Relative Roles of Principal and Intercalated Cells in the Regulation of Sodium Balance and Blood Pressure

2015 ◽  
Vol 17 (4) ◽  
Author(s):  
Régine Chambrey ◽  
Francesco Trepiccione
Keyword(s):  
Blood Pressure ◽  
Sodium Balance ◽  
Intercalated Cells ◽  
Principal And Intercalated Cells

Comparison of fast and slow pressor effects of angiotensin II in the conscious rat

1981 ◽  
Vol 241 (3) ◽  
pp. H381-H388 ◽  
Author(s):  
A. J. Brown ◽  
J. Casals-Stenzel ◽  
S. Gofford ◽  
A. F. Lever ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Control Period ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Pressor Effect ◽  
Ang Ii ◽  
Conscious Rat ◽  
Female Wistar Rats

Female Wistar rats were infused intravenously with 5% dextrose for 3 days, then with angiotensin II (ANG II) in 5% dextrose at 20 ng . kg-1 . min-1 for 7 days, and finally with dextrose for 2.5 days. ANG II raised mean arterial pressure (MAP) gradually; by the 7th day it was 49.7 mmHg higher than during the dextrose control period in the same rats. Control rats were infused with dextrose for 12.5 days; MAP did not change. Plasma ANG II concentration was measured during infusion. In hypertensive rats on the 7th day of ANG II infusion, it was six times higher than in control rats infused with dextrose. Changes of blood pressure and plasma ANG II concentration were compared in further rats infused with much larger doses of ANG II. Rats receiving 270 ng . kg-1 . min-1 for 1 h had an almost maximal direct pressor response, MAP rising 45.3 mmHg and plasma ANG II rising 32-fold compared with controls. Thus, infusion of ANG II at low dose without direct pressor effect gradually raises blood pressure to a level similar to the maximum direct pressor effect produced by larger doses of ANG II. Sodium balance and food and water intakes were also measured and did not change during prolonged infusion of ANG II at 20 ng . kg-1 . min-1. Thus, the slow pressure effect of ANG II develops at a lower and more nearly physiological plasma concentration of the peptide than do the direct pressor effect and the effects on drinking, eating, and urinary sodium excretion.

Abstract 632: Flow-induced TRPV4 Activation Mediates Calcium Influx In The Thick Ascending Limb.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Pablo D Cabral ◽  
Jeffrey L Garvin
Keyword(s):  
Blood Pressure ◽  
Intracellular Calcium ◽  
Calcium Influx ◽  
Ruthenium Red ◽  
Sodium Balance ◽  
Transient Receptor Potential Vanilloid ◽  
No Production ◽  
Thick Ascending Limb ◽  
Fura 2 ◽  
Luminal Flow

Background: The thick ascending limb is critical in the regulation of sodium balance and therefore blood pressure. We previously showed that nitric oxide (NO), which inhibits sodium chloride transport and therefore blood pressure is regulated by luminal flow in this segment. Transient receptor potential vanilloid 4 (TRPV4), a member of the TRPV family of cation channels, is expressed in the thick ascending limb. This calcium permeable channel can be activated by luminal flow in other cell types. Therefore, we hypothesized that in the thick ascending limb luminal flow induces TRPV4 activation thereby increasing calcium influx and NO production. METHODS: We used the TRPV4 antagonists Ruthenium red and RN 1734 and the TRPV4 agonist GSK1016790A and measured intracellular calcium and NO production in the absence and presence of luminal flow in isolated and perfused thick ascending limbs from Sprague Dawley rats. NO production was measured using the NO-sensitive dye DAF FM da. Intracellular calcium was measured using the ratiometric calcium sensitive dye Fura-2 AM. Results: Increasing luminal flow from 0 to 20 nL/min stimulated NO production from 8 ± 3 to 45 ± 12 arbitrary units (AU)/min ( p <0.05, n =5). Increasing luminal flow in the presence of the TRPV4 antagonist Ruthenium red (15 μM) eliminated NO production (from 18 ± 5 to 16 ± 9 AU/min; n = 4). Flow-induced NO production was also prevented by the selective TRPV4 antagonist RN 1734 (10 μM) (from 11 ± 7 to 9 ± 2 AU/min; n = 4). Increasing luminal flow increased Fura 2 ratio units by 113 ± 20 %. However, in the presence of the TRPV4 antagonist Ruthenium red (15 μM) Fura 2 ratio units increased only by 55 ± 12 % in response to luminal flow ( p <0.04, n =6). In the absence of luminal flow, activating TRPV4 using the TRPV4 selective agonist GSK1016790A (1 ηM) increased Fura 2 ratio units by 204 ± 43 %. Conclusion: From these data we conclude that flow-induced TRPV4 activation mediates calcium influx and NO production in the thick ascending limb.

