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PubMed1998

Body fluid volume status and the renal response to atrial natriuretic peptide in rats.

The effect of altering the volumes of different body fluid compartments on the renal response to atrial natriuretic peptide (ANP) was studied in anesthetized rats before and during administration of the peptide at 170 ng/min. Four different groups were used. In the first (De), reduction of total body water content was induced by 48 h water deprivation. In the second (De+NaCl), an acute intravenous infusion after the same 48 h dehydration was used to restore the extracellular, but not the intracellular, fluid compartment. In the third (Eu+NaCl), euvolemic rats were infused with isotonic saline at the same rate as in group De+NaCl to expand both intravascular and interstitial components of extracellular fluid. In the fourth group (Eu+BSA) an infusion of hyperoncotic (6%) bovine serum albumin in isotonic saline was used to expand the intravascular volume while contracting the interstitial volume. Excretion of water and salt was predictably reduced in the De group compared with the others. This reduction was associated with increased tubular reabsorption, both upstream from the medullary collecting duct and in the duct itself. Administration of ANP did not significantly affect diuresis and saluresis, or tubular transport. By contrast, there were marked and similar diuretic and natriuretic responses to ANP in groups De+NaCl and Eu+NaCl, associated with transport inhibition primarily in the medullary collecting duct. Surprisingly, the rats infused with hyperoncotic solution (Eu+NaCl) also failed to show marked excretory or duct transport responses to ANP. According to the study design, the two nonresponding groups had, respectively, a decreased or a normal intracellular compartment, and a decreased or increased plasma volume. The common feature of both nonresponding groups was a decreased interstitial fluid compartment, whereas the two responding groups had normal or increased interstitial volume. We suggest, therefore, that a replete interstitial fluid compartment is essential for the renal response to ANP.

Animals↗
PubMed1980

Cerebral blood flow during normocapnic hyperoxia in the unanesthetized pony.

The effect of hyperoxia on cerebral blood flow (CBF) was examined in 12 unanesthetized ponies. CBF was determined using radioactive microspheres, 15 micrometer in diam, durijng inspriation of the following gases: 1) room air (control); 2) 40% I2 in N2; and 3) approximately 100% O2 with 2.2-4.5% CO2 added to maintain isocapnia. CBF did not change from control values during either level of hyperoxia. However, cerebrospinal fluid (CSF) carbon dioxide tension (PCO2) increased during 40% O2 (delta 1.0 Torr) and approximately 100% O2 (delta 2.9 Torr). This rise in CSF PCO2, not due to a change in CBF, may have resulted from a decrease in the CO2 carrying capacity of cerebral venous blood during hyperoxia (Haldane effect). Although respiration did not change during 40% O2, expired minute volume increased 25% during approximately 100% O2 due to an increase in tidal volume. This rise in respiration was not associated with changes in any of the conventional stimuli to breathing (arterial pH, O2 tension, or PCO2 or CSF pH). One possible explanation was that cerebral extracellular fluid pH, in the vicinity of the central chemoreceptors, or cerebral intracellular fluid pH changed in a direction unlike CSF pH. An alternate explanation was that the CO2 in the inspired gas activated CO2-sensitive receptors in the lungs.

Acid-Base Equilibrium↗
PubMed1992

Use of multi-frequency bioelectrical impedance analysis for the estimation of extracellular fluid.

