Effects of acute NaCl, KCl and KHCO3 loads on renal electrolyte excretion in humans

1992 ◽  
Vol 83 (5) ◽  
pp. 567-574 ◽  
Author(s):  
Marjolijn van Buren ◽  
Ton J. Rabelink ◽  
Herman J. M. van Rijn ◽  
Hein A. Koomans
Keyword(s):  
Sodium Excretion ◽  
Plasma Potassium ◽  
Acid Excretion ◽  
Potassium Salts ◽  
Electrolyte Excretion ◽  
Specific Effects ◽  
Identical Manner ◽  
Natriuretic Effect ◽  
Nacl Load

1. Potassium salts increase sodium excretion in humans. To define the role of the potassium ion in this effect, we compared the effects of equimolar single oral loads of 100 mmol of NaCl and KCl on renal electrolyte excretion in seven healthy subjects. In a second group (n = 7), we infused equimolar loads of NaCl or KCl (0.75 mmol/kg in 2 h). 2. In both experiments the KCl load quickly increased plasma potassium and aldosterone concentrations and potassium and sodium excretion to a maximum by 2 h after the load, whereas the NaCl load had no such effect. 3. In a third group (n = 7) we compared the effects of single oral loads of KCl and KHCO3 (1 mmol/kg), to assess the role of the anion in the natriuretic effect of potassium salts. 4. KCl and KHCO3 transiently stimulated urinary excretion of potassium and sodium in an identical manner. 5. We also followed the changes in acid excretion over time. Whereas both KCl and KHCO3 loading decreased acid excretion, this effect was greater after KHCO3 loading. Interestingly, acid excretion did not decrease further after the first collection hour after the potassium load, although the plasma potassium concentration was still increasing. 6. From these data we conclude (1) that increased excretion of sodium, potassium and chloride and decreased excretion of protons after administration of potassium salts are the specific effects of the potassium component; (2) that potassium also appears to have secondary, indirect effects on proton excretion, the mechanism of which remains to be clarified.

Effects of sodium and potassium salts with anions other than chloride on renin secretion in the dog

1978 ◽  
Vol 234 (1) ◽  
pp. F10-F15
Author(s):  
G. A. Stephens ◽  
J. O. Davis ◽  
R. H. Freeman ◽  
B. E. Watkins
Keyword(s):  
Plasma Potassium ◽  
Sodium Lactate ◽  
Renin Secretion ◽  
Potassium Sulfate ◽  
Plasma Sodium ◽  
Potassium Salts ◽  
Arterial Blood ◽  
Sodium And Potassium ◽  
Venous Plasma

Intrarenal arterial infusions of sodium and potassium salts with anions other than chloride were given to evaluate the role of the chloride ion in influencing renin secretion (RS). The studies were conducted in dogs with thoracic caval constriction. Sodium lactate increased renal venous plasma sodium concentration (RVPNa) from 142 to 166 meq/liter (n, 6); RS decreased from 3,070 to 1,510 ng angiotensin/min (P less than 0.005). Arterial blood pressure and renal blood flow were not changed appreciably. Sodium excretion (ENa) increased, whereas chloride excretion (EC1) fell during the first three 15-min infusion periods. Potassium lactate increased renal venous plasma potassium concentration from 4.1 to 6.2 meq/liter (N, b). RS decreased during the first three 15-min periods of infusion (from 3,470 to 2,180 ng angiotensin/min, P less than 0.01). ENa and EC1 increased during the infusion. Potassium sulfate also decreased RS, and EC1 was usually increased. The results with sodium lactate favor a role for sodium compared with chloride in mediating the decreased renin release, but there are other possible interpretations which have been discussed. Additional studies are needed to resolve the role of chloride during potassium infusion.

Extrarenal potassium adaptation: role of skeletal muscle

1986 ◽  
Vol 251 (2) ◽  
pp. F313-F318 ◽  
Author(s):  
J. D. Blachley ◽  
B. P. Crider ◽  
J. H. Johnson
Keyword(s):  
Skeletal Muscle ◽  
Binding Capacity ◽  
Lethal Dose ◽  
Plasma Potassium ◽  
Potassium Salts ◽  
Ouabain Binding ◽  
High Potassium ◽  
Potassium Adaptation

Following the ingestion of a high-potassium-content diet for only a few days, the plasma potassium of rats rises only modestly in response to a previously lethal dose of potassium salts. This acquired tolerance, termed potassium adaptation, is principally the result of increased capacity to excrete potassium into the urine. However, a substantial portion of the acute potassium dose is not immediately excreted and is apparently translocated into cells. Previous studies have failed to show an increase in the content of potassium of a variety of tissues from such animals. Using 86Rb as a potassium analogue, we have shown that the skeletal muscle of potassium-adapted rats takes up significantly greater amounts of potassium in vivo in response to an acute challenge than does that of control animals. Furthermore, the same animals exhibit greater efflux of 86Rb following the termination of the acute infusion. We have also shown that the Na+-K+-ATPase activity and ouabain-binding capacity of skeletal muscle microsomes are increased by the process of potassium adaptation. We conclude that skeletal muscle is an important participant in potassium adaptation and acts to temporarily buffer acute increases in the extracellular concentration of potassium.

