Renal Interstitial Hydrostatic Pressure Research Articles

Renal interstitial hydrostatic pressure during pressure natriuresis in hypertension

The objective of this study was to test the hypothesis that changes in renal perfusion pressure (RPP) are not fully transmitted to the renal interstitium in spontaneous hypertension in comparison with normotensive states. Okamoto spontaneously hypertensive and normotensive Wistar-Kyoto rats were used in this study. Renal interstitial hydrostatic pressure (RIHP) was measured directly and continuously via a polyethylene matrix that was implanted chronically in the left kidney 3 wk before RIHP measurement. When RPP was allowed to increase from 136 +/- 0.5 to 162 +/- 1.3 mmHg in male spontaneously hypertensive rats, RIHP was not significantly changed from 3.7 +/- 0.9 to 4.6 +/- 1.1 mmHg, and fractional excretion of sodium (FENa) increased significantly from 0.26 +/- 0.12 to 0.65 +/- 0.15% (P less than 0.05). When RPP was allowed to change from 104 +/- 0.9 to 127 +/- 1.3 mmHg in male Wistar-Kyoto rats, RIHP increased markedly from 4.0 +/- 0.3 to 7.2 +/- 0.4 mmHg (P less than 0.05), and FENa was significantly elevated from 0.27 +/- 0.08 to 2.02 +/- 0.55% (P less than 0.05). In conclusion, spontaneously hypertensive rats have a blunted increase in RIHP and pressure natriuresis response in comparison with Wistar-Kyoto rats. Thus, in Okamoto spontaneously hypertensive rats, the effect of RPP on RIHP is attenuated, leading to a blunted pressure natriuresis response.

Prostaglandin blockade blunts the natriuresis of elevated renal interstitial hydrostatic pressure.

Previous studies have shown that renal interstitial volume expansion (RIVE) increases renal interstitial hydrostatic pressure and urinary sodium excretion. In the present study we investigated whether blockade of prostaglandin synthesis inhibits the increase in fractional sodium excretion induced by RIVE. Expansion of the renal interstitial volume was achieved by injecting 50 microliters of 2.5% albumin solution into a polyethylene matrix chronically implanted in the left kidney. Fractional sodium excretion (FENa), renal interstitial hydrostatic pressure (PI), and urinary prostaglandin excretion (UPGE2) were measured before and after RIVE in eight control, seven meclofenamate-treated, and eight indomethacin-treated rats. RIVE in the control animals resulted in significant increases in PI (delta + 4.2 +/- 0.8 mmHg), in FENa (delta + 1.02 +/- 0.27%), and in UPGE2 (% delta + 150 +/- 38%) without significant changes in glomerular filtration rate. Inhibition of prostaglandin synthesis with meclofenamate or indomethacin attenuated the natriuretic response and blocked the increase in UPGE2 associated with RIVE. In summary, direct increases in renal interstitial hydrostatic pressure increase UPGE2 and urinary sodium excretion. This natriuretic response is markedly diminished by inhibition of prostaglandin synthesis. These studies suggest that prostaglandin synthesis may have an important role in mediating the natriuretic effect of increased renal interstitial hydrostatic pressure during renal interstitial volume expansion.

Effect of direct increases in renal interstitial hydrostatic pressure on sodium excretion.

This study examined the effect of increases in renal interstitial hydrostatic pressure (PI) on sodium excretion (UNaV) utilizing a direct technique for increasing renal interstitial volume. PI was increased by renal interstitial volume expansion (RIVE) via injection of 50 microliters of a 2% albumin in saline solution into the renal interstitium through a chronically implanted interstitial catheter. RIVE resulted in a stable increase in PI (4.6 +/- 0.4 to 9.4 +/- 0.8 mmHg) that was sustained over a 30- to 40-min period without significant changes in renal blood flow or glomerular filtration rate. Increases in PI were associated with significant increases in urine flow (13.8 +/- 3.4 to 31.7 +/- 5.0 microliters/min) and UNaV (2.3 +/- 0.6 to 6.2 +/- 1.1 micro eq/min) and fractional excretion of Na (2.6 +/- 0.8 to 6.9 +/- 1.5%). To determine the importance of albumin in maintaining an elevated PI, the effects of renal interstitial injections of saline were compared with albumin in saline solution. Injection of 50 microliters of saline into the renal interstitium had no sustained effect on PI. Injection of 2% albumin in saline solution in the same group of rats resulted in significant elevations in PI and UNaV. These data indicate that direct increases in PI via renal interstitial volume expansion result in significant increases in UNaV, thus supporting a role for PI in controlling UNaV.

