Renal Venous Pressure Elevation Research Articles

Pericyte detachment and renal congestion involve interstitial injury and fibrosis in Dahl salt-sensitive rats and humans with heart failure

Congestive heart failure produces fluid volume overload, central and renal venous pressure elevation, and consequently renal congestion, which results in worsening renal function. Pericyte detachment and pericyte-myofibroblast transition (PMT) were linked to renal interstitial fibrosis. Dahl salt-sensitive hypertensive (DahlS) rats are a non-surgical renal congestion model. The relation, however, between renal interstitial damage, pericyte morphology, and PMT in the renal congestion of DahlS rats has not been reported. DahlS rats (8-week-old) were fed normal salt (NS, 0.4% NaCl) or high salt (HS, 4% NaCl), and the left kidney was decapsulated to reduce renal interstitial hydrostatic pressure (RIHP) at 9 weeks old. One week after capsulotomy, both kidneys were analyzed by molecular and histological techniques. Renal pericyte structure was assessed in the body donors with/without venous stasis. Markers of tubulointerstitial damage, interstitial fibrosis, and PMT were upregulated in the right non-decapsulated kidney of DahlS rats fed HS. Renal tubular injury and fibrosis were detected in the HS diet groups in histological analysis. Pericyte detachment was observed in the right non-decapsulated kidney of DahlS rats fed HS by low vacuum-scanning electron microscopy. Decapsulation in DahlS rats fed HS attenuated these findings. Also, renal pericytes detached from the vascular wall in patients with heart failure. These results suggest that pericyte detachment and PMT induced by increased RIHP are responsible for tubulointerstitial injury and fibrosis in DahlS rats and humans with renal congestion. Renal venous congestion and subsequent physiological changes could be therapeutic targets for renal damage in cardiorenal syndrome.

PS-BPB10-6: THE RELATION BETWEEN PERICYTE DETACHMENT AND INTERSTITIAL FIBROSIS IN DAHL SALT-SENSITIVE HYPERTENSIVE (DAHLS) RATS

Background: Congestive heart failure produces the state of fluid volume overload, central venous pressure (CVP) elevation, and consequently renal venous pressure (RVP) elevation. We have recently developed a novel rat unilateral renal venous congestion model, in which ligation of the inferior vena cava between both renal veins artificially induced renal congestion in the left kidney only. In this model, pericyte detachment and pericyte-myofibroblast transition (PMT) around the vasa recta were involved in interstitial injury and fibrosis. Dahl salt-sensitive hypertensive (DahlS) rats on high salt diets exhibit hypertension, congestive heart failure, fluid volume overload, CVP and RVP elevation, and renal damage, considering to be a non-artificial renal congestion model. The relation, however, between renal interstitial injury and fibrosis, elevated RVP, and pericyte detachment in DahlS rats has not been reported. In the present study, we assessed the relation of pericyte detachment around the vasa recta and PMT with interstitial fibrosis in DahlS rats. Methods: Eight-week-old DahlS rats (Dahl/Mcwi) were divided into three groups: normal diet, 4% NaCl diet, and 8% NaCl diet groups, and their kidneys were analyzed after 2 weeks. Total mRNA and protein expression levels were quantified by real-time PCR and western blot, respectively. Tubulointerstitial damage and fibrosis were identified by histological analysis. Furthermore, we evaluated pericyte detachment around the vasa recta by low-vacuum scanning electron microscopy (LV-SEM). Results: The expression of KIM1, a tubulointerstitial damage marker; CNN1 and αSMA, interstitial fibrosis markers; and TAGLN, a smooth muscle protein22 and PMT marker; was significantly increased in a salt-dependent manner in DahlS rats. In histological analysis, hyperplasia of the extracellular matrix and renal tubular injury were detected in 4% and 8% NaCl diet groups. The positive area of PMT markers in the interstitial space around the vasa recta was also increased in the NaCl diet groups. Pericyte detachment from the vasa recta was observed in the NaCl diet groups by LV-SEM. Conclusions: Pericyte detachment and PMT are involved in tubulointerstitial injury and fibrosis of DahlS rats. Renal venous congestion and subsequent physiological changes could have a role in renal damage and fibrosis. Arterial hypertension has been emphasized for a long time in renal injury, and venous hypertension must also be focused on with the concept of renal congestion. Further understanding of this concept may lead to new therapeutic strategies for renal injury.