Role of transmitters in mediating hypothalamic control of electrolyte excretion

1977 ◽  
Vol 55 (5) ◽  
pp. 1143-1154 ◽  
Author(s):  
M. Morris ◽  
S. M. McCann ◽  
R. Orias
Keyword(s):  
Sodium Excretion ◽  
Adrenergic Receptors ◽  
Male Rats ◽  
Intraventricular Injection ◽  
Urinary Volume ◽  
Electrolyte Excretion ◽  
Hypothalamic Control ◽  
Adrenergic Blocker ◽  
Β Receptor

Changes in urinary volume and electrolyte excretion were monitored after the injection of cholinergic and monoaminergic drugs into the third cerebral ventricle of conscious male rats made diuretic by an intravenous infusion of 5% dextrose. A natriuretic and kaliuretic response was induced by the intraventricular injection of norepinephrine (NE) or carbachol, whereas dopamine (DA) had no effect. The β-receptor stimulator isoproterenol (ISO) induced an antinatriuretic and antikaliuretic effect.Intraventricular injection of the α-adrenergic blocker phentolamine abolished the natriuretic response to NE and carbachol and to intraventricular hypertonic saline (HS). By contrast, the β-adrenergic blocker propranolol induced a natriuresis and kaliuresis when injected alone and an additive effect when its injection was followed by NE or HS. Propranolol potentiated the natriuretic response to carbachol. Cholinergic blockade with atropine diminished the response to NE and blocked the natriuretic response to HS. It is suggested that sodium receptors in the ventricular wall can modify renal sodium excretion via a stimulatory pathway involving cholinergic and α-adrenergic receptors and can inhibit sodium excretion via a tonically active β-receptor pathway.

Atrial natriuretic peptide in preeclampsia: metabolic clearance, sodium excretion and renal hemodynamics

1997 ◽  
Vol 273 (3) ◽  
pp. F483-F487 ◽  
Author(s):  
D. W. Irons ◽  
P. H. Baylis ◽  
T. J. Butler ◽  
J. M. Davison
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Renal Plasma Flow ◽  
Metabolic Clearance ◽  
Significant Difference ◽  
Basal Plasma ◽  
Natriuretic Effect ◽  
Atrial Natriuretic

To further elucidate the role of atrial natriuretic peptide (ANP) in preeclampsia, its metabolic clearance (MCRANP) was determined concomitantly with its effects on sodium excretion (UNa), glomerular filtration rate (GFR), and effective renal plasma flow (ERPF). Ten untreated preeclamptic primigravidae (PET) were studied at 29-37 wk gestation and again 4 mo postpartum (PP). Basal plasma concentration of ANP was significantly increased in PET compared with PP (14.8 +/- 1.9 vs. 4.1 +/- 0.5 pmol/l, respectively; P < 0.0001). MCRANP in PET and PP was 5.0 +/- 0.8 and 4.9 +/- 0.5 l/min [not significant (NS)], respectively. In PET, infusion of ANP produced (basal vs. ANP) a natriuresis (UNa 0.14 +/- 0.02 vs. 0.28 +/- 0.04 mmol/min, P < 0.001) and an increase in GFR (97 +/- 7 vs. 106 +/- 8 ml/min, P < 0.05), with ERPF unchanged (609 +/- 24 vs. 634 +/- 29 ml/min, NS). In PP, ANP infusion also produced a natriuresis (UNa 0.20 +/- 0.02 vs. 0.25 +/- 0.02 mmol/min, P = 0.01), no significant change in GFR (109 +/- 7 vs. 102 +/- 4 ml/min), and a significant reduction in ERPF (514 +/- 22 vs. 409 +/- 18 ml/min, P < 0.0001). Analysis of variance demonstrated a greater natriuretic effect of ANP in PET compared with PP (P < 0.05), similarly a significant difference in the effect of ANP on ERPF (P < 0.01) and GFR (P < 0.05) was seen but not on filtration fraction (P = 0.35).

