Aim and methods: Obesity in humans is associated with proteinuria and an increased glomerular filtration, possibly related to an increase in glomerular capillary pressure. We investigated in obese and lean Zucker rats (10-12 weeks old) whether this might be related to alterations in the diameter of preglomerular and postglomerular microvessels and their reactivity to the resistance regulator angiotensin II (AngII), using the hydronephrotic kidney model.
Results: The obese rats exhibited a hyperinsulinaemic, euglycaemic state and hypertension. Urinary protein concentration and fluid intake were both increased threefold. Basal diameters of distal interlobular arteries (ILAs) and afferent arterioles (AAs) were larger in the obese rat than in the lean rat (ILA: 25.7 +/- 0.3 vs. 23.0 +/- 0.4 microm and AA: 18.8 +/- 0.3 vs. 16.7 +/- 0.5 microm, respectively; p </= 0.01), while diameters of efferent arterioles (EAs) were smaller in obese animals (14.2 +/- 1.1 vs. 18.2 +/- 1.2 microm; p </= 0.05). AngII induced a concentration-dependent constriction in ILA, AA and EA with an augmented response in the obese compared with the lean rats. Thus, at higher concentrations, AngII abolished the diameter difference between obese and lean animals in preglomerular microvessels while exaggerating that in postglomerular arterioles.
Conclusions: Our data indicate that in obese rats, a vasodilated state in small preglomerular microvessels and a vasoconstricted state in the postglomerular arterioles exist. Although AngII cancelled the former, the latter remained. Therefore, these data reveal periglomerular vascular changes that may play a role in glomerular dysfunction and renal pathology associated with obesity.