Continuous Renal Interstitial Hydrostatic Pressure Dynamics During Atrial Natriuretic Peptide Administration

Continuous Renal Interstitial Hydrostatic Pressure Dynamics During Atrial Natriuretic Peptide Administration

Renal interstitial pressure in mineralocorticoid escape.

Studies were performed in normal and DOCA-treated rats to determine renal hydrostatic pressures within superficial peritubular capillaries, the vasa recta, and renal interstitium during mineralocorticoid escape to test the hypothesis that mineralocorticoid escape is associated with elevated renal interstitial hydrostatic pressure. Fractional sodium excretion was greater in the DOCA-treated rats (3.20 +/- 0.51%) compared with control rats (1.23 +/- 0.12%) with no difference in glomerular filtration rate and renal blood flow between the two groups. Superficial peritubular capillary hydrostatic pressure (13.4 +/- 0.6 vs. 8.3 +/- 0.3 mmHg), vasa recta hydrostatic pressure (13.8 +/- 0.5 vs. 9.0 +/- 0.4 mmHg), renal interstitial hydrostatic pressure (9.8 +/- 0.4 vs. 4.5 +/- 0.4 mmHg), and arterial pressure (145 +/- 6 vs. 120 +/- 7 mmHg) were greater in the DOCA-treated compared with the control rats. These studies establish that mineralocorticoid escape is characterized by high renal interstitial hydrostatic pressure.

Regulation of proximal tubular fluid reabsorption in the rat kidney

Epithelia such as the renal proximal tubule reasorb fluid "isotonically" by osmotic coupling to active salt transport. This coupling has a rectifying character which means that solute accumulation on the basolateral side induces higher flow rates than the same accumulation on the apical side (for example, see [9]) and that small rises of hydrostatic pressure on the basolateral side reduce the fluid transport to almost zero but have very little effect from the apical side (for example, see [14]). These phenomena are usually related to the "leakiness" of the basolateral spaces [4], which are believed to be rendered hyperosmotic by the active salt transport and thus be the site where the coupling of salt and fluxes occurs [2]. It has been argued that a pressure gradient opposing the outflow of resorbate from these spaces to the interstitium may result in trapping of solutes and fluid so that the backleak of resorbate through the tight junctions rises and a higher fraction of the accumulated solutes is lost by diffusion from the basolateral spaces into the interstitium [19, 201. For the renal proximal tubule this concept has not only been used to explain rectification and isotonicity of the tubular fluid transport but also the dependency of fluid transport rate on the rate of glomerular filtration [17]. It has been argued that variation of glomerular l~tration rate with its concomitant variations of peritubular blood flow are reflected in appropriate variations of the renal interstitial hydrostatic pressure, which may finally adjust the tubular fluid transport rate to the rate of glomerular filtration by the above mechanism. However, apart from the fact that variations of glomerlar filtration do not induce significant alterations of the peritubular hydrostatic pressure [11], the original concept itself has come under challange through a variety of recent observations. For instance, it was found that water pemeates leaky epithelia predominantly through the cells [18]. In addition, a reinvestigation of the reflection coefficients for Na + and C1in isolated rabbit tubules in vitro found values a good deal closer to I than was originally the case [2, 6, 10]. Furthermore, many obervations on tight epithelia suggest that osmotic or hydrostatic pressure gradients across the epithelium may alter the cellular transport activity directly by unknown mechanisms localized within the cells themselves (for literature see [12]). This seems also to be true for leaky epithelia since, for example, when hydrostatic pressure on the basolateral side of gallbladders is raised, the undirectional sodium flux from the apical to the basolateral side is diminished whereas the opposing flux is only minimally increased [7]. Similarly, the addition of

Mechanism of natriuresis during intrarenal infusion of prostaglandins.

