Intracellular Volume Regulation Research Articles

The Integral Role of Chloride & With-No-Lysine Kinases in Cell Volume Regulation & Hypertension.

Chloride anions are the most abundant in humans. For many years, it has been believed that chloride is simply a counterion of all other cations, ensuring the electroneutrality of the extracellular space. Recent data suggests that chloride anions possess a broad spectrum of important activities that regulate vital cellular functions. It is now evident that, apart from its contribution to the electroneutrality of the extracellular space, it acts as an osmole and contributes to extracellular and intracellular volume regulation. Its anionic charge also contributes to the generation of cell membrane potential. The most interesting action of chloride anions is their ability to regulate the activity of with-no-lysine kinases, which in turn regulate the activity of sodium chloride and potassium chloride cotransporters and govern the reabsorption of salt and excretion of potassium by nephron epithelia. Chloride anions seem to play a crucial role in cell functions, such as cell volume regulation, sodium reabsorption in the distal nephron, potassium balance, and sodium sensitivity, which lead to hypertension. All of these functions are accomplished on a molecular level via complicated metabolic pathways, many of which remain poorly defined. We attempted to elucidate some of these pathways in light of recent advances in our knowledge, obtained mainly from experimental studies.

Dietary potassium intake and blood pressure: possible beneficial effect of Paleolithic diet.

Potassium is one of the most important elements of human organism. Its main distribution in the intracellular space makes it an essential component of intracellular volume regulation on the other hand extracellular/ intracellular potassium ratio determines the resting membrane potential. This later capability of potassium makes essential the necessity of maintaining extracellular potassium levels in a narrow range limit between 3.5 and 5.5 mEq/L in order to avoid dangerous dysfunction of excitable cells such as myocardium, neuronal cells and muscle cells. Because of asymmetric potassium distribution between intracellular and extracellular space there is a continuous need to excrete the excess of potassium ingested by food in a diurnal basis. The main site of potassium excretion is the distal nephron and it is coupled directly with the amount of sodium and solute delivered to this segment of the nephron. Although the very early segment of distal convoluted tubule has no ability to excrete potassium it is capable to regulate the amount of sodium chloride delivered downstream the nephron and by this way is implicated indirectly in potassium excretion. Newer data suggest that this segment of the nephron responds to increased extracellular levels of potassium by reducing sodium chloride cotransporter activity and so increases sodium delivery to distal nephron for exchange with potassium and leads to kaliuresis as well as natriuresis. It is believed that this mechanism is responsible for the beneficial effect of increased potassium intake in ameliorating hypertension even in cases of increased salt intake. In this review article, under the light of recent discoveries, we try to elucidate the complex underlying mechanisms of increased potassium intake and blood pressure regulation as well as the possible beneficial effect of Paleolithic diet upon hypertension.

Branchial carbonic anhydrase activity and ninhydrin positive substances in the Pacific white shrimp, Litopenaeus vannamei, acclimated to low and high salinities

The Pacific white shrimp, Litopenaeus vannamei, acclimated to 30 ppt salinity, was transferred to either low (15 and 5 ppt), or high (45 ppt) salinity for 7 days. Hemolymph osmolality, branchial carbonic anhydrase activity, and total ninhydrin-positive substances (TNPS) in abdominal muscle were then measured for each condition. Hemolymph osmotic concentration was regulated slightly below ambient water osmolality in shrimp acclimated to 30 ppt. At 15 and 5 ppt, shrimp were strong hyper-osmotic regulators, maintaining hemolymph osmolality between 200 and 400 mOsm above ambient. Shrimp acclimated to 30 ppt and transferred to 45 ppt salinity were strong hypo-osmotic and hypo-ionic regulators, maintaining hemolymph osmolality over 400 mOsm below ambient. Branchial carbonic anhydrase (CA) activity was low (approximately 100 micromol CO(2) mg protein(-1) min(-1)) and uniform across all 8 gills in shrimp acclimated to 30 ppt, but CA activity increased in all gills after exposure to both low and high salinities. Anterior gills had the largest increases in CA activity, and levels of increase were approximately the same for low and high salinity exposure. Branchial CA induction appears to be functionally important in both hyper- and hypo-osmotic regulations of hemolymph osmotic concentrations. Abdominal muscle TNPS made up between 19 and 38% of the total intracellular osmotic concentration in shrimp acclimated to 5, 15, and 30 ppt. TNPS levels did not change across this salinity range, over which hemolymph osmotic concentrations were tightly regulated. At 45 ppt, hemolymph osmolality increased, and muscle TNPS also increased, presumably to counteract intracellular water loss and restore cell volume. L. vannamei appears to employ mechanisms of both extracellular osmoregulation and intracellular volume regulation as the basis of its euryhalinity.