RVD in principal and intercalated cells of rabbit cortical collecting tubule

1988 ◽  
Vol 255 (5) ◽  
pp. C612-C621 ◽  
Author(s):  
K. Strange
Keyword(s):  
Mammalian Cells ◽  
Control Volume ◽  
Regulatory Volume Decrease ◽  
Isotonic Saline ◽  
Cell Types ◽  
Intercalated Cells ◽  
Intercalated Cell ◽  
Collecting Tubule ◽  
Principal And Intercalated Cells ◽  
Cortical Collecting Tubule

Cells of the rabbit renal cortical collecting tubule possess significant regulatory volume decrease (RVD) capabilities. After a 100-mosmol/kg reduction in peritubular osmolality, principal and intercalated cells swell 40-45 and 30-35%, respectively, and immediately activate RVD mechanisms. Both cell types downregulate their volume to within 5-6% of control volume at initial rates of 3-6%/min. Return to isotonic saline causes both cell types to shrink (isotonic shrinkage) 25-35% below control volume due to the loss of osmotically active intracellular solutes during RVD. In most mammalian cells studied to date, RVD is mediated largely by passive KCl efflux via KCl cotransport, parallel K+ and Cl- channels, or parallel K+-H+ and Cl- -HCO3- exchange mechanisms. Peritubular application of 0.1 mM ouabain (0 Na+ lumen), bilateral CO2-HCO3- removal, or bilateral application of 0.02 mM bumetanide, 2.0 mM Ba2+, 2.0 mM anthracene-9-carboxylic acid, or 0.5 mM SITS had no significant effect on rates or magnitudes of RVD and isotonic shrinkage in either cell type. Bilateral elevation of K+ from 5 to 52.5 mM reverses or reduces the electrochemical gradient for K+ movement, causing accumulation of this ion in the cytoplasm, but had no effect on the rates or magnitude of principal and intercalated cell RVD. Principal and intercalated cells from K+- or Cl- -depleted tubules (1 h bilateral perfusion with K+- or Cl- -free saline at 37 degrees C) showed normal rates and magnitudes of RVD in K+- or Cl- -free hypotonic saline. Taken together, these results argue against a significant role of passive KCl efflux pathways in mediating principal and intercalated cell RVD.

Minealocorticoid receptors and 11 beta-steroid dehydrogenase activity in renal principal and intercalated cells

1994 ◽  
Vol 266 (1) ◽  
pp. F76-F80 ◽  
Author(s):  
A. Naray-Fejes-Toth ◽  
E. Rusvai ◽  
G. Fejes-Toth
Keyword(s):  
Cell Sorting ◽  
Direct Action ◽  
Collecting Duct ◽  
Cell Types ◽  
Target Cells ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Specific Receptors ◽  
Principal And Intercalated Cells ◽  
Steroid Dehydrogenase

