Membrane abnormalities of vascular smooth muscle of mesenteric arteries of spontaneous diabetic BB rats.
Mesenteric arteries were isolated from the spontaneous diabetic BB rats, non diabetic BB rats and regular Wistar control rats. Gross morphology indicated that the mesenteric vascular bed of the control Wistar rats had a normal development of mesenteric fat pad around the vessels, while that of the diabetic BB rats showed drastically reduced perivascular fat pad, suggesting greater mobilization of fat for energy consumption in the hyperglycemic state of diabetes mellitus. The perivascular mesenteric fat pad of the non-diabetic BB rats was intermediate between those of the Wistar control and diabetic BB rats. The wet weight of the mesenteric arteries following removal of fat, vein and connective tissues was significantly greater in diabetic BB rats than in the corresponding controls. Microsomal membranes isolated from the mesenteric arteries of diabetic BB rats showed increased alkaline phosphatase and 5'-nucleotidase activities compared to those isolated from the two groups of non-diabetic control rats. Acid phosphatase activities were higher in both BB rat groups compared to the Wistar group. The total Ca2+ uptake by the microsomes of mesenteric arteries in the presence of ATP was not different among three experimental groups, but the ATP dependent active transport of Ca2+ was significantly increased and the passive Ca2+ binding was significantly reduced in diabetic group compared to the other two non-diabetic groups. Our results demonstrate that in the spontaneously diabetic BB rats, alterations in both structural and functional parameters may underline the vascular complications associated with type I diabetes mellitus in humans.
Kwan
C Y
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Department of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada. kwancy@fhs.mcmaster.ca
D015720:5'-Nucleotidase / Q000378:metabolism; D000135:Acid Phosphatase / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D001692:Biological Transport / Q000187:drug effects / Q000502:physiology; D017301:Ca(2+) Mg(2+)-ATPase / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism / Q000473:pathology*; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism / Q000473:pathology*; D003576:Electron Transport Complex IV / Q000378:metabolism; D008297:Male; D008638:Mesenteric Arteries / Q000201:enzymology / Q000473:pathology*; D008861:Microsomes / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000201:enzymology / Q000473:pathology*; D009247:NADH, NADPH Oxidoreductases / Q000378:metabolism; D009251:NADPH-Ferrihemoprotein Reductase; D009929:Organ Size; D043264:Phosphodiesterase I; D010727:Phosphoric Diester Hydrolases / Q000378:metabolism; D051381:Rats; D011913:Rats, Inbred BB; D017208:Rats, Wistar
D000255:Adenosine Triphosphate; D009247:NADH, NADPH Oxidoreductases; D009251:NADPH-Ferrihemoprotein Reductase; D003576:Electron Transport Complex IV; D000469:Alkaline Phosphatase; D000135:Acid Phosphatase; D015720:5'-Nucleotidase; D010727:Phosphoric Diester Hydrolases; D043264:Phosphodiesterase I; D017301:Ca(2+) Mg(2+)-ATPase; D002118:Calcium