Diabetes-associated mesenteric vascular hypertrophy is attenuated by angiotensin-converting enzyme inhibition

Mark E. Cooper, Jonathan Rumble, Radko Komers, Du He-Cheng, Karin Jandeleit, Chou Sheung-To

Research output: Contribution to journalArticle

76 Citations (Scopus)

Abstract

In experimental diabetes, the mesenteric vascular tree undergoes hypertrophy, and this is associated with an increase in mesenteric angiotensin-converting enzyme (ACE) levels. The aim of this study was to determine if inhibition of mesenteric ACE by ACE inhibition would influence diabetes-associated mesenteric vascular hypertrophy. Control or streptozocin- induced diabetic rats were randomized to receive no drug or the ACE inhibitor perindopril. In addition, other diabetic rats were randomized to receive either low-dose insulin that does not alter glycemic control or high-dose insulin, administered as a silastic pellet to achieve euglycemia. After 3 weeks, animals were killed for measurement of mesenteric ACE, vessel weight, and wall:lumen ratio. Diabetes was associated with increased mesenteric ACE levels, increased vessel weight, and an increase in the wall:lumen ratio. ACE inhibition, despite no effect on glycemic control, food intake, urinary urea excretion, or gut weight, prevented the increase in mesenteric ACE levels and attenuated mesenteric vascular hypertrophy as assessed by weight or wall:lumen ratio. The increase in staining by an antibody to the endothelial product, von Willebrand factor, in diabetic rats was totally prevented by perindopril treatment. Euglycemia but not low-dose insulin therapy in the diabetic rats normalized mesenteric vessel ACE, weight, and wall:lumen ratio. In conclusion, ACE inhibition may have a specific role in preventing diabetes-associated vascular hypertrophy, an important process in the genesis of micro- and macrovascular diabetic complications.

Original languageEnglish (US)
Pages (from-to)1221-1228
Number of pages8
JournalDiabetes
Volume43
Issue number10
StatePublished - 1994
Externally publishedYes

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Peptidyl-Dipeptidase A
Hypertrophy
Blood Vessels
Weights and Measures
Perindopril
Insulin
von Willebrand Factor
Diabetes Complications
Streptozocin
Angiotensin-Converting Enzyme Inhibitors
Urea
Eating
Staining and Labeling
Antibodies

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Cooper, M. E., Rumble, J., Komers, R., He-Cheng, D., Jandeleit, K., & Sheung-To, C. (1994). Diabetes-associated mesenteric vascular hypertrophy is attenuated by angiotensin-converting enzyme inhibition. Diabetes, 43(10), 1221-1228.

Diabetes-associated mesenteric vascular hypertrophy is attenuated by angiotensin-converting enzyme inhibition. / Cooper, Mark E.; Rumble, Jonathan; Komers, Radko; He-Cheng, Du; Jandeleit, Karin; Sheung-To, Chou.

In: Diabetes, Vol. 43, No. 10, 1994, p. 1221-1228.

Research output: Contribution to journalArticle

Cooper, ME, Rumble, J, Komers, R, He-Cheng, D, Jandeleit, K & Sheung-To, C 1994, 'Diabetes-associated mesenteric vascular hypertrophy is attenuated by angiotensin-converting enzyme inhibition', Diabetes, vol. 43, no. 10, pp. 1221-1228.
Cooper ME, Rumble J, Komers R, He-Cheng D, Jandeleit K, Sheung-To C. Diabetes-associated mesenteric vascular hypertrophy is attenuated by angiotensin-converting enzyme inhibition. Diabetes. 1994;43(10):1221-1228.
Cooper, Mark E. ; Rumble, Jonathan ; Komers, Radko ; He-Cheng, Du ; Jandeleit, Karin ; Sheung-To, Chou. / Diabetes-associated mesenteric vascular hypertrophy is attenuated by angiotensin-converting enzyme inhibition. In: Diabetes. 1994 ; Vol. 43, No. 10. pp. 1221-1228.
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