Thomasset (Lyon Medicine (1962): 207, 107-118; (1963): 209, 1325-1350; (1965): 214, 131-143) and others suggested that low-frequency impedance measurements could be used to estimate extracellular fluid and that high-frequency measurements could be used for the assessment of total body water. It was the purpose of this study to examine the relationship between body fluid compartments and multi-frequency bioelectrical impedance analysis (MF-BIA). Total body water (TBW) and extracellular fluid (ECF) were measured using deuterium and sodium bromide dilution procedures. Intracellular fluid volume (ICF) was calculated as the difference between TBW and ECF. A tetrapolar arrangement of surface electrodes was used to measure whole-body resistance (R), reactance (Xc), impedance (Z), and phase angle (P) at 25 frequencies ranging from 1 kHz to 1.35 MHz. Subjects (n = 60; 40 male and 20 female) were between the ages of 19 and 65 years. Mean ratios (+/- SEM) of ECF/ICF and ECF/TBW were 0.83 +/- 0.021 and 0.45 +/- 0.011, respectively. Individuals with the largest fat-free mass (FFM) had the highest ECF value. Whole-body resistive index values most correlated to ECF were at 224, 300, 400, 548 and 1 kHz with correlations ranging from 0.93 to 0.84. All possible subset regression analysis was used to develop a prediction equation for ECF: R2 = 0.924 and SEE = 1.061: ECF = 5.17753 + (0.09989*RI224) + (0.09322*WT) - (1.3962*SEX), where RI = resistive index (HT2/R) at the specific frequency of 224kHz; WT = weight in kilograms; sex was dummy-coded, males = 0, females = 1.

Adult↗
PubMed1972

On the physiological response of the cerebral cortex to acute stress (reversible asphyxia).

1. Rhesus monkey (Macaca mulatta) foetuses were delivered by Caesarean section 3-10 days before term. Aortic blood and cerebrospinal fluid (c.s.f.) samples were taken, the latter from the cortical subarachnoid space and the cisterna magna. The umbilical cord was clamped and foetal breathing prevented for 14-17 min. Blood and c.s.f. were sampled further during this total asphyxiation and for up to 24 hr thereafter.2. The [K(+)] in the cortical subarachnoid fluid started to rise within 2-3 min after the onset of asphyxia and increased up to 7 times the normal level. The [K(+)] of blood plasma and cisternal fluid also increased, but much more moderately. All these effects reversed rapidly upon resuscitation of the foetus.3. A pronounced rise in the cortical subarachnoid fluid [glucose] and a lesser effect on cisternal fluid [glucose] were noted in most cases by the end of, or immediately following, the period of asphyxia. The onset, magnitude and reversal of these effects on [glucose] were less predictable than the observed effects on [K(+)].4. There were no significant changes in the [Mg(2+)], [Ca(2+)] or [Na(+)] of any of these fluids. The calculated total osmolarity of the cortical subarachnoid fluid and, to a much lesser extent, of cisternal fluid and plasma, increased during asphyxia mainly as a result of increased [K(+)].5. The results are interpreted as indicative of a rapid release of K(+) from cortical cells during total asphyxia. The (immature) haematoencephalic K(+) transport system becomes saturated and thus K(+) accumulates in the extracellular fluid (e.c.f.) whence it diffuses into adjacent regions of the c.s.f. system.6. The intracellular fluid of apical dendrites must become even more hypertonic than the e.c.f., since these cellular processes are known to swell during asphyxia at the expense of the e.c.f. space. This apparent increase in intracellular osmolarity could be accounted for by the release of normally bound intracellular cations.7. On the basis of our results and review of the relevant literature, the following sequence of events is proposed: the cortex responds to acute physiological stress (asphyxia, overstimulation, chemical or physical irritation, etc.) by releasing intracellularly bound cations (K(+) and possibly Na(+)). The increased intracellular osmolarity results in the absorption of water from the e.c.f. space. Passage of water across the blood-brain barrier is restricted; thus the e.c.f. space of the cortex does not swell, but becomes hyperosmotic. Under these circumstances, swelling of the cortical cells is limited by the volume of e.c.f. available.8. It is proposed that the release of intracellularly bound cations is a result of their displacement from their binding sites by NH(4) (+) which is released to, and recovered from, these cation binding sites by a glutamate-glutamine interconversion.9. It is concluded that the apparent organized ;shutdown' of the cortical cells in response to acute stress may contribute to the relative insensitivity of this area of the brain to permanent histopathological damage.

