Papillary Plasma Flow Research Articles

Papillary plasma flow and tissue osmolality in chronic caval dogs

ARTICLESPapillary plasma flow and tissue osmolality in chronic caval dogsP. F. Faubert, S. Y. Chou, J. G. Porush, I. J. Belizon, and S. SpitalewitzP. F. Faubert, S. Y. Chou, J. G. Porush, I. J. Belizon, and S. SpitalewitzPublished Online:01 Apr 1982https://doi.org/10.1152/ajprenal.1982.242.4.F370MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByVisualization of the intrarenal distribution of capillary blood flow22 April 2019 | Physiological Reports, Vol. 7, No. 8Influence of renal prostaglandins and dietary linoleate on hypertension in Dahl S rats.Hypertension, Vol. 4, No. 3_pt_2 More from this issue > Volume 242Issue 4April 1982Pages F370-F378 Copyright & PermissionsCopyright © 1982 the American Physiological Societyhttps://doi.org/10.1152/ajprenal.1982.242.4.F370PubMed7065246History Published online 1 April 1982 Published in print 1 April 1982 Metrics

Renal concentration defect following nonoliguric acute renal failure in the rat

The mechanism of impaired renal concentrating ability following nonoliguric ischemic acute renal failure was studied in the rat. Fifty min of complete occlusion of the renal artery and vein with contralateral nephrectomy resulted in reversible, nonoliguric acute renal failure. Eight days following induction of acute renal failure, a defect in 30 hr dehydration urine osmolality was present when experimental animals were compared with uninephrectomized controls (1,425 +/- 166 versus 2,267 +/- 127 mOsm/kg water respectively, P less than 0.001). Comparable postdehydration plasma vasopressin levels in experimental and control animals and an impaired hydro-osmotic response to exogenous vasopressin in experimental animals documented a nephrogenic origin of the defect in urine concentration. Lower urinary excretion of prostaglandin E2 in experimental animals and a failure of cyclo-oxygenase inhibition with 10 mg/kg of indomethacin to improve dehydration urine osmolality suggested that prostaglandin E2 antagonism of vasopressin action did not contribute to the concentration defect. Postdehydration inner medullary (papillary) interstitial tonicity was significantly reduced in experimental animals versus controls (870 +/- 85 versus 1,499 +/- 87 mOsm/kg water respectively, P less than 0.001). To determine if this decreased interstitial tonicity was due to vascular mechanisms, papillary plasma flow was measured and found to be equivalent in experimental and control animals. To examine a role for biochemical factors in the renal concentration defect, cyclic nucleotide levels were measured in cytosol and membrane fragments. A decrease in vasopressin and sodium fluoride-stimulated adenylate cyclase was found in outer medullary tissue of experimental animals. In contrast, vasopressin-stimulated adenylate cyclase activity was comparable in the inner medullary tissue of control and experimental animals. Our study suggests a defect in generation of renal inner medullary interstitial solute as a mechanism of the impaired urinary concentration observed in this model of acute renal failure.

Potassium Citrate Feeding Protects against Nephron Loss in Severe Sodium Chloride Hypertension in Rats

1. Potassium citrate did not significantly increase plasma flow to the renal papilla in normotensive Dahl R rats on either low or high NaCl diets. Similarly, potassium citrate did not significantly increase papillary plasma flow in mildly hypertensive Dahl S rats on low NaCl diets. Thus potassium citrate feeding did not ordinarily alter papillary plasma flow. 2. When S rats were fed on a high (4%) NaCl diet for 24 weeks, they became severely hypertensive and developed nephrosclerosis with nephron loss. This accounted for the significant reduction in papillary plasma flow in S rats on 4% high NaCl diet with no potassium supplementation. 3. When S rats on high NaCl diet were given a supplement of KCl, they still developed severe hypertension and almost the same fall in papillary plasma flow, suggesting a similar degree of nephron loss from nephrosclerosis. 4. However, when S rats on high NaCl diet were given a supplement of potassium citrate, they still developed the same severe hypertension but, in contrast, they did not have a decrease in papillary plasma flow. This actually increased to 7% higher than in comparable S rats eating the low NaCl diet. Moreover, S rats receiving potassium citrate supplements in their high NaCl diet had a papillary plasma flow which was 34% higher than that of S rats receiving no potassium supplement in the high NaCl diet (P < 0.005) and was 19% higher than that of S rats receiving KCl supplements in the high NaCl diet (P < 0.04). This occurred even though the rats receiving potassium citrate were severely hypertensive. 5. Thus potassium citrate feeding protected against nephron loss from nephrosclerosis during severe NaCl-induced hypertension, whereas KCl feeding did not provide such protection.

Renal function studies in an experimental model of papillary necrosis in the rat.

