Chronic Volume Depletion in Patients with Addisons Disease Due to Undertreatment with Fludrocortisone; Further Evidence for the Role of Aldosterone

1983 ◽  
Vol 64 (2) ◽  
pp. 36P-37P
Author(s):  
S J Smith ◽  
N D Markandu ◽  
R A Banks ◽  
J Bayliss ◽  
M G Prentice ◽  
...  
Keyword(s):  
Volume Depletion ◽  
Addisons Disease

scholarly journals THE ROLE OF VOLUME DEPLETION IN FUROSEMIDE ENHANCED AMINOGLYCOSIDE NEPHROTOXICITY

1980 ◽  
Vol 14 (8) ◽  
pp. 1007-1007
Author(s):  
R D Adelman ◽  
W Spangler ◽  
D Thomson ◽  
F Beasom
Keyword(s):  
Volume Depletion

ACUTE CONFUSIONAL STATES AND DEMENTIA IN THE ELDERLY: THE ROLE OF DEHYDRATION/VOLUME DEPLETION, PHYSICAL ILLNESS AND AGE

1980 ◽  
Vol 9 (3) ◽  
pp. 137-146 ◽  
Author(s):  
D. G. SEYMOUR ◽  
P. J. HENSCHKE ◽  
R. D. T. CAPE ◽  
A. J. CAMPBELL
Keyword(s):  
The Elderly ◽  
Physical Illness ◽  
Volume Depletion ◽  
Confusional States

scholarly journals Role of KCNE1-Dependent K+ Fluxes in Mouse Proximal Tubule

2001 ◽  
Vol 12 (10) ◽  
pp. 2003-2011
Author(s):  
VOLKER VALLON ◽  
FLORIAN GRAHAMMER ◽  
KERSTIN RICHTER ◽  
MARKUS BLEICH ◽  
FLORIAN LANG ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Coupled Transport ◽  
Wild Type ◽  
Electrochemical Gradient ◽  
Volume Depletion ◽  
Luminal Membrane ◽  
Clearance Studies ◽  
Electrophysiological Studies ◽  
Kidney Micropuncture

Abstract. The electrochemical gradient for K+ across the luminal membrane of the proximal tubule favors K+ fluxes to the lumen. Here it was demonstrated by immunohistochemistry that KCNE1 and KCNQ1, which form together the slowly activated component of the delayed rectifying K+ current in the heart, also colocalize in the luminal membrane of proximal tubule in mouse kidney. Micropuncture experiments revealed a reduced K+ concentration in late proximal and early distal tubular fluid as well as a reduced K+ delivery to these sites in KCNE1 knockout (-/-), compared with wild-type (+/+) mice. These observations would be consistent with KCNE1-dependent K+ fluxes to the lumen in proximal tubule. Electrophysiological studies in isolated perfused proximal tubules indicated that this K+ flux is essential to counteract membrane depolarization due to electrogenic Na+-coupled transport of glucose or amino acids. Clearance studies revealed an enhanced fractional urinary excretion of fluid, Na+, Cl-, and glucose in KCNE1 -/- compared with KCNE1 +/+ mice that may relate to an attenuated transport in proximal tubule and contribute to volume depletion in these mice, as indicated by higher hematocrit values.

Role of the adrenal medulla in control of blood pressure and renal function during frusemide-induced volume depletion

1995 ◽  
Vol 13 (2) ◽  
pp. 235???242 ◽  
Author(s):  
Philip Hasbak ◽  
Josrgen S. Petersen ◽  
Michael Shalmi ◽  
Henrik R. Lam ◽  
Niels J. Christensen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Adrenal Medulla ◽  
Volume Depletion

Defining the role of albumin infusion in cirrhosis-associated hyponatremia

2014 ◽  
Vol 307 (2) ◽  
pp. G229-G232 ◽  
Author(s):  
Minhtri K. Nguyen ◽  
Vahram Ornekian ◽  
Liyo Kao ◽  
Anthony W. Butch ◽  
Ira Kurtz
Keyword(s):  
Sodium Concentration ◽  
Albumin Concentration ◽  
Intravascular Volume ◽  
Volume Depletion ◽  
Vitro Assay ◽  
Albumin Infusion ◽  
Donnan Equilibrium ◽  
Intravascular Volume Depletion