I/D ACE gene polymorphism in survival of leukemia patients – hypothesis and pilot study

Angiotensin-I converting enzyme (ACE) is involved not only in intracellular volume regulation but also in proliferation control. Since both ACE gene polymorphism (I/D ACE) and ABO blood group determine ACE level in peripheral blood and probably also in bone marrow, the hypothesis to the interindividual differences in survival of leukemic patients was suggested. The data of 25 patients of both sexes with acute myelogenous (AML), acute lymphatic (ALL), chronic myelogenous (CML) and chronic lymphatic (CLL) leukemia treated by conventional were used for the study. The overall survival (SUR) was estimated as the time from the date of diagnosis to the date of death. The difference between patient’s individual SUR (iSUR) and median SUR according to the type of leukemia (mSUR) was calculated. This difference (iSUR–mSUR) varied with I/D ACE genotype ( p<0.02) but neither with diagnosis nor with ABO blood group. The regression model for iSUR calculation, from mSUR and I/D ACE genotype, has been suggested.

Endothelial Na-K-Cl cotransport regulation by tonicity and hormones: phosphorylation of cotransport protein.

The Na-K-Cl cotransport system of vascular endothelial cells plays a central role in maintenance and regulation of intracellular volume. Activity of the cotransporter is modulated both by hormones and by extracellular tonicity. Vasopressin and other hormones that stimulate the endothelial cotransporter act via a Ca- and calmodulin-dependent pathway. Little is known, however, about the mechanisms that mediate cell shrinkage-induced stimulation of cotransport activity. In the present study, we evaluated the Ca dependence of cell shrinkage-stimulated Na-K-Cl cotransport activity and cell volume recovery of cultured bovine aortic endothelial cells and also the effects of protein kinase and phosphatase inhibitors on these processes. In addition, to investigate the possibility that hormones and/or hypertonicity regulate endothelial Na-K-Cl cotransport via direct phosphorylation of the cotransporter protein, we employed a monoclonal antibody to the human colonic T84 epithelial cell Na-K-Cl cotransport protein (T4 antibody) for Western blot analysis and immunoprecipitation of phosphoprotein. Our studies revealed that both cell shrinkage-stimulated net K uptake and recovery of intracellular volume were Ca dependent. We also found that hypertonicity-induced stimulation of cotransport activity was blocked by several inhibitors of Ca- and calmodulin-dependent protein kinases. Furthermore, inhibitors of myosin light chain kinase blocked cell shrinkage-stimulated cotransport and recovery of intracellular volume, while having no effect on vasopressin-stimulated cotransport. Western blot analysis of bovine aortic and cerebral microvascular endothelial cell membrane preparations revealed a 170-kDa protein recognized by the T4 antibody. In addition, we found that hypertonicity induced a marked increase in phosphorylation of the endothelial cotransport protein, as did vasopressin, bradykinin, okadaic acid, and calyculin A. Our findings indicate that modulation of endothelial cell Na-K-Cl cotransport activity by hypertonicity and by stimulatory hormones occurs via pathways involving Ca- and calmodulin-dependent protein kinases and direct phosphorylation of the cotransport protein.

Na-K-Cl cotransport regulates intracellular volume and monolayer permeability of trabecular meshwork cells

The trabecular meshwork (TM) of the eye plays a critical role in modulating intraocular pressure (IOP) through regulation of aqueous humor outflow, although the underlying mechanisms remain unknown. Ethacrynic acid, an agent known to inhibit Na-K-Cl cotransport of a number of cell types, recently has been reported to increase aqueous outflow and lower IOP through an unknown effect on the TM. In vascular endothelial cells and a variety of other cell types, the Na-K-Cl cotransporter functions to regulate intracellular volume. The present study was conducted to evaluate TM cells for the presence of Na-K-Cl cotransport activity and to test the hypothesis that modulation of cotransport activity alters intracellular volume and, consequently, permeability of the TM. We demonstrate here that bovine and human TM cells exhibit robust Na-K-Cl cotransport activity that is inhibited by bumetanide and by ethacrynic acid. Our studies also show that TM cell Na-K-Cl cotransport is modulated by a variety of hormones and neurotransmitters. Inhibition of the cotransporter either by bumetanide, ethacrynic acid, or inhibitory hormones reduces TM intracellular volume, whereas stimulatory hormones increase cell volume. In addition, shrinkage of the cells by hypertonic media stimulates cotransport activity and initiates a subsequent regulatory volume increase. Permeability of TM cell monolayers, assessed as transmonolayer flux of [14C]sucrose, is increased by hypertonicity-induced cell shrinkage and by bumetanide. These findings suggest that Na-K-Cl cotransport of TM cells is of central importance to regulation of intracellular volume and TM permeability. Defects of Na-K-Cl cotransport may underlie the pathophysiology of glaucoma.