Aldosterone exerts complex effects on the cortical collecting duct (CCD): it increases Na+ and K+ transport, and it also influences H+ and HCO3 transport. Whether these latter effects represent direct action of aldosterone on intercalated cells (ICC) or are secondary to changes in the transport of other electrolytes is unclear. Because the presence of specific receptors is the prerequisite of a direct steroid action, and mineralocorticoid receptors (MR) have not yet been demonstrated in ICC, in this study we determined the density of MR directly in isolated principal cells (PC) and beta-ICC. Purified populations of these two cell types were obtained from rabbit renal cortex by immunodissection and fluorescence-activated cell sorting. We found that both PC and beta-ICC contained a significant number of MR, although receptor density was higher in PC than in beta-ICC (6,704 +/- 912 vs. 2,181 +/- 388 MR sites/cell; P < 0.001). 11 beta-Hydroxysteroid dehydrogenase (11 beta-OHSD), an enzyme that is present predominantly in mineralocorticoid target cells, exhibited a distribution similar to that of MR in the two cell types. 11 beta-OHSD activity, determined by measuring the rate of conversion of [3H]corticosterone to 11-dehydrocorticosterone, was 1.08 +/- 0.14 and 0.34 +/- 0.08 fmol.min-1 x 1,000 cells-1 (P < 0.001) in intact PC and beta-ICC, respectively. 11 beta-OHSD in both cell types utilized NAD as cofactor. These results suggest that beta-ICC are potential direct targets of aldosterone and that MR in both PC and beta-ICC are protected by 11 beta-OHSD.

Insulin's impact on renal sodium transport and blood pressure in health, obesity, and diabetes

2007 ◽  
Vol 293 (4) ◽  
pp. F974-F984 ◽  
Author(s):  
Swasti Tiwari ◽  
Shahla Riazi ◽  
Carolyn A. Ecelbarger
Keyword(s):  
Blood Pressure ◽  
Insulin Infusion ◽  
Type Ii Diabetes Mellitus ◽  
Sodium Balance ◽  
Type I ◽  
Sodium Transporters ◽  
Current State ◽  
Obesity And Diabetes ◽  
Sodium Hydrogen Exchanger ◽  
Insulin Receptor Signaling

Insulin has been shown to have antinatriuretic actions in humans and animal models. Moreover, endogenous hyperinsulinemia and insulin infusion have been correlated to increased blood pressure in some models. In this review, we present the current state of understanding with regard to the regulation of the major renal sodium transporters by insulin in the kidney. Several groups, using primarily cell culture, have demonstrated that insulin can directly increase activity of the epithelial sodium channel, the sodium-phosphate cotransporter, the sodium-hydrogen exchanger type III, and Na-K-ATPase. We and others have demonstrated alterations in the expression at the protein level of many of these same proteins with insulin infusion or in hyperinsulinemic models. We also discuss how this regulation is perturbed in type I and type II diabetes mellitus. Finally, we discuss a potential role for regulation of insulin receptor signaling in the kidney in contributing to sodium balance and blood pressure.

scholarly journals Cortical distal nephron Cl− transport in volume homeostasis and blood pressure regulation

2013 ◽  
Vol 305 (4) ◽  
pp. F427-F438 ◽  
Author(s):  
Susan M. Wall ◽  
Alan M. Weinstein
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Extracellular Volume ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Acid Base Balance ◽  
Relative Contribution ◽  
And Function

Renal intercalated cells mediate the secretion or absorption of Cl− and OH−/H+ equivalents in the connecting segment (CNT) and cortical collecting duct (CCD). In so doing, they regulate acid-base balance, vascular volume, and blood pressure. Cl− absorption is either electrogenic and amiloride-sensitive or electroneutral and thiazide-sensitive. However, which Cl− transporter(s) are targeted by these diuretics is debated. While epithelial Na+ channel (ENaC) does not transport Cl−, it modulates Cl− transport probably by generating a lumen-negative voltage, which drives Cl− flux across tight junctions. In addition, recent evidence indicates that ENaC inhibition increases electrogenic Cl− secretion via a type A intercalated cells. During ENaC blockade, Cl− is taken up across the basolateral membrane through the Na+-K+−2Cl− cotransporter (NKCC1) and then secreted across the apical membrane through a conductive pathway (a Cl− channel or an electrogenic exchanger). The mechanism of this apical Cl− secretion is unresolved. In contrast, thiazide diuretics inhibit electroneutral Cl− absorption mediated by a Na+-dependent Cl−/HCO3− exchanger. The relative contribution of the thiazide and the amiloride-sensitive components of Cl− absorption varies between studies and probably depends on the treatment model employed. Cl− absorption increases markedly with angiotensin and aldosterone administration, largely by upregulating the Na+-independent Cl−/HCO3− exchanger pendrin. In the absence of pendrin [ Slc26a4 (−/−) or pendrin null mice], aldosterone-stimulated Cl− absorption is significantly reduced, which attenuates the pressor response to this steroid hormone. Pendrin also modulates aldosterone-induced changes in ENaC abundance and function through a kidney-specific mechanism that does not involve changes in the concentration of a circulating hormone. Instead, pendrin changes ENaC abundance and function, at least in part, by altering luminal HCO3−. This review summarizes mechanisms of Cl− transport in CNT and CCD and how these transporters contribute to the regulation of extracellular volume and blood pressure.