The presence of negatively charged, impermeant proteins in the plasma space alters the distribution of diffusible ions in the plasma and interstitial fluid (ISF) compartments to preserve electroneutrality and is known as Gibbs-Donnan equilibrium. In patients with hypoalbuminemia due to underlying cirrhosis, the decrease in the plasma water albumin concentration ([Alb−]pw) would be expected to result in a decrease in the plasma water sodium concentration ([Na+]pw) due to an alteration in the distribution of Na+ between the plasma and ISF. In addition, cirrhosis-associated hyponatremia may be due to the renal diluting defect resulting from the intravascular volume depletion due to gastrointestinal losses and overdiuresis and/or decreased effective circulatory volume secondary to splanchnic vasodilatation. Therefore, albumin infusion may result in correction of the hyponatremia in cirrhotic patients either by modulating the Gibbs-Donnan effect due to hypoalbuminemia or by restoring intravascular volume in patients with intravascular volume depletion due to gastrointestinal losses and overdiuresis. However, the differential role of albumin infusion in modulating the [Na+]pw in these patients has not previously been analyzed quantitatively. In the present study, we developed an in vitro assay system to examine for the first time the quantitative effect of changes in albumin concentration on the distribution of Na+ between two compartments separated by a membrane that allows the free diffusion of Na+. Our findings demonstrated that changes in [Alb−]pw are linearly related to changes in [Na+]pw as predicted by Gibbs-Donnan equilibrium. However, based on our findings, we predict that the improvement in cirrhosis-associated hyponatremia due to intravascular volume depletion results predominantly from the restoration of intravascular volume rather than alterations in Gibbs-Donnan equilibrium.

Role of the autonomic nervous system in the reduced maximal cardiac output at altitude

2002 ◽  
Vol 93 (1) ◽  
pp. 271-279 ◽  
Author(s):  
Harm J. Bogaard ◽  
Susan R. Hopkins ◽  
Yoshiki Yamaya ◽  
Kyuichi Niizeki ◽  
Michael G. Ziegler ◽  
...  
Keyword(s):  
Nervous System ◽  
Cardiac Output ◽  
Autonomic Nervous System ◽  
Sea Level ◽  
Maximal Exercise ◽  
Maximal Heart Rate ◽  
Contributing Factors ◽  
Volume Depletion ◽  
Autonomic Nervous

After acclimatization to high altitude, maximal exercise cardiac output (Q˙t) is reduced. Possible contributing factors include 1) blood volume depletion, 2) increased blood viscosity, 3) myocardial hypoxia, 4) altered autonomic nervous system (ANS) function affecting maximal heart rate (HR), and 5) reduced flow demand from reduced muscle work capability. We tested the role of the ANS reduction of HR in this phenomenon in five normal subjects by separately blocking the sympathetic and parasympathetic arms of the ANS during maximal exercise after 2-wk acclimatization at 3,800 m to alter maximal HR. We used intravenous doses of 8.0 mg of propranolol and 0.8 mg of glycopyrrolate, respectively. At altitude, peak HR was 170 ± 6 beats/min, reduced from 186 ± 3 beats/min ( P = 0.012) at sea level. Propranolol further reduced peak HR to 139 ± 2 beats/min ( P = 0.001), whereas glycopyrrolate increased peak HR to sea level values, 184 ± 3 beats/min, confirming adequate dosing with each drug. In contrast, peak O2 consumption, work rate, and Q˙t were similar at altitude under all drug treatments [peak Q˙t = 16.2 ± 1.2 (control), 15.5 ± 1.3 (propranolol), and 16.2 ± 1.1 l/min (glycopyrrolate)]. All Q˙t results at altitude were lower than those at sea level (20.0 ± 1.8 l/min in air). Therefore, this study suggests that, whereas the ANS may affect HR at altitude, peak Q˙t is unaffected by ANS blockade. We conclude that the effect of altered ANS function on HR is not the cause of the reduced maximal Q˙t at altitude.

Vasopressin and Malignant Deoxycorticosterone Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 45s-48s ◽  
Author(s):  
J. Möhring ◽  
B. Möhring ◽  
M. Petri ◽  
D. Haack
Keyword(s):  
Blood Pressure ◽  
Arginine Vasopressin ◽  
Renal Hypertension ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Volume Depletion ◽  
Angiotensin System ◽  
Plasma Arginine ◽  
Normotensive Control

1. The role of arginine-vasopressin in the pathogenesis of malignant deoxycorticosterone (DOC) hypertension of rats was investigated. 2. In rats with malignant DOC hypertension plasma arginine-vasopressin concentrations increased more than tenfold subsequent to volume depletion and a rise of serum osmolality. 3. The injection of a specific antibody serum for arginine-vasopressin caused a marked fall of blood pressure in rats with malignant DOC hypertension, whereas the injection of angiotensin II antiserum did not affect blood pressure. 4. In rats exhibiting a benign course of DOC hypertension plasma concentrations of arginine-vasopressin were increased threefold in comparison with normotensive control rats; the injection of an arginine-vasopressin antiserum induced a significant but small fall of blood pressure. 5. It is concluded that in the pathogenesis of malignant DOC hypertension arginine-vasopressin might play the role that the renin—angiotensin system plays in the pathogenesis of malignant renal hypertension.