Renal interstitial hydrostatic pressure during verapamil-induced natriuresis

1992 ◽  
Vol 262 (3) ◽  
pp. R432-R436 ◽  
Author(s):  
J. P. Granger ◽  
M. J. Solhaug
Keyword(s):  
Angiotensin Ii ◽  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Fractional Excretion ◽  
Electrolyte Excretion ◽  
Filtration Fraction ◽  
Fractional Excretion Of Sodium ◽  
Induced Hypertension ◽  
Renal Vascular

Infusion of calcium antagonists results in significant increases in sodium excretion, an effect that is exacerbated in hypertensive animals. The mechanism responsible for the increase in sodium excretion has not been elucidated. The purpose of this study was to determine the role of renal interstitial hydrostatic pressure (RIHP) in mediating increases in sodium excretion produced by the calcium antagonist verapamil. Changes in renal hemodynamics and electrolyte excretion were examined in response to an intrarenal infusion of verapamil (100 micrograms/min) in normal dogs and in dogs with angiotensin II-induced hypertension. Infusion of verapamil in normal dogs increased renal blood flow by 18% and had no effect on glomerular filtration rate. Renal vascular resistance and filtration fraction both decreased in response to verapamil. Absolute (5.1 +/- 2.3 to 176 +/- 45.8 mueq/min) and fractional excretion of sodium (0.21 +/- 0.13 to 7.36 +/- 3.12%) also increased significantly. Despite renal vasodilation, the natriuresis was not associated with significant increases in RIHP (6.4 +/- 0.9 to 5.8 +/- 0.9 mmHg). Infusion of verapamil into dogs with angiotensin II hypertension resulted in a natriuresis (4.2 +/- 1.6 to 338.7 +/- 78.3 mueq/min) that was much greater than under normal conditions. Although the renal vasodilation was significantly higher in the angiotensin II-hypertensive dogs, the enhanced natriuresis in these animals was not associated with increases in RIHP. The results of this study indicate that increases in RIHP are not responsible for the natriuresis produced by verapamil in normal or angiotensin II-hypertensive dogs.

scholarly journals Role of cytochrome P-450 metabolites in the regulation of renal function and blood pressure in 2-kidney 1-clip hypertensive rats

2011 ◽  
Vol 300 (6) ◽  
pp. R1468-R1475 ◽  
Author(s):  
Alexandra Sporková ◽  
Libor Kopkan ◽  
Šárka Varcabová ◽  
Zuzana Husková ◽  
Sung Hee Hwang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Sodium Excretion ◽  
Blood Pressure Lowering Effect ◽  
Pressure Lowering ◽  
Natriuretic Effect ◽  
Pressure Natriuresis ◽  
Cytochrome P 450 ◽  
2K1c Hypertension

Alterations in renal function contribute to Goldblatt two-kidney, one-clip (2K1C) hypertension. A previous study indicated that bioavailability of cytochrome P-450 metabolites epoxyeicosatrienoic acids (EETs) is decreased while that of 20-hydroxyeicosatetraenoic acids (20-HETE) is increased in this model. We utilized the inhibitor of soluble epoxide hydrolase cis-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid ( c-AUCB) and HET-0016, the inhibitor of 20-HETE production, to study the role of EETs and 20-HETE in the regulation of renal function. Chronic c-AUCB treatment significantly decreased systolic blood pressure (SBP) (133 ± 1 vs. 163 ± 3 mmHg) and increased sodium excretion (1.23 ± 0.10 vs . 0.59 ± 0.03 mmol/day) in 2K1C rats. HET-0016 did not affect SBP and sodium excretion. In acute experiments, renal blood flow (RBF) was decreased in 2K1C rats (5.0 ± 0.2 vs . 6.9 ± 0.2 ml·min−1·g−1). c-AUCB normalized RBF in 2K1C rats (6.5 ± 0.6 ml·min−1·g−1). HET-0016 also increased RBF in 2K1C rats (5.8 ± 0.2 ml·min−1·g−1). Although RBF and glomerular filtration rate (GFR) remained stable in normotensive rats during renal arterial pressure (RAP) reductions, both were significantly reduced at 100 mmHg RAP in 2K1C rats. c-AUCB did not improve autoregulation but increased RBF at all RAPs and shifted the pressure-natriuresis curve to the left. HET-0016-treated 2K1C rats exhibited impaired autoregulation of RBF and GFR. Our data indicate that c-AUCB displays antihypertensive properties in 2K1C hypertension that are mediated by an improvement of RBF and pressure natriuresis. While HET-0016 enhanced RBF, its anti-natriuretic effect likely prevented it from producing a blood pressure-lowering effect in the 2K1C model.

