Intrarenal Distribution of Blood Flow during Elevation of Ureteral Pressure in Dogs

Abstract

The ^Kr method was used to determine the effect of elevated ureteral pressure on total cortical and outer medullary nutrient renal blood flow of pentobarbital-anesthetized dogs. Increased ureteral pressure during mild saline diuresis resulted in increased total nutrient blood flow from 316 to 402 ml/100 g/min. Autoradiographs demonstrated that the increased blood flow is confined to the renal cortex and that juxtamedullary cortical and outer medullary flow is unchanged. Elevated ureteral pressure decreased total renal blood flow from 473 to 381 ml/g/min during copious mannitol diuresis. This is due at least partly to decreased cortical blood flow; we were unable to measure juxtamedullary cortical plus outer medullary blood flow during mannitol diuresis. Isolated renal arteries relaxed when placed in a physiologic salt solution containing 70 mM mannitol. Renin release is increased during elevation of ureteral pressure. We concluded that the mechanism for increased renal blood flow during ureteral occlusion selectively involves the nutrient circulation of the renal cortex.

Compensatory hypertrophy of the contralateral kidney after unilateral ureteral ligation

“…It has been shown repeatedly in acute experiments that the blocking of one ureter or the elevation of ureteral pressure produces an immediate increase of the blood flow to that kidney (Selkurt, 1963;Carlson & Sparks, 1970;Suki et al 1971). It has been shown in experiments on rabbits that 24 hr after the obstruction of one ureter the blood supply to that kidney had decreased (Herdman & Jaco, 1950) and that after 1 week it had dropped by 60% (Idbohrn & Muren, 1956).…”

Microcomputed tomography of kidneys following chronic bile duct ligation

“…This redistribution of intrarenal blood flow has been described in a variety of conditions such as reduccapacity secondary to increased portal pressure has been reported in cirrhotic rats without ascites [45]. Furthertion of renal artery perfusion pressure [35], hemorrhagic hypotension [36], ureteral occlusion [37], sodium restricmore, increased renal venous pressure has been reported in human cirrhosis [46]. The increase in renal venous tion [38], and renal venous pressure elevation [39].…”

Effect of Local Metabolic Factors on Vascular Smooth Muscle

“…no evidence of release of vasoactive substances into renal venous blood (88). Cortical blood flow was raised by hypertonic mannitol which also relaxed isolated renal artery strips (38). The vasoconstriction response to angiotensin I1 was markedly reduced by elevated arterial osmolarity (171).…”