Enhanced prostaglandin production is postulated to contribute to altered vascular reactivity and glomerular hyperfiltration in early insulin-deficient diabetes mellitus. Rats with streptozocin-induced diabetes (STZ-D) show glomerular hyperfiltration and develop renal disease. BB rats with genetic diabetes (BB-D) also hyperfilter but have only minor renal lesions. We therefore compared glomerular and mesangial prostaglandin E2 (PGE2) production and glomerular contractility in response to pressors as a reflection of in vitro vascular reactivity in these models. Glomeruli isolated from rats with 3 wk of STZ-D produced significantly more PGE2 under basal and ionophore A23187-stimulated conditions than those from control rats. Glomeruli from BB-D rats under basal and stimulated conditions, however, generated amounts of PGE2 that were comparable to either those of nondiabetic litter mates or of normal Wistar rats. Mesangial cells cultured from glomeruli of STZ-D, BB-D, and control rats all had identical prostaglandin profiles judged by conversion of [14C]arachidonic acid. They also produced comparable amounts of PGE2 under basal conditions and after stimulation with angiotensin II or A23187, as determined by radioimmunoassay. Planar surface area of glomeruli isolated from control rats showed a dose-dependent decrease in response to angiotensin II (10−11-10−9 M). This response to angiotensin II was at least as great in glomeruli from STZ-D rats. Contraction of glomeruli from control and STZ-D rats was also comparable after vasopressin or norepinephrine. Similarly, glomeruli from BB-D and BB control rats contracted in a comparable fashion to angiotensin II and norepinephrine. We conclude that in vitro PGE2 production is enhanced in glomeruli from STZ-D rats but not in those from BB-D rats, as compared with their respective controls. Because the contractile response of isolated glomeruli to pressors was comparable in all groups, our in vitro results argue against a major role of prostaglandins in the hyperfiltration of diabetes mellitus.
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Original Articles|
December 01 1987
Comparison of Glomerular and Mesangial Prostaglandin Synthesis and Glomerular Contraction in Two Rat Models of Diabetes Mellitus
Richard Barnett;
Richard Barnett
Renal Division, Department of Medicine, Albert Einstein College of Medicine
Bronx, New York
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Linda Scharschmidt;
Linda Scharschmidt
Renal Division, Department of Medicine, Albert Einstein College of Medicine
Bronx, New York
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Young-Hyeh Ko;
Young-Hyeh Ko
Renal Division, Department of Medicine, Albert Einstein College of Medicine
Bronx, New York
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Detlef Schlondorff
Detlef Schlondorff
Renal Division, Department of Medicine, Albert Einstein College of Medicine
Bronx, New York
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Current address of R.B.: Department of Medicine, SUNY, Stony Brook, New York.
Address correspondence and reprint requests to Dr. Detlef Schlondorff, Division of Nephrology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461.
Diabetes 1987;36(12):1468–1475
Article history
Received:
April 04 1987
Revision Received:
May 04 1987
Accepted:
May 04 1987
PubMed:
3119406
Citation
Richard Barnett, Linda Scharschmidt, Young-Hyeh Ko, Detlef Schlondorff; Comparison of Glomerular and Mesangial Prostaglandin Synthesis and Glomerular Contraction in Two Rat Models of Diabetes Mellitus. Diabetes 1 December 1987; 36 (12): 1468–1475. https://doi.org/10.2337/diab.36.12.1468
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