Intrarenal Hemodynamic Changes Research Articles

Effect of renal sympathetic nerve stimulation on proximal water and sodium reabsorption.

The renal responses to sympathetic nerve stimulation were studied in saline-expanded rats. The left kidney was partially denervated by crushing the left greater splanchnic nerve. Then the distal portion of the nerve was stimulated with square wave pulses of 0.5 ms duration, voltage twice threshold, and 1 or 2 Hz frequency while monitoring the compound action potential. Fibers with conduction speeds of 13-17 m-s-1 and of 0.7-1 m-s-1 were identified. Only stimulation of the latter appeared to produce changes in renal Na and water excretion. Whole kidney and individual nephron studies were performed alternating control and nerve stimulation periods. Nerve stimulation produced approximately a 25% reduction of the left kidney urine volume and sodium excretion. Glomerular filtration rate and renal plasma flow remained unchanged. Right kidney Na and water excretion, glomerular filtration rate, and renal plasma flow remained constant. In the left kidney, during nerve stimulation, the tubular fluid to plasma inulin concentration ratio increased significantly in the late proximal tubule. We conclude that the antidiuresis and antinatriuresis seen during sympathetic nerve stimulation were caused by increased sodium and water reabsorption in the proximal tubule, probably mediated by the stimulation of slowly conducting unmyelinated fibers. These responses appeared to be unrelated to systemic or intrarenal hemodynamic changes.

Effects of acute unilateral renal denervation in the rat.

Studies were undertaken to characterize the renal responses to acute unilateral renal denervation and the mechanisms involved in these responses. Denervation was produced in anesthetized nondiuretic rats by application of phenol to the left renal artery. Studies were also performed in sham-denervated nondiuretic rats. Whole kidney and individual nephron studies were performed before and after denervation or sham denervation. Denervation increased urine volume from the left kidney to about twice its control value (P less than 0.001) and increased urinary sodium excretion from 332 neq min minus -1 to 1,887 neq min minus -1 (P less than 0.001). Glomerular filtration rate (GFR) and renal plasma flow (RPF) remained unchanged in both kidneys after the procedure. The innervated right kidney showed no changes in urine volume or in sodium excretion. After denervation, late proximal ratio of tubular fluid inulin concentration to that of plasma [(F/P)In] decreased from 2.23 to 1.50 (P less than 0.001) while single nephron GFR remained unchanged. Absolute reabsorption decreased from 16.5 to 9.9 n. min minus -1 (P less than 0.001). (F/P)In ratios were also decreased in early distal (from 6.21 to 3.18, P less 0.001) and late distal convolutions (from 16.41 to 8.33, P less than 0.001) during the experimental period. (F/P)Na ratios remained unchanged in the early distal convolutions, but increased from 0.18 to 0.38 (P less than 0.01) in late distal convolutions after denervation. Absolute Na reabsorption after denervation increased in the loop of Henle, distal convolution, and collecting ducts. Any changes in intrarenal hydrostatic pressures after denervation were always small. There were no changes in GFR, RPF, urine volume, urinary sodium excretion, or late proximal (F/P)In after sham denervation. We conclude that the diuresis and natriuresis seen after acute renal denervation were caused by a marked depression of sodium and water reabsorption in the proximal tubule with partial compensation in more distal nephron segments. These responses appeared to be unrelated to systemic or intrarenal hemodynamic changes. The results demonstrate an effect of the renal nerves on proximal tubular function.

Sequential changes in intrarenal hemodynamics during saline infusion in the dog

Intrarenal blood flow and volume (indicator-dilution technique), kidney volume (mercury-in-rubber resistance gage), intr-renal venous pressure, filtration fraction, and sodium excretion were determined dequentially before and during a l-h infusion of isotonicsaline 80 ml/kg in anesthetized dogs. The cortical fraction of renal blood flow roseduring the first 20 min of infusion from an average of 70 to 77%, butreturned nearly to control levels during the last 20 min of infusion because ofa low rise in noncortical flow. During the first 20 min a 23% increase in cortical blood volume accounted for one-third of the 8.5% increase in kidney volume, whereasin the last 20 min cortical blood volume had fallen nearly to control values and kidneyvolume was increased by 17.2%. Intrarenal resistances calculated from intrarenalpressure and flow indicated persistent cortical prevenous dilatation, progressive cortical venous constriction, and only a slight late reduction in noncortical resistance. These data indicate that hemodynamics are shanging continuously during saline infusion and the natriuresis probably is multifactorial.

Renal vascular resistance and aortic pressure as determinants of sodium reabsorption.

During induced renal vasodilatation, angiotensin and norepinephrine result in an increased excretion of sodium (UNaV), which has been attributed to transmission of elevated aortic pressure (PA) to peritubular capillaries and not to direct effects of the drugs on sodium reabsorption. The importance of PA, intrarenal hemodynamics, and other possible effects of angiotensin and norepinephrine was examined in anesthetized dogs in which one kidney was vasodilated by denervation or acetylcholine, and the opposite kidney served as control. During elevation of aortic pressure, following bilateral carotid occlusion and vagotomy (B.C.O. and V), infusion of angiotensin and norepinephrine, increased UNaV occurred on only the vasodilated side. Changes in UNaV on both sides are related inversely to renal vascular resistance (R.V.R.) before elevation PA, but not to changes in R.V.R., glomerular filtration rate (G.F.R.), or filtration fraction following elevation of PA. When renal perfusion pressure was controlled during aortic constriction, persistent increases in UNaV and urine flow rate were abolished during infusion of norepinephrine and after B.C.O. and V, and markedly reduced during infusion of angiotensin. These effects could not be attributed to changes in intrarenal hemodynamics. Thus increased sodium and water excretion following infusion of norepinephrine and angiotensin, and B.C.O. and V, can be largely attributed to an interplay of increased renal perfusion pressure and reduced preset renal vascular resistance.