Restricted postexercise pulmonary diffusion capacity and central blood volume depletion

1997 ◽  
Vol 83 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Birgitte Hanel ◽  
Inge Teunissen ◽  
Alan Rabøl ◽  
Jørgen Warberg ◽  
Niels H. Secher
Keyword(s):  
Blood Volume ◽  
Electrical Impedance ◽  
Control Group ◽  
Central Blood Volume ◽  
Volume Depletion ◽  
Diffusion Capacity ◽  
Pulmonary Diffusion ◽  
Before And After ◽  
Pulmonary Diffusion Capacity

Hanel, Birgitte, Inge Teunissen, Alan Rabøl, Jørgen Warberg, and Niels H. Secher. Restricted postexercise pulmonary diffusion capacity and central blood volume depletion. J. Appl. Physiol. 83(1): 11–17, 1997.—Pulmonary diffusion capacity for carbon monoxide (Dl CO), regional electrical impedance (Z0), and the distribution of technetium-99m-labeled erythrocytes together with concentration of plasma atrial natriuretic peptide (ANP) were determined before and after a 6-min “all-out” row in nine oarsmen and in six control subjects. Two and one-half hours after exercise in the upright seated position, Dl CO was reduced by 6 (−2 to 21; median and range) %, the thoracic-to-thigh electrical impedance ratio (Z0 thorax/Z0 thigh) rose by 14 (−1 to 29) %, paralleled by a 7 (−3 to 11) % decrease and a 3 (−5 to 12) % increase in the thoracic and thigh blood volume, respectively. These responses were associated with a decrease in the plasma ANP concentration from 15 (13–31) to 12 (9–27) pmol/l ( P < 0.05). Similarly, in the supine position, Z0 thorax/Z0 thighincreased by 10 (−5 to 28) % when Dl CO was reduced 12 (6–26) % ( P < 0.05), whereas Dl COremained stable in the control group. The increase in Z0 thorax/Z0 thighand the corresponding redistribution of the blood volume in both body positions show that approximately one-half of the postexercise reduction of Dl CO is explained by a decrease in the pulmonary blood volume. The role of a reduced postexercise central blood volume is underscored by the lower plasma ANP, which aids in upregulating the blood volume after exercise in athletes.

scholarly journals Protein phosphatase 1 modulates the inhibitory effect of With-no-Lysine kinase 4 on ROMK channels

2012 ◽  
Vol 303 (1) ◽  
pp. F110-F119 ◽  
Author(s):  
Dao-Hong Lin ◽  
Peng Yue ◽  
Jesse Rinehart ◽  
Peng Sun ◽  
Zhijian Wang ◽  
...  
Keyword(s):  
Protein Phosphatase ◽  
Collecting Duct ◽  
Inhibitory Effect ◽  
Protein Phosphatase 1 ◽  
Cortical Collecting Duct ◽  
Channel Activity ◽  
Serine Residue ◽  
Volume Depletion ◽  
K Secretion

With-no-Lysine kinase 4 (WNK4) inhibited ROMK (Kir1.1) channels and the inhibitory effect of WNK4 was abolished by serum-glucocorticoid-induced kinase 1 (SGK1) but restored by c-Src. The aim of the present study is to explore the mechanism by which Src-family tyrosine kinase (SFK) modulates the effect of SGK1 on WNK4 and to test the role of SFK-WNK4-SGK1 interaction in regulating ROMK channels in the kidney. Immunoprecipitation demonstrated that protein phosphatase 1 (PP1) binds to WNK4 at amino acid (aa) residues 695–699 (PP1#1) and at aa 1211–1215 (PP1#2). WNK4−PP1#1 and WNK4−PP1#2, in which the PP1#1 or PP1#2 binding site was deleted or mutated, inhibited ROMK channels as potently as WNK4. However, c-Src restored the inhibitory effect of WNK4 but not WNK4−PP1#1 on ROMK channels in the presence of SGK1. Moreover, expression of c-Src inhibited SGK1-induced phosphorylation of WNK4 but not WNK4−PP1#1 at serine residue 1196 (Ser1196). In contrast, coexpression of c-Src restored the inhibitory effect of WNK4−PP1#2 on ROMK in the presence of SGK1 and diminished SGK1-induced WNK4 phosphorylation at Ser1196 in cells transfected with WNK4−PP1#2. This suggests the possibility that c-Src regulates the interaction between WNK4 and SGK1 through activating PP1 binding to aa 695–9 thereby decreasing WNK4 phosphorylation and restoring the inhibitory effect of WNK4. This mechanism plays a role in suppressing ROMK channel activity during the volume depletion because inhibition of SFK or serine/threonine phosphatases increases ROMK channel activity in the cortical collecting duct of rats on a low-Na diet. We conclude that regulation of phosphatase activity by SFK plays a role in determining the effect of aldosterone on ROMK channels and on renal K secretion.

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