Microspheres with diameters of from 10 to 30 mum were injected into the renal arteries of three anesthetized dogs. The six kidneys were studied by light microscopy. The diameters of the spheres trapped in the afferent arterioles and of all spheres recovered in the kidneys were recorded. On the basis of the distribution of diameters in these two populations of spheres, the average diameter of the afferent arteriole and the distribution of the afferent arteriolar diameters were estimated. The average diameter of the afferent arterioles was 16.3 mum (S.D. 2.2 mum), without any difference between three cortical layers of equal thickness. The mean diameter of spheres trapped in the interlobular arteries was 25.7 mum (S.D. 2.6). It is suggested that the pressure drop along some interlobular arteries may be of physiological importance, affecting the autoregulation of blood flow in the renal cortex.

The effect on the intracortical distribution of microspheres and radioactivity caused by steric hindrance of the free movement of spheres into afferent arterioles are described by two mathematical models. The results are compared with corresponding experimental data obtained in six kidneys from normotensive dogs. The first model (A) assumes that spheres are distributed as blood flow, regardless of their size, except for those having diameters greater than that of an afferent arteriole and which do not enter this vessel. The second model (B) includes the Ferry correction. The experimental data show that the percent recovery of spheres with diameters of 20-25 mum was significantly greater in the outer cortex and significantly less in the juxtamedullary cortex than recovery of the smaller spheres, and that the distribution of spheres with diameters of 10 mum to about 17 mum seems uninfluenced by the sphere size. The experimental results we have obtained fit best with model A. We found that according to both models steric restriction is a factor of major importance in relation to the intracortical distribution of spheres, and the analysis shows that the blood flow in the inner part of the renal cortex is grossly underestimated by the method of isotope labeled microspheres when diameters of 15 +/- 5 mum are used in the dog. Furthermore we found that dilation of the afferent arterioles will change the steric hindrance so that a redistribution of spheres and radioactivity may occur without any redistribution of blood flow. It is suggested that the results interpreted as redistribution of blood flow can be explained as due to altered steric hindrance alone, i.e., as a methodological artifact.

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SUMMARY Afferent arteriolar diameters, relative flow distribution, and flow conductance factors are estimated by nonlinear regression analysis of the sieving effect on microspheres in different vascular structures of the dog renal cortex. The data presented are from experiments in which microspheres of 10-30 fim were injected into the abdominal aorta during normotension and after lowering the blood pressure to the lower limit of autoregulation. Microscopic examination of the spheres trapped in the glomeruli and the renal arteries showed an increasing exclusion of microspheres greater than 15 fim from the afferent arterioles during normotension. This effect was most pronounced for the deeper cortical layers and can be explained mainly as geometrical exclusion of spheres from afferent arterioles. During hypotension, progressively larger microspheres entered glomeruli and afferent arterioles, presumably due to vasodilation of the vessels. There was a significant redistribution of microspheres larger than 15fim from the outer to the inner cortex during hypotension without a corresponding redistribution of smaller spheres or the estimated blood flow. Approximately the same degree of dilation of afferent arterioles was observed during autoregulatory hypotension in three cortical layers.IT IS commonly believed that the variation of the preglomerular vascular resistance during autoregulation takes place in the afferent arteriole. There is no direct evidence supporting this; neither hydrostatic pressure in this vessel nor its diameter has been measured during autoregulation. The autoregulatory changes in preglomerular vascular resistance may take place exclusively in the interlobular artery or in addition to the afferent arteriole.It also is not clear whether the variation in the preglomerular vascular resistance is identical in all of the so-called cortical layers. Lack of autoregulation in the inner medulla (dog)' and outer cortex (rat), 2 as well as identical autoregulation in all layers'' (dog), have been reported by measuring the local blood flow with various indirect methods.The intension of this study was to measure the variation in diameter of the afferent arteriole in the autoregulating dog kidney. For this purpose we used an original version of the microsphere method, the principle of which is to record the diameter population of the spheres which become trapped in (or pass through) the afferent arterioles and the population of sphere diameters presented to these vessels. 4 ' 5 Methods Mongrel dogs of either sex (body weight, 17-25 kg) were anesthetized with sodium pentobarbital (25 mg/kg given intravenously as an initial dose), and N 2 O was supplied by conventional anesthetic apparatus connected to an endotracheal tube. The arterial oxygen saturation, pH, and Pco 2 were within normal limits during the experFrom Medical Department A, University School of Medicine, Bergen, Norway.Address for reprints: Professor J. Ofstad, Medical Department A, University School of Medicine, 5016 Haukeland, Bergen, Norway.Receiv...

SUMMARY Peritubular capillary hydrostatic and oncotic forces and their relationship to the renal excretion of sodium (U Na V) were examined in 19 patients with moderate and uncomplicated essential hypertension (HT) and compared with data from 20 normotensire subjects (NT). Observations were made in hydropenia (C) and during sustained isotonlc saline volume expansion (E; 3% increase in body weight). 1 ' a The hypothesis states that this relationship is altered in essential hypertension so that a higher BP is needed for the renal excretion of a given quantity of sodium. At normal BP, sodium is therefore retained until the BP has increased enough to establish sodium and water balance.8 ' The mediators of this abnormal relationship between