Re-investigation of the effect of adrenaline and noradrenaline on renal function in situ.

Abstract

1. Adrenaline or noradrenaline in single doses (0.01-0.10 mug/kg) or by continuous infusion (0.3-3.0 mug.kg(-1) min(-1)) into anaesthetized dogs has been administered by different routes. The changes in femoral arterial B.P., hepatic portal venous pressure, renal venous pressure, intrarenal venous pressure, kidney volume, renal plasma flow (RPF), glomerular filtration rate, urine flow and plasma protein concentration have been followed. The effects varied with route of administration, with dose and time.2. Direct injection of single doses of these drugs (</= 0.02 mug/kg) into the renal artery reduced RPF and urine flow without affecting the systemic B.P. or hepatic portal venous pressure.3. When the catecholamines were administered in single small doses (</= 0.02 mug/kg), I.M. or S.C. or via the hepatic or common carotid arteries, only a slight effect on systemic B.P. was observed. There was little effect on hepatic portal venous pressure, and no diuresis was observed.4. Single injection of these drugs (</= 0.02 mug/kg) into the mesenteric artery caused an immediate fall of hepatic portal venous pressure without a direct effect on the kidney. A subsequent rise in hepatic portal venous pressure was associated with an increase in urine flow.5. Administration of these drugs (0.01-0.10 mug/kg) into the femoral vein, inferior vena cava or internal jugular vein caused a great rise in systemic B.P., a decrease in hepatic portal venous pressure and an antidiuresis, but this was usually followed by a rise of hepatic portal venous pressure and by an associated diuresis, as systemic B.P. returned to normal values.6. The total and segmental renal vascular resistance were calculated from parameters measured during ureteral occlusion. The primary effect of the catecholamines was to increase the resistance in all renal vascular segments and produce antidiuresis; subsequently a drastic drop of all segmental resistances occurred and this was accompanied by a diuresis.7. After block of the alpha-adrenergic receptors by dibenzyline or ergotamine, manipulations which increased the hepatic portal venous pressure could still evoke an immediate reflex diuresis.8. Since the primary renal effect of catecholamines is a vasoconstriction and antidiuresis, it seems that the subsequent reduction of the renal vascular resistance and the associated diuresis is caused by some other mechanism.9. It is concluded that the complex effects of catecholamine on renal function represent the resultant of direct intrarenal together with indirect extrarenal actions and that the relative significance of these various actions depends on dose, time and the route of administration.