Chronic, Combined Cardiac and Renal Dysfunction Exacerbates Renal Venous Pressure-Induced Suppression of Renal Function in Rats.

Background and ObjectiveIncreased renal venous pressure (RVP) is common in combined heart and kidney failure. We previously showed that acute RVP elevation depresses renal blood flow (RBF), glomerular filtration rate (GFR), and induces renal vasoconstriction in the absence of changes in blood pressure in healthy rats. We used our established rodent model of chronic combined heart and kidney failure (H/KF) to test whether RVP elevation would impair cardiovascular stability, renal perfusion and exacerbate renal dysfunction.MethodsMale rats were subjected to 5/6 nephrectomy (SNx or Sham) and 6% high salt diet followed 7 weeks later by ligation of the left anterior descending coronary artery (CL or Sham). Experimental groups: CL + SNx (n = 12), Sham CL + SNx (n = 9), CL+ Sham SNx (n = 6), and Sham Control (n = 6). Six weeks later, anesthetized rats were subjected to an acute experiment whereupon mean arterial pressure (MAP), heart rate (HR), RVP, RBF, and GFR were measured at baseline and during elevation of RVP to 20–25 mmHg for 120 min.ResultsBaseline MAP, HR, RBF, and renal vascular conductance (RVC) were comparable among groups. Baseline GFR was significantly depressed in CL + SNx and Sham CL + SNx groups compared to Sham Control and CL + Sham SNx groups. Upon RVP increase, MAP and HR fell in all groups. Increased RVP exacerbated the reduction in RBF in CL + SNx (−6.4 ± 0.9 ml/min) compared to Sham Control (−3.7 ± 0.9 ml/min, p < 0.05) with intermediate responses in Sham CL + SNx (−6.8 ± 1.3 ml/min) and CL + Sham SNx (−5.1 ± 0.4 ml/min) groups. RVP increase virtually eliminated GFR in CL + SNx (−99 ± 1%), Sham CL + SNx (−95 ± 5%), and CL + Sham SNx (−100%) groups compared to Sham Control (−84 ± 15% from baseline; p < 0.05). Renal vascular conductance dropped significantly upon RVP increase in rats with HF (CL + SNx: −0.035 ± 0.011; CL + Sham SNx: −0.050 ± 0.005 ml/min·mmHg−1, p < 0.05) but not Sham CL + SNx (−0.001 ± 0.019 ml/min·mmHg−1) or Control (−0.033 ± mL/min·mmHg−1).ConclusionChronic combined heart and kidney failure primarily impairs renal hemodynamic stability in response to elevated RVP compared to healthy rats.

Chronic elevation of renal venous pressure induces extensive renal venous collateral formation and modulates renal function and cardiovascular stability in rats.

Acutely increased renal venous pressure (RVP) impairs renal function, but the long-term impact is unknown. We investigated whether chronic RVP elevation impairs baseline renal function and prevents exacerbation of renal dysfunction and cardiovascular instability upon further RVP increase. RVP elevation (20-25 mmHg) or sham operation (sham) was performed in rats. After 1 wk (n = 17) or 3 wk (n = 22), blood pressure, RVP, renal blood flow (RBF), renal vascular conductance (RVC), and glomerular filtration rate (GFR) were measured at baseline and during superimposed RVP increase. Chronic RVP elevation induced extensive renal venous collateral formation. RVP fell to 6 ± 1 mmHg at 1 wk and 3 ± 1 mmHg at 3 wk. Baseline blood pressure and heart rate were unaltered compared with sham. RBF, RVC, and GFR were reduced at 1 wk but normalized by 3 wk. Upon further RVP increase, the drop in mean arterial pressure was attenuated at 3 wk compared with 1 wk (P < 0.05), whereas heart rate fell comparably across all groups; the mean arterial pressure-heart rate relationship was disrupted at 1 and 3 wk. RBF fell to a similar degree as sham at 1 wk (-2.3 ± 0.7 vs. -3.9 ± 1.2 mL/min, P = 0.066); however, at 3 wk, this was attenuated compared with sham (-1.5 ± 0.5 vs. -4.2 ± 0.7 mL/min, P < 0.05). The drop in RVC and GFR was attenuated at 1 and 3 wk (P < 0.05). Thus, chronic RVP elevation induced by partial renal vein ligation elicits extensive renal venous collateral formation, and although baseline renal function is impaired, chronic RVP elevation in this manner induces protective adaptations in kidneys of healthy rats, which attenuates the hemodynamic response to further RVP increase.