Twenty four hours after i.v. injection of bromoethylamine-hydrobromide (BEA) in rats, a uniform papillary necrosis is observed. The present study investigates the renal functional and the papillary haemodynamics in response to acute volume expansion (12% of body weight) in this model. Renal function studies were performed in hydropenic and volume expanded sham- or BEA-injected rats. In hydropenic normal animals a GFR of 1.97 +/- 0.14 ml/min, an urinary osmolarity (UOsm) of 1 011 +/- 94.5 mOsm/kg and a fractional sodium excretion (FENa) of 0.18 +/- 0.026% were obtained. In contrast, BEA-treated hydropenic animals showed a lower GFR (1.16 +/- 0.14 ml/min), UOsm (469 +/- 30.31 mOsm/kg) and a higher FENa (0.37 +/- 0.06%). In volume expansion a similar UOsm and FENa were obtained in both groups. The papillary plasma flow (PPF) was measured in each of the experimental groups by the albumin accumulation technique. The mean value in hydropenic normal animals was 50.65 +/- 2.12 m 100 g-1 min-1 and increased to 66.02 +/- 2.00 ml 100 g-1 min-1 after volume expansion (P less than 0.001). In BEA rats the PPF was 58.86 +/- 2.33 ml 100 g-1 min-1 in hydropenia (P less than 0.01 vs. control animals) and remained unchanged after volume expansion. Thus, during hydropenia, BEA-induced papillary necrosis results with a salt wasting state and an urinary concentration defect. After volume expansion no disturbance in sodium excretion capacity was observed. These results are compatible with the nephron-heterogeneity concept in the regulation of sodium excretion. The histological lesions cannot be explained by a decreased renal papillary plasma flow.

Role of medullary hemodynamics in the natriuresis of drug-induced renal vasodilation in the rat.

In contrast to most renal vasodilators, such as acetylcholine (ACh), secretin increases renal blood flow in the dog without a marked effect on sodium excretion (UNaV). To investigate this observation, we studied the relationship between renal vasodilation, UNaV, and papillary plasma flow (PPF) in rats, infused either with ACh or secretin into the aorta at the level of both renal arteries. ACh significantly increased GFR, PAH clearance, and UNaV (delta + 0.35 ml/min, + 2.11 ml/min and + 1.77 muEq/min, respectively; P < 0.05). PPF rose from 50 +/- 2.6 ml/min 100 g (mean +/- SE) in control rats to 91 +/- 4.7 ml/min 100 g after ACh (p < 0.001). Despite a similar increase in PAH clearance after secretin (+ 2.21 ml/min; P < 0.01), UNaV remained unchanged and PPF was only slightly, although significantly, increased (from 50 +/- 2.6 ml/min 100 g to 65 +/- 2.75 ml/min 100 g; P < 0.05). Both total kidney and papillary vasodilation, and the increase in UNaV after ACh were blocked by previous administration of meclofenamate (M), a prostaglandin inhibitor. No effect of M in secretin-infused rats was observed. In conclusion, the relationship between a total renal vasodilation and natriuresis was dissociated with secretin, but not with ACh. However, a relationship between the natriuresis and influence on papillary hemodynamics was observed with both vasodilators. Finally, the renal hemodynamic and natriuretic effects of ACh are probably mediated by prostaglandin release.

Effect of potassium deficiency on papillary plasma flow in the rat.

Chronic potassium (K+) deficiency has been shown previously to cause a reduction in solute content in the renal papilla, an effect that is potentially important as a contributing factor to the concentrating defect seen in this circumstance. The cause of the decrease in papillary solute content has not been adequately explained. Because alterations in the blood flow rate through the renal papilla may affect the solute content of the papilla, the present experiments examined the effect of chronic K+ deficiency on papillary plasma flow (PPF) in the rat. PPF was measured by the radioactive albumin accumulation technique. Sprague-Dawley rats were fed identical quantities of water and either a normal or a K+-deficient diet for 21 days. Total GRR in the control rats, 1.7 +/- 0.17 (SE) ml/min, was similar to that in K+-deficient rats, 1.4 +/- 0.14 ml/min (P greater than 0.01). Total [3H]PAH clearance was also comparable in the two groups, i.e., 4.4 +/- 0.47 in control and 4.7 +/- 0.45 ml/min in K+-deficient rats (P greater than 0.06). PPF was significantly lower in K+-deficient rats, 19.7 +/- 1.1 ml-min-1-100 g-1, than in control rats, 59.8 +/- 1.6 ml-min-1-100 g-1 (P less than 0.001). The decrease in PPF in the K+-deficient rat may reflect a reduction in perfusion to the juxtamedullary nephrons, thereby resulting in a diminution in both solute delivery and blood flow to the papilla.

