Format

Send to

Choose Destination
Am J Hypertens. 1995 Sep;8(9):915-20.

Insulin induces medial hypertrophy of myocardial arterioles in rats.

Author information

1
Department of Internal Medicine, Edith Wolfson Medical Center, Holon, Israel.

Abstract

To investigate the effect of hyperinsulinemia on arteriolar hypertrophy, myocardial hypertrophy, and blood pressure, we administered insulin intraperitoneally to SHR and WKY rats for 3 consecutive weeks. To prevent hypoglycemia, the drinking water contained 10% sugar, and to accentuate the blood pressure, their chow contained 8% table salt. Blood pressure was measured by the tail-cuff method. Heart weights were factored with body weights. Arterioles of approximately 100 microns in diameter were examined at the end of the experiment and the vascular wall thickness was factored with the lumen diameter. At the end of 3 weeks, blood pressure rose in the SHR but not in the WKY rats. The heart weights in the WKY normotensive rats did not increase, whereas in the SHR they did. Furthermore, there was a significant rise in vessel wall thickness in the rats that received insulin, whether there was a rise in blood pressure or not and whether they had an increase in heart weight or not. There was a similar rise in blood glucose in all the groups, with slightly more accentuated rise in the SHR that received insulin. Nevertheless the increase in vascular wall thickness occurred only in the groups which received insulin. This seems to preclude the importance of hyperglycemia per se as the causative agent for the increase in vascular wall thickness in this study. The increase was in the form of medial hypertrophy without any sign of atherosclerosis. It seems, therefore, that hyperinsulinemia is associated with hypertrophy of the media of arterioles regardless of the increase in heart weight or the rise in blood pressure.

PMID:
8541007
DOI:
10.1016/0895-7061(95)00157-K
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Silverchair Information Systems
Loading ...
Support Center