Sodium intake but not renal nerves attenuates renal venous pressure-induced changes in renal hemodynamics in rats.

Increased central venous pressure and renal venous pressure (RVP) are associated with worsening of renal function in acute exacerbation of congestive heart failure. We tested whether an acute isolated elevation of RVP in one kidney leads to ipsilateral renal vasoconstriction and decreased glomerular filtration rate (GFR) and whether this depends on dietary salt intake or activation of renal nerves. Male Lewis rats received a normal (1% NaCl, NS) or high-salt (6% NaCl) diet for ≥14 days before the acute experiment. Rats were then randomized into the following three groups: time control and RVP elevation to either 10 or 20 mmHg to assess heart rate, renal blood flow (RBF), and GFR. To increase RVP, the left renal vein was partially occluded for 120 min. To determine the role of renal nerves, surgical denervation was conducted in rats on both diets. Renal sympathetic nerve activity (RSNA) was additionally recorded in a separate group of rats. Increasing RVP to 20 mmHg decreased ipsilateral RBF (7.5 ± 0.4 to 4.1 ± 0.7 ml/min, P < 0.001), renal vascular conductance (0.082 ± 0.006 to 0.060 ± 0.011 ml·min-1·mmHg-1, P < 0.05), and GFR (1.28 ± 0.08 to 0.40 ± 0.13 ml/min, P < 0.05) in NS rats. The reduction was abolished by high-salt diet but not by renal denervation. Furthermore, a major increase of RVP (1.6 ± 0.8 to 24.7 ± 1.2 mmHg) immediately suppressed RSNA and decreased heart rate ( P < 0.05), which points to suppression of both local and systemic sympathetic activity. Taken together, acute elevated RVP induces renal vasoconstriction and decreased GFR, which is more likely to be mediated via the renin-angiotensin system than via renal nerves.

Sodium excretion during elevation of renal venous pressure: modulation by dDAVP.

Studies were performed to determine the effects of elevation of renal venous pressure on sodium excretion by the isolated perfused rat kidney in the presence and absence of a specific V2-receptor agonist, 1-des-amino-8-D-arginine vasopressin (dDAVP), at a concentration (1 ng/ml) expected to have maximal antidiuretic activity but minor vasopressor action. In either the presence or absence of dDAVP, increments in venous pressure led to falls in perfusate flow rate and glomerular filtration rate, which became significant at an imposed pressure greater than or equal to 18.75 mmHg. In the absence of dDAVP, absolute sodium excretion fell as venous pressure increased, and there was a negative correlation between fractional sodium excretion (FENa) and renal venous pressure (RVP) within each experiment and when all data points were combined: FENa = 3.46-0.072RVP (r = -0.608, P less than 0.01). In contrast, in the presence of dDAVP, absolute sodium excretion was unchanged, and in four of five experiments FENa rose as venous pressure increased (in one it remained unchanged). Linear regression analysis of all data points showed a positive correlation between FENa and RVP: FENa = 1.27 + 0.127RVP (r = 0.392, P less than 0.05). The slopes of the two regression lines were significantly different (P less than 0.001). It is postulated that this effect of dDAVP may be mediated via changes in the distal tubular pressure response to elevation of RVP. Such an effect of vasopressin could explain the observation that the response to renal vein constriction in vivo is dependent on volume status.