Basolateral localization of Na +-HCO 3− cotransporter activity in alveolar epithelial cells

We investigated the polarized distribution of Na +- and HCO 3 −-dependent recovery from intracellular acidification in alveolar epithelial cell monolayers. Rat alveolar type II cells were grown in primary culture on detachable tissue culture-treated Nuclepore filters. Each filter was mounted in a cuvette containing two fluid compartments (apical and basolateral) separated by the monolayer. Cells were loaded with the pH-sensitive dye BCECF and intracellular pH (pH i) measured spectrofluorometrically. Monolayers were studied at ambient temperature on days 3–4 in culture, coincident with the development of high tissue resistance (R T ≥ 1000 Ω·cm 2). After the cells were acidified by NH 3 prepulse, pH i recovered to baseline when Na + was present in the basolateral fluid, but did not recover when Na + was present only in the apical fluid. This basolateral Na +-dependent pH i recovery in the presence of HCO 3 − CO 2 was reduced, but present, in experiments where dimethylamiloride (DMA, 100 μM) or the stilbene derivative DIDS (500 μM) was in basolateral fluid. However, recovery was completely inhibited when both DMA and DIDS were present basolaterally. pH i recovery was not inhibited under Cl −-free conditions, indicating that cytoplasmic realkalinization was not effected by Na +-dependent Cl −-HCO 3 − exchange. These data indicate that alveolar epithelial cells express a basolateral Na +- and HCO 3 −-dependent, DIDS-sensitive, Cl −-independent pH i recovery process that probably represents Na +-HCO 3 −-cotransport (symport). Basolateral Na +-HCO 3 − cotransport modulates pH i in alveolar epithelial cells, may contribute to regulation of intracellular volume and osmolarity, and may participate in signal transduction by hormones and growth factors.

Cerebral microvascular endothelial cell Na-K-Cl cotransport: regulation by astrocyte-conditioned medium.

Brain microvascular endothelial cells play an important role in regulation of ion and fluid movement between the blood and the brain interstitium. Astrocytes have been shown to induce blood-brain barrier properties in the endothelial cells, including formation of tight junctions and increased expression and asymmetric distribution of enzymes and ion transport systems. Previous studies have demonstrated that endothelial cells of bovine aorta possess a highly active Na-K-Cl cotransport system that participates in intracellular volume regulation. The present study was conducted to evaluate Na-K-Cl cotransport activity of cerebral microvascular endothelial cells and to determine whether astrocyte-conditioned medium (CM) influences Na-K-Cl cotransport activity of these cells. We found the brain microvascular endothelial cells to exhibit a robust Na-K-Cl cotransport activity, comprising 50% of the total K influx. Activity of the cotransporter was stimulated by agents that elevate intracellular Ca and by hypertonicity and was inhibited by agents that elevate adenosine 3',5'-cyclic monophosphate, guanosine 3',5'-cyclic monophosphate, or activate protein kinase C. Exposure of the cells to primary astrocyte- or C6 glial cell-CM but not A7r5 or A10 vascular smooth muscle cell-CM also increased cotransport activity. However, this effect required > 1 h of exposure to CM, was additive with the effects of vasopressin, calcium ionophore, and hypertonicity, and was blocked by the protein synthesis inhibitor cycloheximide.(ABSTRACT TRUNCATED AT 250 WORDS)

Responses of the marsh periwinkle,Littoraria (Littorina) irroratato temperature, salinity and desiccation, and the potential physiological relationship to climbing behavior

