/min/rabbit) caused a prompt and dose-dependent decrease in urine volume, glomerular filtration rate (GFR), renal plasma flow (RPF), filtration fraction (FF), electrolyte excretion and free water clearance (CH₂O), the effect being much more profound with CHA than with NECA. The NECA infusion resulted in a profound decrease of systemic blood pressure, but the CHA infusion did not. Both NECA and GHA infusions caused a prompt and dose-dependent decrease in renin secretion rate, again the effect being greater with CHA than with NEGA. These results suggest that both A₁ and A₂ adenosine receptors may be involved in the intrinsic control of renal function and renin release, and that the A₁ receptors plays a more important role than the A_{2 receptor in the regulation of renal fnction.}