Papillary plasma flow in experimental pyelonephritis in rats: effect of antibiotic therapy and indomethacin.

Abstract A defect in Umax is the earliest functional abnormality in pyelonephritis. Administration of inhibitors of renal prostaglandin synthesis (e.g., indomethacin) rapidly and transiently reverse the defect in Umax, suggesting that the defect is mediated by renal prostaglandins. Because medullary prostaglandin synthesis may increase papillary plasma flow which may result in a defect in Umax, papillary plasma flow was determined by measuring the accumulation of 125 I-albumin in the renal papilla of normal rats and rats with early bilateral enterococcal pyelonephritis. In addition, the effect of antibiotic treatment and indomethacin on papillary plasma flow in the infected kidney was determined. Papillary plasma flow was found to be significantly lower in infected rats than in normal rats: 21.9 vs. 31.8 ml/min/100 gm (p

Studies on the mechanism of reduced urinary osmolality after exposure of renal papilla.

Studies were performed in Munich-Wistar rats to determine whether changes in papillary plasma flow might be responsible for the concentrating defect which occurs after exposure of the extrarenal papilla. Papillary plasma flow was measured by (125)I-albumin accumulation. Initial studies in hydropenic animals revealed that papillary plasma flow was 40% higher in the kidney with the exposured papilla, 41 vs. 29 ml/min per 100 g of papilla (P < 0.001). This increase in papillary plasma flow was detectable 15 or 45 min after removing the ureter. Because it was unclear whether the rise in papillary plasma flow was a cause or the result of the fall in urine osmolality, similar studies were performed in animals undergoing a water diuresis. In this setting, papillary plasma flow still increased on the exposed side compared to the control side, 81 vs. 60 ml/min per 100 g, despite similarly low urine osmolalities of 155 and 174 mosmol/kg, respectively. This finding is compatible with the possibility that papillary exposure per se causes an increase in papillary plasma flow and that this hemodynamic alteration may lead to a reduction in urinary osmolality secondary to washout of the medullary interstitium. A final group of hydropenic rats was given either indomethacin or meclofenamate before removing the ureter. In these studies, there was no difference in either the papillary plasma flow or the urine osmolality between control and exposed kidneys. It is therefore suggested that opening the ureter induces an increase in papillary plasma flow by some mechanism which may involve an alteration in prostaglandin synthesis.

Low renal papillary plasma flow in both Dahl and Kyoto rats with spontaneous hypertension.

Abnormally low plasma flow to renal papilla characterizes Dahl hypertension. When eating a normal Na diet (0.3% NaCl) both hypertension-sensitive (S) rats and hypertension-resistant (R) rats, 16 weeks old, have fairly normal blood pressure (BP), averaging 144 and 129 mm Hg, respectively. However, even in this barely hypertensive state, 18 S rats had a 31% lower papillary plasma flow (Lilienfield method) than 22 R rats, 19.2 ml/100 g of papilla per min compared to 25.6 (P less than 0.001). When a high (8%) NaCl diet was fed for 7 days, R rats increased papillary plasma flow from 25.6 on 0.3% NaCl to 33.8 on 8% NaCl, a 32% rise (P less than 0.001). S rats increased papillary flow from 20.4 to 24.8, a 22% rise (P less than 0.05). When a high (8%) NaCl diet was fed for 4 weeks, R rats increased papillary plasma flow from 25.7 ml/100 g per min on 0.3% NaCl to 29.5 ml/100 g per min on 8% NaCl, a 15% rise (P less than 0.025). S rats increased papillary flow from 17.7 to 20.0 ml/100 g per min (not significant). S rats on 8% NaCl had a papillary flow 32% lower than R rats on 8% NaCl (P less than 0.001). BP of S rats rose to 162 mm Hg after 4 weeks on 8% NaCl; in R rats, BP did not rise at all. S rats on 0.3% NaCl have a low papillary flow even in a borderline hypertensive state. When challenged with 8% NaCl, R rats increased papillary flow, an adaptation possibly important for the natriuresis. S rats failed to achieve this same high papillary flow. Lacking this adaptation, hypertension may then conceivably occur in S rats to accomplish natriuresis through a "pressure natriuresis" mechanism. Papillary flow also decreased by 11% in 26 Kyoto 17-week-old spontaneously hypertensives (BP, 182 mm Hg) compared to 24 Kyoto normotensives (BP, 118 mm Hg), 29.5 vs 33.2 ml/100 g per min (P less than 0.001). Thus, low papillary flow exists in both hypertensions.

Does the kidney autoregulate papillary plasma flow in chronic postsalt hypertension?

Does the kidney autoregulate papillary plasma flow in chronic postsalt hypertension?