Effect of renal venous pressure elevation on tubular sodium and water reabsorption in the dog kidney.

This study was performed in order to quantify the effects of renal venous pressure (RVP) elevation on absolute and fractional reabsorption rates of sodium and water in proximal and distal segments of the nephron in dog kidneys. Renal blood flow (RBF) was measured electromagnetically. Clearance of [51Cr]EDTA was used as a measure of the rate of glomerular filtration (GFR). GFR, urinary excretion rates of sodium and water, and lithium clearance were used for assessing the absolute and fractional reabsorption rates of sodium and water in the proximal as well as in more distal segments of the nephron. In the kidneys with intact innervation RVP elevation to 19.9 +/- 0.1 mmHg caused significant increases in both absolute (APR) and fractional (FPR) proximal reabsorption rates from 33.4 +/- 4.2 to 38.7 +/- 2.0 ml min-1 and from 0.62 +/- 0.04 to 0.71 +/- 0.04, respectively. These responses were unaffected by acute surgical denervation of the kidneys. In contrast, chronic renal denervation or infusion of phentolamine (5 micrograms kg-1 min-1) into the renal artery eliminated the increase in APR and FPR during RVP elevation to 20 mmHg. Chronic, but not acute renal denervation depleted renal tissue content of adrenaline and noradrenaline. The results suggest that the increase in APR and FPR during RVP elevation is due mainly to local sympathetic reflex mechanisms.

Hemodynamic relationship between renal venous pressure and blood flow regulation during positive end-expiratory pressure.

The hemodynamic relationship between renal venous pressure (RVP) and renal blood flow (RBF) during PEEP was investigated using adult mongrel dogs. When continuous mechanical ventilation (CMV) with 10 cm H2O of PEEP was applied to dogs previously on CMV with zero PEEP, RVP increased from 6.6 to 8.7 mm Hg (p less than .01), and left RBF decreased from 66 to 57 ml/min (p less than .05). RBF recovered by 49% of the difference as soon as PEEP was discontinued when the RVP elevation was maintained at the level observed during 10 cm H2O of PEEP. With 20 cm H2O of PEEP, RVP increased further to 10 mm Hg (p less than .01) and left RBF decreased to 48 ml/min (p less than .05). When the left renal vein was occluded and the RVP was maintained at the level seen during 20 cm H2O of PEEP, left RBF recovered only 50% of the difference from the flow during zero PEEP. We conclude that the reduction in RBF with PEEP application is caused by several factors; however, RVP elevation during CMV with PEEP is influential in decreasing RBF.

Angiotensin II and tubular transport responses to renal venous pressure elevation in the dog kidney.

Angiotensin II and tubular transport responses to renal venous pressure elevation in the dog kidney.

Renal vascular adjustments to partial renal venous obstruction in dog kidney.

Blood flow studies were conducted in neurolept anesthetized dogs to characterize the involvement of renal nerves in ipsilateral renal vasoconstriction seen during acute elevation of renal venous pressure above 30 mm Hg. Renal blood flow was measured electromagnetically. The vasoconstrictor response was almost abolished by acute surgical denervation of the kidney, since renal vascular conductance remained unchanged during renal venous pressure elevation from 30-60 mm Hg. However, following additional alpha-adrenoceptor blockade or chronic renal denervation, renal vascular conductance increased progressively during renal venous pressure elevation to 60 mm Hg. The effect of acute decapsulation of kidney was studied in another group of dogs. Decapsulation induced a vasoconstriction. The decrease in renal vascular conductance observed during renal venous pressure elevation was unaffected by acute surgical denervation of decapsulated kidney, but was almost abolished following additional alpha-adrenoceptor blockade or chronic denervation. In decapsulated chronically denervated kidney, the increase in renal vascular conductance during renal venous pressure elevation to 60 mm Hg was still present but considerably attenuated as compared with the chronically denervated kidney with intact capsule. The renin-angiotensin system did not participate in acute vascular adjustments to renal venous stasis in intact kidney or in decapsulated acutely surgically denervated kidney. The data favor the view that neurogenic and myogenic mechanisms significantly influence the vasoconstrictor response to renal venous pressure elevation in dog kidney. The neurogenic contribution to the vasoconstrictor response comprises intrarenal and extrarenal vasoconstrictor mechanisms evoked reflexively by renal venous pressure elevation, and the myogenic contribution to the vasoconstrictor response comprises opposing vasodilator mechanisms due to increase in renal interstitial tissue pressure during renal venous pressure elevation.