Animals↗
PubMed1999

Another look at: fuel + O2 --> CO2 + H2O. Developing a water-oriented perspective.

Water plays many vital roles which must be maintained despite constant threat of water stress from the environment. Mechanisms to maintain these roles over the long-term involve intermediates of many metabolic pathways, such as glycerol, sucrose, free amino acids and their derivatives. In addition to viewing metabolic products as intermediates along energy-related pathways, nutrition researchers and epidemiologists should consider them as determinants of intracellular fluid maintenance. Satiety processes, oxidative-fuel selection, hormonal control, and intracellular-signaling processes can all be interpreted in terms of water-oriented metabolism. Water intake and hydration status can vary considerably, and may be inadequate for a sizeable proportion of Western adults. Due to the metabolic adaptations required to compensate for perpetually inadequate water, chronic sub-optimal water intakes may be highly relevant to chronic disease etiology. Preliminary evidence links water-oriented metabolism to obesity, diabetes, cardiovascular disease, hypertension and cancer. Development of a water-oriented perspective may reveal an important new area of research in human nutrition and epidemiology.

Adult↗
PubMed2002

Thirst and salt appetite responses in young and old Brown Norway rats.

Male Brown Norway rats aged 4 mo (young) and 20 mo (old) received a series of experimental challenges to body fluid homeostasis over approximately 3 mo. Water was available for drinking in some tests, and both water and 0.3 M NaCl were available in others. The series included three episodes of extracellular fluid depletion (i.e., furosemide + 20 h of sodium restriction), two tests involving intracellular fluid depletion (i.e., hypertonic saline: 1 or 2 M NaCl at 2 ml/kg body wt sc), one test involving overnight food and fluid restriction, and testing with captopril adulteration of the drinking water (0.1 mg/ml) for several days. Old rats were significantly heavier than young rats throughout testing. Old rats drank less water and 0.3 M NaCl after sodium deprivation than young rats, in terms of absolute and body weight-adjusted intakes. Old rats drank only half as much water as young rats in response to subcutaneous hypertonic NaCl when intakes were adjusted for body weight. Old rats drank less 0.3 M NaCl than young rats after overnight food and fluid restriction when intakes were adjusted for body weight. In response to captopril adulteration of the drinking water, young rats significantly increased daily ingestion of 0.3 M NaCl when it was available as an alternative to water and significantly increased daily water intakes when only water was available, in terms of absolute and body weight-adjusted intakes. Old rats had no response to captopril treatment. These results add important new information to previous reports that aging rats have diminished thirst and near-absent salt appetite responses to regulatory challenges.

Aging↗
PubMed2001

cAMP-dependent fluid secretion in rat inner medullary collecting ducts.

We used an unambiguous in vitro method to determine if inner medullary collecting ducts (IMCD) have intrinsic capacities to absorb and secrete solutes and fluid in an isotonic medium. IMCD(1), IMCD(2), and IMCD(3) were dissected from kidneys of young Sprague-Dawley rats. 8-Bromo-3',5'-cyclic monophosphate (8-BrcAMP) stimulated lumen formation and progressive dilation in all IMCD subsegments; lumen formation was greatest in IMCD(1.) Benzamil potentiated the rate of lumen expansion in response to 8-BrcAMP. Fluid entered tubule lumens by transcellular secretion rather than simple translocation of intracellular fluid. Secreted lumen solutes were osmometrically active. Inhibition of protein kinase A with H-89 and Rp diastereomer of adenosine 3',5'-cyclic monophosphorothioate blocked fluid secretion. The rate of lumen expansion was reduced by the selective addition of ouabain, barium, diphenyl-2-carboxylate, bumetanide, glybenclamide, or DIDS, or reduction of extracellular Cl(-). We conclude that IMCD absorb and secrete electrolytes and fluid in vitro and that secretion is accelerated by cAMP. We suggest that salt and fluid secretion by the terminal portions of the renal collecting system may have a role in modulating the composition and volume of the final urine.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1986

Protons, osmolytes, and fitness of internal milieu for protein function.

