Capillary hypertension is suggested to be the underlying cause of microvascular disease affecting the kidney, the retina, and other organs and tissues in diabetic patients and animals. Hyperglycemia causes an expansion of extracellular volume, which induces a vasodilatory response. Hemodynamic adaptation to vasodilation leads to an increase in intracapillary hydraulic pressure, which subs quently causes vascular damage. In experimental animals, restoration of capillary pressure to normal levels by ingestion of a low-protein diet or administration of an angiotensin l-converting enzyme inhibitor has been s own to prevent microvascular damage in the kidney, and dietary protein restriction limits injury in the retina as well. Atrial natriuretic peptide, which is secreted by atrial myocytes in response to volume expansion, may be involved in mediation of the hemodynamic adaptation (vasodilatory response) that results in diabetic microvascular disease.

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