The possibility of a metabolic control of glomerular filtration rate (GFR) has been considered unlikely to exist as stated by Renkin & Gilmore (1973). This conclusion is based on the assumption that increased metabolism would lead to vasodilatation as in other organs like heart and skeletal muscle. In the kidney renal blood flow (RBF) determines metabolism in as much as increase of RBF leads to an increase of GFR which in turn increases tubular load with sodium chloride and subsequent tubular sodium reabsorption. If increased sodium reabsorption lead to vasodilatation, we would have a case of a positive feedback with no way of regulating constancy of RBF and GFR. Therefore, it was postulated that a vasoconstrictive signal operates in the kidney to limit renal metabolism ie mainly tubular sodium chloride reabsorption (Thurau, 1964).

Since adenosine is a vasoconstrictor in the kidney (Osswald, 1975; Osswald et al., 1975, 1978a, 1978b; Thurau, 1964) and since adenosine is present in the normal kidney (Osswald et al., 1977). The question arises whether adenosine plays a role in regulation renal blood flow under physiological conditions (Oss-wald et al., 1977, 1978; Schnermann et al., 1977). The present studies were undertaken to measure adenosine tissue content during periods of increased