Mechanism of the glucocorticoid-induced increase in glomerular filtration rate.
In order to investigate the mechanism(s) by which glucocorticoids increase GFR the determinants of glomerular ultrafiltration were measured in two groups of seven Munich-Wistar rats. Group 1 rats were normal controls and group 2 rats were pretreated with methylprednisolone (MP), 15 mg/kg per day for 4 days prior to study. In rats given MP mean values for SNGFR were about 25% higher than in the control group, averaging 33.6 +/- 1.6 (SE) vs. 27.0 +/- 1.0 nl/min. Mean values for initial glomerular plasma flow rate (QA) were also about 25% higher in MP-treated rats, averaging 83.4 +/- 3.9 vs. 65.9 +/- 1.9 nl/min in controls. Mean values of the transglomerular hydraulic pressure difference (deltaP) as well as afferent (IIA) and efferent (IIE) oncotic pressures were essentially similar between control and MP-treated rats. Filtration pressure equilibrium, i.e., equality between IIE and deltaP, obtained in both groups and the mean minimum estimates of the ultrafiltration coefficient (Kf) were also similar between control and MP-treated rats. Thus, the rise in SNGFR following MP is entirely due to the increase in AQ, rather than to changes in the other determinants of ultrafiltration.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D005919:Glomerular Filtration Rate / Q000187:drug effects*; D007668:Kidney / Q000098:blood supply; D008297:Male; D008775:Methylprednisolone / Q000494:pharmacology*; D011312:Pressure; D051381:Rats; D012039:Regional Blood Flow / Q000187:drug effects; D013268:Stimulation, Chemical; D014655:Vascular Resistance / Q000187:drug effects
D008775:Methylprednisolone