Intrarenal infusion of the natural prostaglandin PGE2 increases renal blood flow, renal interstitial hydrostatic pressure, and urinary sodium excretion. A newly synthesized prostaglandin analogue, 4-3-[3-[2-(1-hydroxycyclohexyl)- ethyl]-4-oxo-2-thiazolidinyl]propyl benzoic acid, increases renal blood flow without increasing sodium excretion. To investigate the role of renal interstitial hydrostatic pressure in this dissociation, comparisons were made between PGE2 and the prostaglandin analogue. Intrarenal infusion of PGE2 increased renal blood flow, renal interstitial hydrostatic pressure, and urinary sodium excretion. Following a similar increase in renal blood flow with intrarenal infusion of prostaglandin analogue, renal interstitial hydrostatic pressure and urinary sodium excretion were not changed. To determine whether increases in urinary sodium excretion due to PGE2 infusion are causally related to the increase in renal interstitial hydrostatic pressure rather than to the increase in renal blood flow, responses to PGE2 were obtained in the absence of increases in interstitial pressure. When renal interstitial hydrostatic pressure was held constant, urinary sodium excretion did not change although there was a marked increase in renal blood flow. We conclude that increased renal interstitial hydrostatic pressure is necessary to produce an increase in urinary sodium excretion with prostaglandin-mediated renal vasodilation.

Tubuloglomerular feedback and interstitial pressure in obstructive nephropathy

The possible role of the tubuloglomerular feedback (TGF) mechanism in the altered glomerular hemodynamics and tubular reabsorption which occur with prolonged (24-hr) ureteral obstruction and the changes in renal interstitial hydrostatic and oncotic pressure which may modulate TGF sensitivity were examined. The proximal tubule stop-flow pressure (PSF) response to increased distal tubular flow rates (TGF activity) was determined in rats with sham operation, 24-hr unilateral ureteral obstruction (UUO), or 24-hr bilateral ureteral obstruction (BUO), both before and for 2 hr after relief of obstruction. Subcapsular hydrostatic pressure, lymph flow and oncotic pressure, clearance and excretory data were measured in the second series of animals. During and after release of UUO, TGF sensitivity was increased, as indicated by the marked decrease in the loop perfusion rate at which 50% of the maximum decrease in PSF occurred (the turning point of TGF activation). Interstitial oncotic pressure but not hydrostatic pressure was significantly increased in UUO kidneys. In BUO rats, the turning point for TGF activation was slightly higher than the controls and the change in PSF with maximum loop perfusion rates was reduced, indicating a blunting of the TGF response before and particularly during postobstructive diuresis after release of BUO. Interstitial hydrostatic and oncotic pressures were both slightly increased resulting in no changes in net interstitial Starling forces. We conclude that enhanced TGF sensitivity after release of prolonged UUO, associated with increased interstitial oncotic pressure, may play a role in preventing postobstructive diuresis, while the blunting of TGF sensitivity after BUO may contribute to this phenomenon.

Role of hydrostatic and oncotic pressures in renal sodium reabsorption.

Physical factors, and renal interstitial hydrostatic pressure in particular, have an important effect on sodium excretion by the kidney. Changes in hydrostatic and oncotic pressures in the peritubular microcirculation may have effects on proximal tubule reabsorption under some, but not all, circumstances. In regard to control of sodium excretion, the loop of Henle may be a particularly important segment which is sensitive to transepithelial hydrostatic pressure changes. There is little evidence to support an effect of physical factors on sodium reabsorption by the distal tubule. The collecting tubule may be another pressure-sensitive site; however, changes in sodium reabsorption by deep nephrons in the kidney may account for changes that have been attributed to the collecting duct. Changes in intrarenal pressure may be an important link in the regulation of sodium excretion, particularly in pathological circumstances, such as the exaggerated natriuresis of hypertension and the sodium retention seen in congestive heart failure.

Effect of increased peritubule protein concentration on proximal tubule reabsorption in the presence and absence of extracellular volume expansion.

