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Laboratory of Experimental Hypertension and Vasoactive Peptides, Clinical Research Institute of Montreal, Université de Montréal, Montreal, Quebec, Canada H2W 1R7
It has been shown
that glomerular ANG II receptors are downregulated and protein kinase C
(PKC) activity is enhanced in diabetes mellitus. Therefore, we
investigated glomerular and preglomerular vascular ANG II receptors and
PKC isoform regulation in streptozotocin (STZ)-diabetic rats treated
with insulin and/or captopril. Diabetic rats were prepared by injecting
STZ (60 mg/kg). Those that developed diabetes after 48 h were treated
with low or high doses of insulin, or with a low dose of insulin as
well as captopril, and killed 14 days later. Their glomeruli and
preglomerular vessels were purified, competitive binding studies were
performed by using the ANG II antagonists losartan and PD-123319, and
PKC analysis was carried out by Western blotting. Competitive binding
studies showed that the AT1 receptor was the only ANG II
receptor detected on both glomeruli and preglomerular vessels of all
groups. Preglomerular vascular AT1 receptor density
(Bmax) was significantly upregulated in low insulin-treated
STZ rats, whereas glomerular AT1 Bmax was downregulated. Furthermore, both the captopril- and high
insulin-treated groups had less glomerulosclerosis and vascular damage
than the low insulin-treated group. PKC
, PKC
, PKC
, and PKCµ
isoforms found in preglomerular vessels were upregulated by captopril
and high insulin doses, respectively, whereas no such regulation
occurred in glomeruli. We conclude that in STZ-diabetic rats ANG II
receptors and PKC isoforms on preglomerular vessels and glomeruli are
differentially regulated by treatment with insulin and/or captopril.
angiotensin-converting enzyme; receptors; streptozotocin; insulin
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