The composition of the intracellular milieu shows striking similarities among widely different species. Only certain values of intracellular pH, values that generally reflect alphastat regulation, and only narrow ranges of inorganic ion concentrations are found in the cytoplasm of the cells of most animals, plants, and microorganisms. In water-stressed organisms only a few types of low-molecular-weight organic molecules (osmolytes) are accumulated. These highly conserved characteristics of the intracellular fluids reflect the need to maintain critical features of macromolecules within narrow ranges optimal for life. For proteins these features include maintaining adequate rates of catalysis, a high level of regulatory responsiveness, and a precise balance between stability and lability of structure (tertiary conformation, subunit assembly, and multiprotein complexes). The optimal values for these functional and structural features of proteins often lie near the midrange of possible values for these properties, and only under specific conditions of intracellular pH, ionic strength, and osmolyte composition are these optimal midrange values conserved. In dormant cells the departure of solution conditions from values that are optimal for protein function and structure may be instrumental in reducing or shutting down metabolic functions. Seen from a broad evolutionary perspective, the evolution of the intracellular milieu is an important complement to macromolecular evolution. In certain instances appropriate modifications of the internal milieu may reduce the need for adaptive amino acid replacements in proteins.

Acid-Base Equilibrium↗
PubMed1991

Monitoring of intracellular ammonium in perfused rat salivary gland by nitrogen-14 nuclear magnetic resonance spectroscopy.

We have observed the changes in the intracellular ammonium (NH4+) content and the intracellular pH during administration of 20 mM NH4Cl (the ammonium pulse experiment) using nitrogen-14 and phosphorus-31 nuclear magnetic resonance spectroscopy (14N and 31P NMR) at 8.45 T. In the isolated perfused rat mandibular salivary gland, resonances of trimethylamines (-328 p.p.m.) and betaine (-329 p.p.m. from the resonance of NO3-) were detected. A chemical shift reagent, 10 mM of dysprosium triethylenetetramine-N,N,N',N",N"',N"'-hexaacetic acid (Dy(TTHA], was used to discriminate between the resonances from the extracellular NH4+ (-352 p.p.m.) and the intracellular NH4+ (-355 p.p.m.). During the NH4Cl application, the intracellular NH4+ content [( NH4+]i) increased quickly to ca. 50 mmol per litre intracellular fluid (ICF), then increased gradually to ca. 70 mmol per litre ICF. The intracellular pH (pHi), calculated from the 31P chemical shift of inorganic phosphate, increased transiently by 0.5 pH units and then decreased gradually in spite of the high level of [NH4+]i. The initial increase of [NH4+]i, which was observed by 14N NMR, was larger than that calculated from the intracellular pH on an assumption of a non-ionic diffusion process for ammonia. These results suggest a possibility of influx of NH4+, and also suggest an activation of cellular buffering mechanism that extrudes the excess bases from the cells.

Ammonia↗
PubMed1981

The dipsogenic activity of prolactin in male and female rats.

1. Ovine prolactin injected intravenously in doses of 10.0, 5.0, 1.0, 0.1 and 0 mg/kg body wt. caused neither drinking nor a change in urine output in normal water replete male and female rats. 2. The water intake of male rats subjected to 48 hr water deprivation was substantially increased after injection of prolactin. 3. The water intake of male and female rats injected I.P. with a hyperoncotic solution of polyethylene glycol (20 M) was significantly increased after injection of prolactin. 4. Prolactin ws found to act synergistically with a subthreshold dose of angiotensin II amide to cause significant drinking and fluid retention. 5. The drinking responses of male and female rats injected I.V. with hypertonic saline were not modified by prolactin. 6. It is concluded that prolactin may act to increase the net water gain of animals suffering a deficit of the extracellular fluid space but is without effect on stimuli arising from deficits in the intracellular fluid space.

Angiotensin II↗
PubMed1990

[Fluid balance and postoperative lung function].

