Angiotensin receptors in glomeruli differ from those in renal arterioles.

Angiotensin receptors in afferent and efferent arterioles and in the glomerulus are strategically located to influence renal perfusion and glomerular function. With the size of isolated glomeruli as the index, we have demonstrated identical dose-response relationships for graded concentrations (10(-13) to 10(-3) g/liter) of angiotensin II (AII) and angiotensin III (AIII). An octapeptide analogue (saralasin 10(-6) to 10(-2) g/liter) was equally effective at blocking glomerular responses to both AII and AIII, but two heptapeptide analogues (des-asp, 8-ile AII and des-asp, 8-gly AII; 10(-6) to 10(-2) g/liter) failed to block responses to either agonist. The relative influence of octapeptide and heptapeptide analogues on GFR was examined in anesthetized dogs with partial occlusion of the thoracic inferior vena cava. In 18 dogs, caval occlusion reduced renal blood flow (35%), GFR (29%), and arterial pressure (13%). Saralasin (300 to 3000 ng/kg/min, i.v.) and des-asp, 8-ile AII (100 to 3000 ng/kg/min, i.v.) increased renal blood flow by 0.41 +/- 0.11 and 0.62 +/- 0.11 ml/g/min, respectively, but only the octapeptide induced a concomitant increase in GFR (octapeptide: delta GFR = 0.11 +/- 0.03 ml/g/min; heptapeptide: delta GFR = -0.08 +/- 0.07 ml/g/min; P less than 0.025). As octapeptide and heptapeptide analogues were equally effective on renal blood flow in this and in previous studies, but only the octapeptide was effective in isolated glomeruli and in increasing GFR in the intact animal, we conclude that renal vascular and glomerular receptors differ. Furthermore, the glomerular receptor may be the more important in modulating the glomerular functional response to angiotensin.