Glomerular hemodynamic alterations during acute hyperinsulinemia in normal and diabetic rats

• Published in: Kidney international Vol. 42; no. 5; pp. 1160 - 1168
• Main Authors: Tucker, Bryan J., Anderson, Christen M., Thies, R. Scott, Collins, Rose C., Blantz, Roland C.
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Legacy CDMS Elsevier Inc 01.11.1992; Nature Publishing
• Subjects: Acute Disease; Animals; Associated diseases and complications; Biological and medical sciences; Diabetes Mellitus, Experimental - complications; Diabetes Mellitus, Experimental - drug therapy; Diabetes Mellitus, Experimental - physiopathology; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Hydrostatic Pressure; Hyperinsulinism - complications; Hyperinsulinism - physiopathology; Imidazoles - pharmacology; Insulin - pharmacology; Kidney Glomerulus - blood supply; Kidney Glomerulus - drug effects; Kidney Glomerulus - physiopathology; Life Sciences (General); Male; Medical sciences; Rats; Rats, Wistar; Renal Circulation - drug effects; Renal Circulation - physiology; Space life sciences; Thromboxane-A Synthase - antagonists & inhibitors; Non-Nasa Center; Nasa Discipline Cardiopulmonary; Endocrinopathy; Glomerulonephritis; Hyperinsulinemia; Animal model; Urinary system disease; Pathophysiology; Rat; Arachidonic acid derivatives; Diabetes mellitus; Rodentia; Renal disease; Insulin; Renal glomerulus; Vertebrata; Mammalia; Animal; Complication; Hemodynamics; Thromboxane; NASA Discipline Cardiopulmonary; Non-NASA Center
• ISSN: 0085-2538; 1523-1755
• DOI: 10.1038/ki.1992.400

Glomerular hemodynamic alterations during acute hyperinsulinemia in normal and diabetic rats. Treatment of insulin dependent diabetes invariably requires exogenous insulin to control blood glucose. Insulin treatment, independent of other factors associated with insulin dependent diabetes, may induce changes that affect glomerular function. Due to exogenous delivery of insulin in insulin dependent diabetes entering systemic circulation prior to the portal vein, plasma levels of insulin are often in excess of that observed in non-diabetics. The specific effects of hyperinsulinemia on glomerular hemodynamics have not been previously examined. Micropuncture studies were performed in control (non-diabetic), untreated diabetic and insulin-treated diabetic rats 7 to 10 days after administration of 65 mg/kg body weight streptozotocin. After the first period micropuncture measurements were obtained, 5 U of regular insulin (Humulin-R) was infused i.v., and glucose clamped at euglycemic values (80 to 120 mg/dl). Blood glucose concentration in non-diabetic controls was 99 ± 6 mg/dl. In control rats, insulin infusion and glucose clamp increased nephron filtration rate due to decreases in both afferent and efferent arteriolar resistance (afferent greater than efferent) resulting in increased plasma flow and increased glomerular hydrostatic pressure gradient. However, insulin infusion and glucose clamp produced the opposite effect in both untreated and insulin-treated diabetic rats with afferent arteriolar vasoconstriction resulting in decreases in plasma flow, glomerular hydrostatic pressure gradient and nephron filtration rate. Thromboxane A2 (TX) synthetase inhibition partially decreased the vasoconstrictive response due to acute insulin infusion in diabetic rats preventing the decrease in nephron filtration rate. However, the action of TX inhibition decreased nephron filtration rate prior to insulin infusion in both diabetic and control rats, which may indicate participation of other neuro-humoral agents potentiated by TX inhibition.