Littoraria irrorata climb the vertical stems of Sparlina alterniflora in the face of an advancing tide. This behavior, while allowing escape from predators, may also be correlated with the physiological responses of the organism to variations in physical factors typically found in an estuarine salt marsh. To test this hypothesis, snails were exposed to changes in environmental salinity, their resistance to desiccation was determined, and their ability to take up oxygen from both water and air was measured at varying temperatures. L. irrorata were found to be tolerant to wide variations in salinity. The mechanism employed appears to be intracellular volume regulation, which is common in many other marine and estuarine species. This species is also very tolerant of desiccation, surviving after losing nearly 70% of its soft tissue weight over a period of two weeks. Upon contact with water, it quickly rehydrates, regaining its initial weight within one hour. At low temperature (20°C) aquatic and aerial oxygen...

The relationship between plasma proteins and intracellular free amino acids during osmotic regulation in Carcinus maenas

AbstractThe osmoregulatory behavior of the Adriatic population of the shore crab Carcinus maenas is similar to that of more northern populations. Hyperosmotic regulation of the hemolymph is initiated below about 95–85% seawater (973–871 m Osm/kg) and slight hypo‐osmotic regulation appears to occur above approximately 110% seawater (1,127 m Osm/kg). Extracellular volume is actively regulated, and changes in levels of amino acids imply effective regulation of intracellular volume. Serum protein levels increase immediately after transfer of the crabs from high to low salinity, although the changes are much smaller than those reported by other investigators. Levels of free amino acids in serum decrease after transfer from high to low salinity and labeled leucine is incorporated into hemocyanin at a greater rate after such a transfer than in the absence of a change in salinity. However, the rate of incorporation of leucine is also greater at low than at high ionic strength in vitro, in cell‐free preparations. This result suggests that the experiment does not demonstrate storage of intracellular free amino acids by the extracellular oxygen carrier, but rather reflects “passive” binding to hydrophobic sites on the hemocyanin molecule.

Salinity responses of the juvenile penaeid shrimp Penaeus japonicus: II. Free amino acids

The free amino acids (FAA) of juvenile Penaeus japonicus were measured after 48 h of exposure of the shrimps to hypo- and hyperosmotic salinity stress. The concentrations of FAA decreased linearly with decreasing salinity from 50‰ to 10‰. The highest amounts of individual FAA in seawater-adapted P. japonicus are exhibited by glycine (51%), followed by taurine (14%), arginine (10%), proline (9%), and alanine (6%). The main osmoeffectors are glycine, proline, and alanine, which together lower the FAA pool by 80% after a hypoosmotic shock from 40 to 10‰. The concentrations of taurine, arginine, ornithine, and glutamate are not affected by external salinity change. Under hypoosmotic conditions taurine, glutamate, and arginine decrease by only 13–15%, and asparate, ornithine, and lysine by 28–34%. All other amino acids in the FAA pool are reduced by 50 to 88% — the greatest loss is shown by proline (by 96%). Below 25‰ intracellular volume regulation is maintained entirely by proline and glycine, whereas the other FAA concentrations remain more or less constant. After hyperosmotic shock, the concentrations of nearly all FAA increase. This is also true for the essential FAA (+ 86%) — indicating protein hydrolysis. A salinity range between 25 and 40‰ is recommended for the extensive aquaculture of P. japonicus.

The effect of hyponatremia on the regulation of intracellular volume and solute composition.

The effect of hyponatremia on the regulation of intracellular volume and solute composition.

Volume regulation in an intertidal oligochaete, Clitellio arenarius (Müller). I. Short‐term effects and the influence of the supra‐ and subesophageal ganglia