O-190 - The effects of renal venous pressure elevation on prostaglandins and thromboxane release from the canine kidney

O-190 - The effects of renal venous pressure elevation on prostaglandins and thromboxane release from the canine kidney

Renal interstitial pressure measured in the subcapsular space using an in vivo oncometer.

Continuous measurements of renal interstital pressure are of importance for several reasons. The present paper describes an in vivo oncometer developed for this purpose. A piece of dialysis tubing was filled with a 0.15 M NaCl solution containing 5 g albumin 100 ml-1. For detecting the hydrostatic pressure inside the tubing, a thin catheter and a silver wire were inserted into it and both ends of the tubing were sealed with glue. The catheter and the silver wire were connected to a servo-nulling pressure device. The oncometer was then placed under the renal capsule. The pressure inside the dialysis tubing was pi onc+Psc-pi sc, and since pi onc was known, the net interstitial pressure (Pnet, i.e. Psc-pi sc) could be measured continuously in the subcapsular space. Measurements were made during (I) intravenous bolus injection of 2 ml of 0.9% NaCl, (2) saline expansion of 5% of body weight, and (3) elevation of renal venous pressure to 20 mmHg by clamping the renal vein. In the control situation, Pnet averaged-3.3 mmHg, a value in good accordance with findings in earlier studies in which the hydrostatic and oncotic pressure components have been measured separately. Following bolus injection of fluid, Pnet increased transiently by 2.6 mmHg, whereas volume expansion produced a permanent increase in Pnet of almost the same magnitude. During elevated renal venous pressure Pnet was unaffected, except for a minor increase on clamping and a minor decrease on release of the clamp. The results show that reproducible and accurate measurements of Pnet in the renal subcapsular space can be made with an in vivo oncometer.

Pentobarbital inhibits the vasoconstrictor response to renal venous pressure elevation in the dog kidney.

Pentobarbital inhibits the vasoconstrictor response to renal venous pressure elevation in the dog kidney.

Sympathetic reflex-induced vasoconstriction during renal venous stasis elicited from the capsule in the dog kidney.

The study was performed in order to determine the effect of venous pressure elevation induced by unilateral partial renal venous ligation upon total renal blood flow and filtration fraction in the dog kidney. An anaesthesia with no known inhibitory effect on sympathetically mediated vasoconstriction was used. During control conditions instantaneous increase in renal venous pressure to 60 mmHg induced a decrease in renal blood flow (66 +/- 4%) corresponding to an ipsilateral vasoconstriction which was completely abolished following (1) surgical denervation of the kidney, (2) local alpha-receptor blockade of the kidney, and (3) application of lidocaine on the kidney surface. The most striking feature during step increase in renal venous pressure to 40 mmHg was an increase in renal vascular conductance. Renal venous pressure elevation of more than 40 mmHg induced a vasoconstriction, but the vasoconstrictor response was less pronounced as compared with that observed during instantaneous increase in renal venous pressure to the same level. The results strongly suggest that venous stasis of more than 40 mmHg activates an adrenergic sympathetic vasoconstrictor reflex comprising the spinal cord. The reflex is probably elicited from stretch receptors located in the renal capsule. Changes in filtration fraction at venous stasis during the experimental conditions indicate that renal venous pressure elevation activates mechanisms other than neural ones accounting for the reduction in the filtration fraction.

Renal hemodynamic responses to increased renal venous pressure: role of angiotensin II.

