Insulin causes renal vasodilatation independently of renal prostaglandins in healthy humans.
The effect of physiological hyperinsulinaemia on renal haemodynamics and renal sodium handling was studied in nine healthy males on two separate study occasions with and without indomethacin pretreatment, using the euglycaemic insulin clamp technique. Renal haemodynamics and segmental tubular sodium handling were evaluated by determining the inulin, PAH, sodium and lithium clearances. Changes in urinary dopamine excretion were also studied. Insulin infusion caused similar increases in renal plasma flow with as well as without indomethacin pretreatment, but no change in glomerular filtration rate in both experimental settings. Following indomethacin pretreatment, the basal sodium clearance decreased from 1.6 +/- 0.2 to 0.8 +/- 0.2 ml/min and the basal urinary dopamine excretion decreased from 107 +/- 8 to 86 +/- 6 nmol/h. In conclusion, the present study demonstrates a direct renal vasodilatory effect of insulin in healthy subjects that does not seem to be dependent on renal prostaglandins. Moreover, under the present experimental circumstances indomethacin reduced the basal urinary dopamine output, which could reflect a reduction in the filtered load of sodium following indomethacin pretreatment.
Stenvinkel
P
P
Karolinska Institute, Department of Renal Medicine, Huddinge University Hospital, Stockholm, Sweden.
Alvestrand
A
A
D000328:Adult; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology*; D007668:Kidney / Q000187:drug effects* / Q000502:physiology; D008297:Male; D011453:Prostaglandins / Q000502:physiology*; D012964:Sodium / Q000378:metabolism; D014664:Vasodilation / Q000187:drug effects*
D007328:Insulin; D011453:Prostaglandins; D012964:Sodium; D007213:Indomethacin