AbstractTerrestrial oligochaetes demonstrate significant volume and osmoregulatory abilities that are under neurosecretory control. In the marine Oligochaete, little is known of volume or osmoregulatory capacities. However, histological evidence has linked cerebral neurosecretion and osmoregulation. The present study investigates water, ion, and volume regulation in an intertidal oligochaete and the effects of ablation of primary neurosecretory centers (supra‐and subesophageal ganglia) on these parameters. Control, sham‐operated, and ablated Clitellio arenarius were acutely transferred to diluted seawaters. Osmolality and Na, K, Cl (mEq/liter) concentrations were determined in total tissue water and in extracellular fluids. Extracellular volume was determined (using micropuncture techniques) as the fraction of the total tissue water in which 14C‐polyethylene glycol was distributed. With transfer to diluted seawater, all worms demonstrated hyperosmotic conformity. Tissue osmolality decreased in all animals at the same rate indicating no effect of ablation on integumental water permeability. Two phases of volume regulation were observed. In phase 1 (0–6 hours) osmolality decreased while water content (gm H2O/gm solute free dry weight = s.f.d.w.) increased both intra‐ and extracellularly. During this period, some volume regulation was accomplished in the control groups, particularly during the first 5 minutes, by the excretion of extracellular Na and Cl (μmoles/gm s.f.d.w.) which limited water gain. Ablated worms, reflecting less extracellular solute loss, gained more water than control groups. In phase 2 (6–18 hours) osmolality was constant, and all groups demonstrated a slow intra‐ (IC) and extracellular (EC) regulatory volume decrease. The solutes that accompanied volume loss were Na (EC), Cl (IC), and unmeasured solutes (IC). Reduction in intracellular solute content was the most significant loss occurring during this period with little difference among the groups tested. We hypothesize the primary effect of ablation is on extra‐ rather than intracellular volume regulation.

Physiological basis of the species abundance-salinity relationship in molluscs: A speculation

The relationship between the osmotic pressures of the blood and the ambient medium was determined for 4 species of bivalve molluscs whose habitats represent distinct salinity regimes within the range from fresh to full seawater. These organisms included 3 corbiculids: Corbicula manilensis (freshwater); Polymesoda caroliniana (brackish-water); Pseudocyrena floridana (marine) and 1 unionid: Elliptio lanceolata. On the basis of the data and similar measurements from the literature, we have placed the molluscs into 5 categories: marine stenohaline, marine euryhaline, oligohaline, fresh-water euryhaline and freshwater stenohaline. Marine stenohaline and euryhaline species are osmoconformers. They differ only in the size of the free amino acid pool available for intracellular volume regulation, and thus in the range of salinities that they tolerate. Oligohaline species tolerate salinities from seawater down to freshwater; they not only possess a large capacity for volume regulation, but can also osmoregulate below 3‰ S. Freshwater species also osmoregulate below 3‰ S, but they are usually limited to salinities below 2‰. Presumably, in evolving from the marine to the freshwater habit, they have lost the ability to volume-regulate in response to hyperosmotic stress. We propose that the varying physiological characteristics underlie the well-known relationship that species abundance declines from both freshwater and full seawater to a minimum between 3 and 5‰ S. We have related this species minimum to physical-chemical discontinuities in the ionic composition of seawater which are, again, reflected in the physiological mechanisms of the molluscs.

Regulation of renal tubule cell volume in hypotonic media.

Regulation of renal tubule cell volume in hypotonic media.

Effect of osmolarity on canine renal vascular resistance.