The effect of increased peritubule capillary oncotic pressure on sodium reabsorption by the proximal tubule of the dog was investistigated after extracellular volume expansion (ECVE) with Ringer's solution or during continued hydropenia. Control measurements were made after ECVE or during hydropenia and again during renal arterial infusion with hyperoncotic albumin solution. Absolute reabsorption by the proximal tubule was calculated from fractional reabsorption and single nephron filtration rates as determined by micropuncture. Direct measurements of efferent arteriole protein were used to determine efferent arteriolar oncotic pressure. Albumin infused into the renal artery after ECVE significantly increased efferent oncotic pressure by 17.6 plus or minus 5.3 mm Hg. Fractional and absolute reabsorption by the proximal tubule increased from 20 plus or minus 6 to 37 plus or minus 5% and from 22 plus or minus 6 to 36 plus or minus 7 nl/min, respectively. During hydropenia, the albumin infusion significantly increased efferent oncotic pressure by 15.0 plus or minus 4.4 mm Hg. However, in contrast to the effect seen during ECVE, neither fractional nor absolute reabsorption was changed, delta equals 0.3 plus or minus 1.5% and 3 plus or minus 5 nl/min, respectively. Single nephron filtration rates were not significantly different between the groups and were unchanged by the albumin infusion. Peritubule capillary hydrostatic pressures, measured with a null-servo device, were not changed by the albumin infusion in either group. Renal interstitial hydrostatic pressure, measured from chronically implanted polyethylene capsules, was decreased significantly from 7.2 plus or minus 0.9 to 3.4 plus or minus 0.6 mm Hg in the hydropenic group and from 0.6 plus or minus 0.6 to 4.8 plus or minus 0.7 mm Hg in the Ringer's expanded group. In the hydropenic group, the increase in efferent oncotic pressure was nearly compensated for by changes in interstitial forces so that the calculated net force for capillary uptake was almost unchanged, 17.8 mm Hg before vs. 21.4 mm Hg during the albumin infusion. The increased efferent oncotic pressure in the Ringer's expanded group was not compensated, so that the calculated net force for uptake was increased, 11.9 mm Hg before to 22.2 mm Hg during the albumin infusion. Thus, while the increase in efferent oncotic pressure during albumin infusion was not significantly different between the groups, absolute and fractional reabsorptions were increased only in the animals in which the extracellular volume was expanded. The results suggest that ECVE alters the effect of increased peritubule oncotic pressure on sodium reabsorption by the proximal tubule.

Effect of increases in blood pressure on pressure and reabsorption in the proximal tubule.

ARTICLESEffect of increases in blood pressure on pressure and reabsorption in the proximal tubuleTP Dresser, RE Lynch, EG Schneider, and FG KnoxTP Dresser, RE Lynch, EG Schneider, and FG KnoxPublished Online:01 Feb 1971https://doi.org/10.1152/ajplegacy.1971.220.2.444MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByRenal Autoregulation in Health and DiseaseMattias Carlström, Christopher S. Wilcox, and William J. Arendshorst1 April 2015 | Physiological Reviews, Vol. 95, No. 2Elevations in Renal Interstitial Hydrostatic Pressure and 20-Hydroxyeicosatetraenoic Acid Contribute to Pressure NatriuresisHypertension, Vol. 49, No. 3Effect of sodium delivery on superoxide and nitric oxide in the medullary thick ascending limbMichiaki Abe, Paul O'Connor, Mary Kaldunski, Mingyu Liang, Richard J. Roman, and Allen W. Cowley1 August 2006 | American Journal of Physiology-Renal Physiology, Vol. 291, No. 2Acute hypotension induced by aortic clamp vs. PTH provokes distinct proximal tubule Na+ transporter redistribution patternsPatrick K. K. Leong, Li E. Yang, Harrison W. Lin, Niels H. Holstein-Rathlou, and Alicia A. McDonough1 October 2004 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 287, No. 4Mechanisms of pressure natriuresisCurrent Hypertension Reports, Vol. 4, No. 2Effect of Renal Perfusion Pressure on Excretion of Calcium, Magnesium, and Phosphate in the Rat3 July 2009 | Clinical and Experimental Hypertension, Vol. 17, No. 8Control of Sodium Excretion: An Integrative Approach1 January 2011Response of superficial proximal convoluted tubule to decreased and increased renal perfusion pressure. In vivo microperfusion study in rats.Circulation Research, Vol. 66, No. 5Diuretic Effects of L-Threo-3,4-Dihydroxyphenylserine (L-Threo-DOPS) in Anesthetized RatsJapanese Journal of Pharmacology, Vol. 52, No. 34 Control of blood and extracellular volumeBaillière's Clinical Endocrinology and Metabolism, Vol. 3, No. 2Pressure-diuresis in volume-expanded rats. Cortical and medullary hemodynamics.Hypertension, Vol. 12, No. 2Pressure-diuresis in volume-expanded rats. Tubular reabsorption in superficial and deep nephrons.Hypertension, Vol. 12, No. 2Renal Hemodynamics and Sodium Chloride ExcretionRole of renal papillae in the regulation of sodium excretion during acute elevation of renal perfusion pressure in the rat.Hypertension, Vol. 6, No. 6_pt_1Arterial pressure and exaggerated natriuresis in spontaneously hypertensive rats.Hypertension, Vol. 3, No. 3Autoregulation of superficial nephron function in the alloperfused dog kidneyPflügers Archiv - European Journal of Physiology, Vol. 382, No. 1Renal Hemodynamic Factors and the Regulation of Sodium ExcretionAutoregulatory responses of superficial nephrons and their association with sodium excretion during arterial pressure alterations in the dog.Circulation Research, Vol. 41, No. 4The effect of an acute increase in renal perfusion pressure on sodium transport in the rat kidney.Circulation Research, Vol. 39, No. 5Quantitative aspects of autoregulation in the canine kidneyPfl�gers Archiv European Journal of Physiology, Vol. 353, No. 1Role of physical and neuroendocrine factors in proximal electrolyte reabsorptionMetabolism, Vol. 23, No. 8Correlation between luminal hydrostatic pressure and proximal tubular fluid reabsorption in the rat kidneyPfl�gers Archiv European Journal of Physiology, Vol. 350, No. 2Über die antidiuretische und saluretische Aktivität des Jugularvenenblutes narkotisierter Ratten bei einer beidseitigen Abklemmung der A. carotis communisResearch in Experimental Medicine, Vol. 160, No. 2Hydrostatic pressures in proximal tubules and peritubule capillaries in the dogKidney International, Vol. 2, No. 1 More from this issue > Volume 220Issue 2February 1971Pages 444-447 Copyright & PermissionsCopyright © 1971 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1971.220.2.444PubMed5540895History Published online 1 February 1971 Published in print 1 February 1971 Metrics