Studies were performed to quantitate the effects of progressive increases in renal venous pressure (RVP) on renin secretion (RS) and renal hemodynamics. RVP was raised in 10 mmHg increments to 50 mmHg. Renin secretion rate increased modestly as RVP was increased to 30 mmHg and then increased sharply after RVP exceeded 30 mmHg. Glomerular filtration rate (GFR), renal blood flow (RBF), and filtration fraction (FF) did not change significantly when RVP was elevated to 50 mmHg. GFR and RBF were also measured after the renin-angiotension system (RAS) was blocked with the angiotensin converting enzyme inhibitor (CEI) SQ 14225. After a 60-min CEI infusion, RBF was elevated (32%), GFR was unchanged, FF was decreased, and total renal resistance (TRR) was decreased. As RVP was increased to 50 mmHg, GFR and FF decreased to 36.3 and 40.0% of control, respectively, RBF returned to a value not significantly different from control, and TRR decreased to 44.8% of control. The data indicate that the RAS plays an important role in preventing reductions in GFR during increased RVP because blockade of angiotensin II (ANG II) formation by the CEI results in marked decreases in GFR at high RVPs. The decreases in GFR after ANG II blockade and RVP elevation were not due to lack of renal vasodilation, since TRR was maintained below while RBF was maintained either above or at the pre-CEI levels.

Intrarenal distribution of blood flow and renin release during renal venous pressure elevation

Intrarenal distribution of blood flow and renin release during renal venous pressure elevation. The effects of renal venous pressure (RVP) elevation on the intrarenal distribution of blood flow and renin secretion were studied in mongrel dogs anesthetized with pentobarbital sodium. The intrarenal distribution of blood flow was determined with the radioactive xenon ( 133 Xe) washout technique. Elevation of RVP to 30 mm Hg caused a significant change in the intrarenal distribution of blood flow and a significant increase in renin secretion rate without changes in total renal blood flow (RBF) and glomerular filtration rate (GFR). At this RVP, the percentage of distribution and relative volume increased significantly in the second flow component and decreased significantly in the first flow component. When RVP was elevated above 30 mm Hg, further redistribution of flow from first flow component to second flow component occurred, and RBF and GFR began to decrease. Thus, there was an inverse relationship between RVP and the percentage of RBF into first flow component (P

Effect of renal alpha-adrenergic stimulation on proximal tubular sodium reabsorption.

ARTICLESEffect of renal alpha-adrenergic stimulation on proximal tubular sodium reabsorption Gill JR Jr, and AG Casper Gill JR Jr, and AG CasperPublished Online:01 Nov 1972https://doi.org/10.1152/ajplegacy.1972.223.5.1201MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByLandscape of GPCR expression along the mouse nephronBrian G. Poll, Lihe Chen, Chung-Lin Chou, Viswanathan Raghuram, and Mark A. 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Part A: Theory and Practice, Vol. 4, No. 4-5Dietary Sodium and Renal α2-Adrenergic Receptors in Dahl Hypertensive Rats3 July 2009 | Clinical and Experimental Hypertension. Part A: Theory and Practice, Vol. 4, No. 4-5Sodium Intake Alters the Effects of Norepinephrine on the Renin System and the KidneyAmerican Journal of Kidney Diseases, Vol. 1, No. 3IMPLICATIONS OF ANTIHYPERTENSIVE THERAPY ON SODIUM BALANCE AND SODIUM AND WATER RETENTION26 July 2012 | British Journal of Clinical Pharmacology, Vol. 12Effects of Adrenergic Activators and Inhibitors on Kidney FunctionInfluence of renal nerve activity on arteriolar resistance, ultrafiltration dynamics and fluid reabsorptionPfl�gers Archiv European Journal of Physiology, Vol. 389, No. 2Renin/aldosterone in pheochromocytomaThe Journal of Pediatrics, Vol. 95, No. 4Akute kombinierte Alpha- und Betarezeptorenblockade bei essentieller Hypertonie: Wirkungen auf Blutdruck, Nierenfunktion, Renin und AldosteronKlinische Wochenschrift, Vol. 57, No. 14The effect of renal vasodilation and hypotonic volume expansion on water excretion in dogs after anesthesia and surgeryLife Sciences, Vol. 20, No. 12The effect of an acute increase in renal perfusion pressure on sodium transport in the rat kidney.Circulation Research, Vol. 39, No. 5Control of renin release: A review of experimental evidence and clinical implicationsThe American Journal of Cardiology, Vol. 37, No. 4Effect of Vasopressors and Hemorrhage on Intrarenal OxygenationRole of Cyclic Nucleotides in the Regulation of Intestinal Ion TransportMetabolism of Isolated Kidney Tubules Independent Actions of Catecholamines on Renal Cyclic Adenosine 3': 5'-Monophosphate Levels and GluconeogenesisEuropean Journal of Biochemistry, Vol. 52, No. 2Antagonism between parathyroid hormone and norepinephrine on cyclic adenosine-3?:5?-monophosphate (cAMP) levels in isolated tubules from rat kidney cortexPfl�gers Archiv European Journal of Physiology, Vol. 354, No. 2Effects of adrenergic nervous system and catecholamines on systemic and renal hemodynamics, sodium and water excretion and renin secretionKidney International, Vol. 6, No. 5Natriuretic HormonesControl of Proximal Reabsorption of Sodium in the KidneyIFAC Proceedings Volumes, Vol. 6, No. 4 More from this issue > Volume 223Issue 5November 1972Pages 1201-1205 Copyright & PermissionsCopyright © 1972 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1972.223.5.1201PubMed4143967History Published online 1 November 1972 Published in print 1 November 1972 Metrics