ARTICLESEffect of osmolarity on canine renal vascular resistanceS Gazitua, JB Scott, CC Chou, and FJ HaddyS Gazitua, JB Scott, CC Chou, and FJ HaddyPublished Online:01 Oct 1969https://doi.org/10.1152/ajplegacy.1969.217.4.1216MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByDivergent Effects of Hypertonic Fluid Resuscitation on Renal Pathophysiological and Structural Parameters in Rat Model of Lower Body Ischemia/Reperfusion-Induced Sterile InflammationShock, Vol. 50, No. 6Is Contrast Medium Osmolality a Causal Factor for Contrast-Induced Nephropathy?BioMed Research International, Vol. 2014Hypertonic saline solution for prevention of renal dysfunction in patients with decompensated heart failureInternational Journal of Cardiology, Vol. 167, No. 1Impact of Hypertonic and Hyperoncotic Saline Solutions on Ischemia-Reperfusion Injury in Free FlapsPlastic and Reconstructive Surgery, Vol. 122, No. 1Local and Systemic Effects of Hypertonic Solution (NaCl 7.5%) in Experimental Acute PancreatitisPancreas, Vol. 32, No. 1Assessment of changes in blood volume in response to resuscitative fluid administration in dogsJournal of Veterinary Emergency and Critical Care, Vol. 15, No. 3SMALL VOLUME HYPERTONIC RESUSCITATION OF CIRCULATORY SHOCKClinics, Vol. 60, No. 2Anteroventral third ventricle lesions impair cardiovascular responses to intravenous hypertonic saline infusionAutonomic Neuroscience, Vol. 117, No. 1Effects of hypertonic dextran in hypovolaemic shock: a prospective clinical trialInjury, Vol. 35, No. 5Resuscitation of Severe Uncontrolled Hemorrhage 7.5% Sodium Chloride/6% Dextran 70 vs 0.9% Sodium ChlorideAcademic Emergency Medicine, Vol. 7, No. 8Hypertonic SalineVeterinary Clinics of North America: Food Animal Practice, Vol. 15, No. 3Comparison of the acute hemodynamic effects of hypertonic or colloid infusions immediately after mitral valve repairCritical Care Medicine, Vol. 27, No. 10Fluid and Electrolyte Disorders in the Surgical PatientSmall-volume Resuscitation beim hypovolämischen Schock7 November 2016 | Der Anaesthesist, Vol. 46, No. 4Effect of 7.2% Hypertonic Saline/6% Hetastarch on Left Ventricular Contractility in Anesthetized HumansAnesthesiology, Vol. 82, No. 6Fluid and Electrolyte Disorders in the Surgical PatientHaemodynamic effects of small volume hypertonic saline in experimentally induced haemorrhagic shockEquine Veterinary Journal, Vol. 22, No. 4Chlorure de sodium hypertonique et choc hémorragiqueAnnales Françaises d'Anesthésie et de Réanimation, Vol. 9, No. 6Treatment of uncontrolled hemorrhagic shock by hypertonic saline and external counterpressureAnnals of Emergency Medicine, Vol. 18, No. 10Small-volume resuscitationBaillière's Clinical Anaesthesiology, Vol. 2, No. 3Analysis of the cardiovascular effects of arginine vasopressin in conscious dogs.Hypertension, Vol. 9, No. 4A comparison of several hypertonic solutions for resuscitation of bled sheepJournal of Surgical Research, Vol. 39, No. 6The peritoneal microcirculationThe effect of hyponatremia on the regulation of intracellular volume and solute composition.Circulation Research, Vol. 54, No. 5Contrast Media in the Cardiovascular SystemInduced hyperosmolality effects on extracellular fluid volume, lymph flow and osmolar equilibrium: studies in the ratActa Physiologica Scandinavica, Vol. 116, No. 3Feedback-mediated reduction of glomerular filtration rate during infusion of hypertonic salineKidney International, Vol. 20, No. 4The Peritoneal MicrocirculationEffect of Local Metabolic Factors on Vascular Smooth Muscle1 January 2011In situ hypothermic renal perfusion Evaluation of three intracellular solutionsUrology, Vol. 15, No. 5The mechanism of neuronal noradrenaline and dopamine β-hydroxylase release by a sodium-deficient solution substituted with ureaNeuroscience, Vol. 5, No. 2Microvascular and clinical effects of altered peritoneal dialysis solutionsKidney International, Vol. 15, No. 6Management of 136 consecutive supratentorial berry aneurysmsJournal of Neurosurgery, Vol. 49, No. 6Hyper/Hypo-Osmotic Peritoneal Dialysis7 July 2009 | Journal of Dialysis, Vol. 2, No. 5-6Fetal pathology and mechanism of fetal death in saline-induced abortion: A study of 143 gestations and critical review of the literatureAmerican Journal of Obstetrics and Gynecology, Vol. 120, No. 3Ex vivo renal surgeryThe American Journal of Surgery, Vol. 128, No. 3Experiments in Renal Preservation: 48 and 72-hour Canine Kidney Preservation by Initial Perfusion and Hypothermic StorageJournal of Urology, Vol. 111, No. 4Mechanism of the acute pressor action of hypokalemia, hypomagnesemia, and hypo-osmolalityAmerican Heart Journal, Vol. 85, No. 5CANINE KIDNEY PRESERVATION USING A NEW PERFUSATEThe Lancet, Vol. 301, No. 7811The Nature of Renal Perfusion in Normal, Oliguric and Anuric States29 October 2018 | Urologia Journal, Vol. 39, No. 6Influence of Plasma Hypertonicity on Blood Viscosity Studied in Vitro and in an Isolated Vascular BedActa Physiologica Scandinavica, Vol. 84, No. 4Effects of renal artery infusion of various hypertonic solutions on the renal blood flow and renal handling of PAH in the dogPfl�gers Archiv European Journal of Physiology, Vol. 334, No. 1 More from this issue > Volume 217Issue 4October 1969Pages 1216-1223 Copyright & PermissionsCopyright © 1969 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1969.217.4.1216PubMed5824323History Published online 1 October 1969 Published in print 1 October 1969 Metrics