To evaluate renal microcirculation during acute cyclosporin (CsA) administration (50 mg/kg, i.v.), seven euvolaemic Munich–Wistar rats were studied. CsA infusion caused a significant decrease in total glomerular filtration rate (GFR) (0.96±0.04 vs 0.47±0.07 ml/min) and in single-nephron GFR (SNGFR) (27.90±3.4 vs 14.02±3.5 nl/min). The efferent arteriolar resistance increased substantially (P<0.05) while the afferent resistance rose moderately. Consequently, there was an increase (P<0.05) in mean glomerular capillary hydraulic pressure (P¯GC), from 45±1 to 55±4 mmHg, together with an important decrease in mean glomerular plasma flow rate (QA), from 100±17 to 44±13 nl/min. Since tubular hydraulic pressure was maintained unaltered, an elevated transglomerular hydraulic pressure difference was observed (P<0.05). The lower values of SNGFR were accounted for by both the decrease in QAand in the glomerular ultrafiltration coefficient (Kf). The latter was reduced from 0.096±0.03 to 0.031±0.010 nl/sec per mmHg(P<0.05) by CsAAdditionally, three groups of Munich–Wistar rats were previously treated with captopril (2 mg/kg per h, i.v.), verapamil (20μg/kg per min, i.v.) or indomethacin (2 mg/kg, i.v.). Both captopril and verapamil minimised the renal effects of CsA, with a decline of∼25instead of∼50on GFR and RPF.Thus CsA infusion caused a decline on SNGFR due to an important reduction in QAand Kfwith an impressive increase on arteriolar resistance, a mark of angiotensin II stimulation. However, indomethacin was unable to prevent glomerular haemodynamic changes, suggesting that prostaglandins have a minor effect, if any, in impairing glomerular haemodynamics during
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