Abstract 527: Natriuretic Effect Mediated by the Renal Medullary α7 Nicotinic Acetylcholine Receptor

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Weili Wang ◽  
Wei-Qing Han ◽  
Qing Zhu ◽  
Imad Damaj ◽  
Pin-Lan Li ◽  
...  
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Α7 Nicotinic Acetylcholine Receptor ◽  
Nicotinic Acetylcholine ◽  
Renal Sodium Excretion ◽  
Α7 Nachr ◽  
Natriuretic Effect

Although there are extensive studies on the regulation of renal sodium excretion by adrenergic pathway, the role of cholinergic pathway in the renal sodium excretion is largely unknown. The present study characterized the expression of α7 nicotinic acetylcholine receptor (nAChR) in the kidneys and determined the functional role of this nAChR subtype in urinary sodium excretion in Sprague Dawley rats. RT-PCR and Western blot analyses showed that α7 nAChR was present in the kidneys. Immunohistochemistry analysis demonstrated that the strongest immunostaining of α7 nAChR was observed in the distal tubules and collecting ducts in the kidneys. Infusion of an α7 nAChR agonist PNU-282987 (2.7 μM, 10 μl/min) into the renal medulla dramatically increased the urine volume (from 15.4 ± 2.1 to 42.5 ± 3.9 μl/min/g kwt) and sodium excretion (from 1.26 ± 0.18 to 4.15 ± 0.60 μmole/min/g kwt), which was blocked by an α7 nAChR antagonist methyllycaconitine (MLA, 5 μM, 10 μl/min), in anesthetized rats. Infusion of PNU-282987 did not cause any change in renal medullary blood flow as measured by Laser Doppler flowmeter. In addition, intra-renal medullary infusion of MLA (5 μM, 10 μl/min) significantly inhibited the volume expansion-induced increase of urine volume and sodium excretion by 25%. These data suggest that activation of renal medullary α7 nAChR produces a natriuretic effect through its tubular action in rats. (Supported by NIH grant HL89563 and HL106042)

scholarly journals Monoclonal Antibodies as Neurological Therapeutics

2021 ◽  
Vol 14 (2) ◽  
pp. 92
Author(s):  
Panagiotis Gklinos ◽  
Miranta Papadopoulou ◽  
Vid Stanulovic ◽  
Dimos D. Mitsikostas ◽  
Dimitrios Papadopoulos
Keyword(s):  
Monoclonal Antibodies ◽  
Molecular Mechanisms ◽  
Neurological Diseases ◽  
Therapeutic Agents ◽  
Medical Specialties ◽  
Specific Effects ◽  
Different Types ◽  
Neurological Conditions ◽  
Disease Pathways

Over the last 30 years the role of monoclonal antibodies in therapeutics has increased enormously, revolutionizing treatment in most medical specialties, including neurology. Monoclonal antibodies are key therapeutic agents for several neurological conditions with diverse pathophysiological mechanisms, including multiple sclerosis, migraines and neuromuscular disease. In addition, a great number of monoclonal antibodies against several targets are being investigated for many more neurological diseases, which reflects our advances in understanding the pathogenesis of these diseases. Untangling the molecular mechanisms of disease allows monoclonal antibodies to block disease pathways accurately and efficiently with exceptional target specificity, minimizing non-specific effects. On the other hand, accumulating experience shows that monoclonal antibodies may carry class-specific and target-associated risks. This article provides an overview of different types of monoclonal antibodies and their characteristics and reviews monoclonal antibodies currently in use or under development for neurological disease.

scholarly journals Expectancy of Stress-Reducing Aromatherapy Effect and Performance on a Stress-Sensitive Cognitive Task

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Irina Chamine ◽  
Barry S. Oken
Keyword(s):  
Task Performance ◽  
Stress Reduction ◽  
Cognitive Task ◽  
Reaction Times ◽  
Event Related Potentials ◽  
Specific Effects ◽  
N200 Amplitude ◽  
Related Potentials ◽  
And Performance

Objective. Stress-reducing therapies help maintain cognitive performance during stress. Aromatherapy is popular for stress reduction, but its effectiveness and mechanism are unclear. This study examined stress-reducing effects of aromatherapy on cognitive function using the go/no-go (GNG) task performance and event related potentials (ERP) components sensitive to stress. The study also assessed the importance of expectancy in aromatherapy actions.Methods. 81 adults were randomized to 3 aroma groups (active experimental, detectable, and undetectable placebo) and 2 prime subgroups (prime suggesting stress-reducing aroma effects or no-prime). GNG performance, ERPs, subjective expected aroma effects, and stress ratings were assessed at baseline and poststress.Results. No specific aroma effects on stress or cognition were observed. However, regardless of experienced aroma, people receiving a prime displayed faster poststress median reaction times than those receiving no prime. A significant interaction for N200 amplitude indicated divergent ERP patterns between baseline and poststress for go and no-go stimuli depending on the prime subgroup. Furthermore, trends for beneficial prime effects were shown on poststress no-go N200/P300 latencies and N200 amplitude.Conclusion. While there were no aroma-specific effects on stress or cognition, these results highlight the role of expectancy for poststress response inhibition and attention.

Sign in / Sign up

Export Citation Format

Share Document