Hypertension in short-term experimental diabetes. possible role of nitric oxide

Abstract EN

Background: cardiovascular disease is the most frequent cause of death and disability in diabetes mellitus.

Complications of IDDM represent vascular dysfunction that has its origin in the endothelium.

Dysfunction of vascular endothelium is important in the pathogenesis of micro-and macro-angiopathy.

Lack of nitric oxide is incriminated in the pathogenesis of vascular dysfunction and small vessel complications.

Aim of the work: the study was planned to investigate the mechanism(s) of vascular dysfunction in diabetes by assessment of vascular reactivity in experimentally-induced diabetic rats.

Materials & Methods: this comprised 2 groups of rats.

Group I: 2-week control group.

Group II: 2-week diabetic group, in which experimental diabetes was induced by injection of streptozotocin (STZ) in a dose of 40 mg / kg body weight.

Two weeks from the onset of diabetes, animals were subjected to determination of body weight, blood glucose, recording of ECG and assessment of baroreflex function.

In vitro vascular reactivity was studied, using isolated aortic rings, to determine the contractile and relaxant responses to vasoactive agents.

Nitrate, the metabolic end-product of nitric oxide (NO), was measured in plasma and aortic tissues. Results: STZ-induced diabetes produced rise of blood glucose >300 mg / dl and loss of body weight.

Associated with this 2-week diabetes, all blood pressure parameters rose significantly above levels reached in non-diabetic controls.

Baroreflex function revealed that the net pressor responses to phenylepherine were unaltered, while the net depressor responses to sodium nitroprusside were exaggerated.

The Baroreflex calculated gain was not significantly changed.

Reductions in plasma nitrate levels were displayed by the 2-week diabetic rats.

In vitro reactivity of aortic rings isolated from diabetic rats showed a significant inhibition of their response to acetylcholine.

These effects were associated with significant reduction in aortic tissue nitrate levels. Conclusions: hypertension was produced in experimental diabetes as early as two weeks.

It may be explained by the defective vasorelaxation, as a result of hyperglycemia and reduced nitric oxide availability.