Répercussions hémodynamiques rénales de la surcharge salée aiguë isotonique chez le chien

Intrarenal hemodynamic changes during acute isotonic saline loading in the dog. 85 Kr autoradiograms, perfusions of silastic and injections of thioflavine S labelled red blood cells (R.B.C.) have been used to study the intrarenal hemodynamic changes induced in the dog by an acute isotonic expansion of the extracellular fluid volume. The silastic injected specimens showed a generalized vasodilatation, without however, any change of the diameter of the glomerular tufts. As the ratio of the number of labelled R.B.C. of the superficial glomeruli to the number of the R.B.C. of the juxtamedullary glomeruli has decreased, we can conclude that the relative juxtamedullary glomerular capillary volume has increased. The autoradiographs showed that the velocity of the blood flow increased in the superficial cortex and the vasa recta and decreases in the juxtamedullary cortical region. This slowing seems to be due to the marked dilatation of the capillary bed of the latter region. It is then concluded that the natriuresis could be linked mainly to changes of peritubular factors induced by the vasodilatation which is itself more marked in the juxtamedullary cortex. Repercussions hemodynamiques renales de la surcharge salee aigue isotonique chez le chien. Les changements hemodynamiques intrarenaux ont ete etudies chez des chiens soumis a une surcharge salee isotonique aigue, a l'aide d'autoradiographies au Kr 85 , de perfusion de silastic et d'injections de globules rouges marques a la Thioflavine S. La surcharge a entraine une vasodilatation renale generalisee (moules au silastic). Le decompte des globules rouges marques par glomerule montra une diminution du leur nombre dans les glomerules superficiels par rapport aux glomerules juxtamedullaires. Ceci traduit une augmentation relative du volume capillaire glomerulaire juxtamedullaire. Par ailleurs, la vitesse du flux sanguin (autoradiographies) a augments dans le cortex superficiel, les vasa recta et diminue dans la region juxtamedullaire. Une dilatation excessive du lit capillaire de cette derniere semble expliquer le ralentissement de son flux sanguin. Le diametre des floculi glomerulaires n'a pas change sous l'effet de la surcharge. La natriurese peut ainsi etre reliee principalement a la baisse de reabsorption tubulaire secondaire aux changements des facteurs peritubulaires induits par la vasodilatation, elle-meme maximale au niveau du cortex interne.

Intrarenal hemodynamics in glycerol-induced myohemoglobinuric acute renal failure in the rat.

A modified 138 Xe washout technique was used to study changes in intrarenal hemodynamics during glycerol-induced acute renal failure in the rat. Within 10 minutes after glycerol injection, the flow fraction supplied to component 1 of the washout curve ("cortex A") decreases, reaching minimum values 24 hours afer glycerol (31% of control conditions). Seven days thereafter five of the rats, still uremic, showed cortical flow fractions less than 50% of control values. Nine others had recovered. Twenty-four hours after glycerol, renal blood flow was 27% and increased to 86% of control conditions in the recovered rats 7 days after glycerol. 85 Kr autoradiographs and silicone rubber casts of the renal vasculature demonstrated a severe cortical hypoperfusion at the height of oliguria that gradually disappeared in parallel with the functional recovery of the kidney. These observations, in good agreement with micropuncture data, suggest that oliguria and renal insufficiency in this experimental model are the result of a primary decrease in glomerular filtration rate due to an increased preglomerular resistance.

Effects of diazoxide on renal function in the dog.

SummaryRenal clearance and stop flow studies were done in dogs before and after infusion of diazoxide directly into the left renal artery. In all animals the left kidney showed a prompt diuresis, natriuresis and increase in creatinine or inulin clearance when diazoxide was given. No inhibition of distal tubular sodium reabsorption following diazoxide administration was found using the stop flow technique. The natriuresis produced by infusing diazoxide directly into the renal artery is probably due to renal vasodilation and resulting changes in intrarenal hemo-dynamics.

Intrarenal hemodynamic changes following acute partial renal artery occlusion.

BRAKE, CHARLES M.; REINS, DALE; WITTMERS, LORENZ E.; HINSHAW, LERNER B. Author Information

EFFECT OF MANNITOL ON THE KIDNEY: CHANGES IN INTRARENAL HEMODYNAMICS.

THE use of hypertonic mannitol as an osmotic diuretic has captured the attention and imagination of investigators and clinicians alike in the past several years. First used widely by physiologists to promote urine flow during studies of general renal physiology, it was reported in 1945 by Selkurt1 to improve renal function in a dog's kidney after a period of ischemia. This study led to the use of mannitol in clinical situations involving a decrease in renal blood flow or the presence of circulating nephrotoxic substances.2,3 The result of this interest has led to significant investigation of the renal, as . . .

ANGIOGRAPHIC ANALYSIS OF RENAL VASOCONSTRICTION.

The effects of renal nerve stimulation, catecholamine infusion, and renal vein constriction on intrarenal vessel calibers were studied in dogs with a technique which combined renal perfusion at constant flow with selective angiography of the kidney. Equivalent elevations of total renal vascular resistance by nerve stimulation and catecholamine infusion resulted in different intrarenal hemodynamic changes. Nerve stimulation elicited constriction of both the large and small arterial segments, whereas the catecholamines constricted only the smaller segments while the renal and interlobar segments were passively dilated. Either no change or a decrease in the size of the interlobar and arcuate arteries was noted during renal vein constriction. It was concluded that intrarenal hemodynamics are affected differentially by the neurogenic and humoral components of the sympathetic nervous system.

Mechanisms of intrarenal hemodynamic changes following acute arterial occlusion.

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.