Role of physical factors in the natriuresis induced by acetylcholine.

ARTICLESRole of physical factors in the natriuresis induced by acetylcholineJP Hayslett, DT Domoto, M Kashgarian, and FH EpsteinJP Hayslett, DT Domoto, M Kashgarian, and FH EpsteinPublished Online:01 Mar 1970https://doi.org/10.1152/ajplegacy.1970.218.3.880MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByNeural Control of Renal Function1 January 2011Synthesis and release of acetylcholine in the rabbit kidney cortexLife Sciences, Vol. 51, No. 22Prostaglandin E2 induced changes in renal blood flow, renal interstitial hydrostatic pressure and sodium excretion in the ratProstaglandins, Vol. 40, No. 6Cholinergic effect on rat proximal convoluted tubulePflügers Archiv European Journal of Physiology, Vol. 415, No. 5Regional blood flow during paraoxon infusion in rabbitsArchiv f�r Toxikologie, Vol. 50-50, No. 3-4Comparison of Effects of Cyanide and Acetylcholine on Renal Hemodynamics and Sodium ExcretionJournal of Pharmaceutical Sciences, Vol. 71, No. 1The Regulation of Glomerular Filtration Rate in Mammalian KidneysA possible sympathetic cholinergic mechanism in the renal reflex elicited by stimulation of abdominal viscera in the dogClinical and Experimental Pharmacology and Physiology, Vol. 2, No. 2Role of physical and neuroendocrine factors in proximal electrolyte reabsorptionMetabolism, Vol. 23, No. 8Studies on a New 1, 5-Benzothiazepine Derivative (CRD-401)Japanese Journal of Pharmacology, Vol. 24, No. 4Renal vasodilation and uncoupling of blood flow and filtration rate autoregulationKidney International, Vol. 4, No. 1Sieving equations and effective glomerular filtration pressureKidney International, Vol. 2, No. 3Glomerular filtration in single nephronsKidney International, Vol. 1, No. 4Chapter 10. Diuretics More from this issue > Volume 218Issue 3March 1970Pages 880-885 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.218.3.880PubMed5414049History Published online 1 March 1970 Published in print 1 March 1970 Metrics