Three distinct cell populations in rat kidney collecting duct

1987 ◽  
Vol 253 (2) ◽  
pp. C323-C328 ◽  
Author(s):  
H. Holthofer ◽  
B. A. Schulte ◽  
G. Pasternack ◽  
G. J. Siegel ◽  
S. S. Spicer
Keyword(s):  
Collecting Duct ◽  
Rat Kidney ◽  
Morphological Characteristics ◽  
Anion Channel ◽  
Band 3 ◽  
Cell Populations ◽  
Intercalated Cells ◽  
Distinct Cell ◽  
Collecting Ducts ◽  
Principal And Intercalated Cells

The morphologically heterogeneous cell populations in the collecting ducts of the rat kidney were studied using immunocytochemical detection of Na+-K+-ATPase and the anion channel (band 3) glycoprotein. Both enzymes were localized to the basal aspect of separate and morphologically distinct subpopulations of cells in various segments of the collecting duct. Na+-K+-ATPase appeared to be present exclusively in principal cells as identified by their morphology, whereas band 3 antibodies reacted only with intercalated cells. However, 5-20% of cells with the morphological characteristics of intercalated cells failed to react with either antisera in various segments of collecting ducts. As band 3 glycoprotein serves in exchanging intracellular bicarbonate for chloride, it is highly likely that the cells positive for this antigen secrete protons. The method introduced here appears thus useful for distinguishing between principal and intercalated cells by differences in their enzyme content and further for revealing two subpopulations of intercalated cells. This method promises to provide a useful approach for studying the principal and intercalated cell populations in various metabolic states.

scholarly journals Effects of AT1A receptor deletion on blood pressure and sodium excretion during altered dietary salt intake

2002 ◽  
Vol 283 (3) ◽  
pp. F447-F453 ◽  
Author(s):  
Amy J. Mangrum ◽  
R. Ariel Gomez ◽  
Victoria F. Norwood
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Wild Type ◽  
Compensatory Mechanisms ◽  
Wide Range ◽  
Blood Pressures ◽  
Pressure Natriuresis

The present study was performed to investigate the role of type 1A ANG II (AT1A) receptors in regulating sodium balance and blood pressure maintenance during chronic dietary sodium variations in AT1A receptor-deficient (−/−) mice. Groups of AT1A (−/−) and wild-type mice were placed on a low (LS)-, normal (NS)-, or high-salt (HS) diet for 3 wk. AT1A(−/−) mice on an LS diet had high urinary volume and low blood pressure despite increased renin and aldosterone levels. On an HS diet, (−/−) mice demonstrated significant diuresis, yet blood pressure increased to levels greater than control littermates. There was no effect of dietary sodium intake on systolic blood pressures in wild-type animals. The pressure-natriuresis relationship in AT1A (−/−) mice demonstrated a shift to the left and a decreased slope compared with wild-type littermates. These studies demonstrate that mice lacking the AT1A receptor have blood pressures sensitive to changes in dietary sodium, marked alterations of the pressure-natriuresis relationship, and compensatory mechanisms capable of maintaining normal sodium balance across a wide range of sodium intakes.

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