Mechanisms of intrarenal hemodynamic changes following acute arterial occlusion

¹ Civil Aeromedical Research Institute, Federal Aviation Agency, and Department of Physiology, University of Oklahoma Medical School, Oklahoma City, Oklahoma

The hemodynamic response of the kidney to acute arterial occlusion is poorly understood. The purpose of the present study was to determine intrarenal hemodynamic changes in intact and isolated kidneys following arterial occlusion. The relative roles of metabolic, myogenic, and tissue pressure influences on the postocclusion response were evaluated. The response of the kidney to occlusion was found to be complex, depending on the interaction of a variety of physical and humoral forces. Increases in renal resistance appeared to be due, in part, to adrenergic agents and were enhanced by extending time of occlusion and lowering the arterial pressure. The combined effects of prevenous dilatation and diminished tissue pressure resulted in a decreased resistance following shorter periods of occlusion. Prevenous dilatation was accounted for by depressed vascular sensitivity to pressor agents and the presence of vasodilator substances. Changes in venous segment resistance were found to be of primary importance in both the autoregulatory phenomenon and the postocclusion hyperemic response to short (15-sec) occlusion periods.

Note:
With the Assistance of Frederick D. Masucci

Key Words: renal arterial occlusion • intrinsic renal humoral agents • renal ischemia and hyperemia • renal reactive hyperemia • renal constriction and dilatation • autoregulation and reactive hyperemia • intrinsic renal constrictor mechanisms • renal segmental resistances • kidney and hypotension (shock) • renal vascular resistance • renal hypoxia

Submitted on April 30, 1963