Effects of renal venous pressure elevation on renal hemodynamics, urine formation and renin release.

Effects of renal venous pressure (RVP) elevation on the renal hemodynamics, urine formation and renin secretion rate (RSR) were studied in the pentobar-bital anesthetized dogs. Gradual increment of RVP produced no changes in RBF and GFR till 30 mmHg but a significant decrease in them at RVP above 35 mmHg. The urine flow response to RVP elevation was divided into two groups: an increased urine flow with an increase of sodium excretion and a decreased urine flow with a decrease of sodium excretion. In the former group, gradual RVP elevation produced a significant increase in UNaV, Na/K ratio and TCH20 without changes in UKV and Cosm, while the latter group showed a decrease in UNaV, UKV and TCH20. Renin secretion rate (RSR), the product of RPF and renal venous-arterial difference of plasma renin activity, increased significantly as function of RVP elevation. This RSR increment seemed to be independent of changes in RBF, GFR, urine flow, or UNaV and the increased mechanism of RSR was discussed. It is concluded that tubular handling of sodium is not essential but intrarenal baroreceptor mechanism seems to be responsible for renin release in case of RVP elevation.

Effect of amiloride, ouabain, and furosemide on distal tubular function in the rat

DUARTE, CRISTOBAL G., FRANCOISE CHOMETY, AND GERHARD GIEBISCH. Effects of amiloride, ouabain, and furosemide on distal tubular function in the rat. Am. J. Physiol. 221(Z) : 632-639. 1971 .-Freeflow samples of tubular fluid (TF) were collected from superficial distal rat tubules and analyzed for inulin-14C, sodium (Na), and potassium (K). The effects of the three diuretic agents, a,miloride, ouabain, and furosemide, were studied. Amiloride completely suppressed K secretion at the distal tubular level with only small modifications of distal tubular Na reabsorption. Ouabain induced distal kaliuresis and natriuresis in animals kept on a low-potassium diet. The effects of ouabain upon distal tubular electrolyte transport consisted in depression of both tubular Na and K reabsorption. The distal potassium effects of ouabain were independent of any increase in distal sodium delivery and are thought to be due to depression of active potassium uptake across the luminal cell membrane of distal tubule cells. The main kaliuretic effect of furosemide on distal potassium transport is related to the delivery to the distal tubule of a much greater than normal fraction of fluid. After furosemide administration, despite a very significant elevation of distal tubular sodium concentration, fractional Na reabsorption rate control values. along this tubular segment greatly exceeded

Intrarenal regulatory factors of salt excretion during renal venous pressure elevation.

Intrarenal regulatory factors of salt excretion during renal venous pressure elevation.