Vascular Changes in Renal Ischemia Cell Mitosis in the Media of Arteries

Abstract

Pathological studies of the kidneys of chronically hypertensive dogs with renal ischemia by Goldblatt, Lynch, Hanzal, and Summer-ville, 1 by Verney and Vogt, 2 and by others have in general revealed only degenerative changes chiefly of the tubules, arterioles and to a lesser extent of the glomeruli. These changes have been attributed directly to the ischemia. No changes have previously been described which might have a direct relationship to the hypertensive principle of the ischemic kidney. In order to see if such changes exist studies of the more immediate as well as the chronic effects of partially obstructing the renal arteries are being made by one of us (Goormagh-tigh).

The kidneys of 12 dogs sacrificed 2 days to 18 months after compression of the renal arteries by Golblatt clamps applied at 2 consecutive lumbar operations, or by externally adjustable clamps 3 applied simultaneously have been studied. The most striking change has been observed in the media of the interlobular and glomerular arteries.

The media of these vessels is composed not only of ordinary smooth muscle cells but also of larger, more afibrillar and probably less contractile cells. 4 , 5 In the kidney these cells are found all along the arterial vascular tree and accumulate in groups at the vascular poles of the glomeruli to form the “juxta glomerular apparatus” or “polkissen”. Elsewhere in the body these cells are particularly abundant in the arterial vessels of the glomus carotidum and glomus aorticum 6 and in the vascular glomi of the skin. They are also found in a subendothelial position in the region of the carotid sinus. 6 Their close association with the carotid sinus and cardioaortic presso and chemo receptor regions suggests that their function may be connected with vaso-motor regulation.