Postoperative volume therapy: 1. Replacement of fluid loss. 2. Therapy of intravasal hypovolaemia in case of permeability damage or intracellular fluid shift. Monitoring: 1. Circulation (HR, CVP, art. pressure). 2. Homeostasis (Na, K). 3. Metabolic changes (BE, pH). 4. Kidney function. In complications like sepsis or ARDS with pulmonary problems and increase of pulmonary vascular resistance the use of a pulmonary artery catheter is necessary. Differential treatment has to be based on additional measurement of cardiac output and pulmonary capillary pressure. Volume treatment in postoperative complications is essential because of intravasal hypovolaemia. Kidney and cardiac failure have to be ruled out.

Acid-Base Equilibrium↗
PubMed1987

Body composition changes in marrow transplant recipients receiving total parenteral nutrition.

Nine patients with acute lymphocytic leukemia in remission, aged 12-35 years, undergoing allogeneic bone marrow transplantation (BMT) were studied for changes in body fluid balance and body composition. Body composition and fluids were assessed the first 4 weeks following BMT, using isotope dilution and anthropometry. Oral and parenteral nutrient intakes were recorded daily. Tracer dilution techniques were used to assess body fluid volumes and estimate body cell, lean body, and body fat masses. Body cell mass was lost (mean -1.62 kg, P less than 0.05) without significant changes in body fat or lean body masses. There was an expansion of the extracellular fluid compartment (mean +0.8 l, P less than 0.05) and a loss in the intracellular fluid compartment (mean -1.3 l, P less than 0.05) with little change in total body water volume. Changes in body weight correlated poorly with body cell mass or fluid volume changes. Change in arm muscle area correlated well with changes in body cell mass (r = 0.61, P less than 0.05) and lean body mass (r = 0.68, P less than 0.05), while that of arm fat area did not reflect its isotope dilution-derived counterpart. Instead, the change in arm fat area was related to shifts in fluid compartments. Prealbumin decreased significantly (mean -9.3 mg/dl, P less than 0.05), while albumin decreased slightly (mean -0.1 mg/dl), and both were related to changes in body cell mass. Nitrogen balance was negative throughout the study and the overall mean was related to the change in body cell mass (r = 0.60, P less than 0.05). Calorie and protein intakes were not associated with the changes in body composition, implying other causal factors.

Adolescent↗
PubMed1988

Shift in body fluid compartments after dehydration in humans.

To investigate the influence of [Na+] in sweat on the distribution of body water during dehydration, we studied 10 volunteer subjects who exercised (40% of maximal aerobic power) in the heat [36 degrees C, less than 30% relative humidity (rh)] for 90-110 min to produce a dehydration of 2.3% body wt (delta TW). After dehydration, the subjects rested for 1 h in a thermoneutral environment (28 degrees C, less than 30% rh), after which time the changes in the body fluid compartments were assessed. We measured plasma volume, plasma osmolality, and [Na+], [K+], and [Cl-] in plasma, together with sweat and urine volumes and their ionic concentrations before and after dehydration. The change in the extracellular fluid space (delta ECF) was estimated from chloride distribution and the change in the intracellular fluid space (delta ICF) was calculated by subtracting delta ECF from delta TW. The decrease in the ICF space was correlated with the increase in plasma osmolality (r = -0.74, P less than 0.02). The increase in plasma osmolality was a function of the loss of free water (delta FW), estimated from the equation delta FW = delta TW - (loss of osmotically active substance in sweat and urine)/(control plasma osmolality) (r = -0.79, P less than 0.01). Free water loss, which is analogous to "free water clearance" in renal function, showed a strongly inverse correlation with [Na+] in sweat (r = -0.97, P less than 0.001). Fluid movement out of the ICF space attenuated the decrease in the ECF space.(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗
PubMed1993

Regulation of fluid secretion and intracellular messengers in isolated rat pancreatic ducts by acetylcholine.

1. We have studied the effects of acetylcholine (ACh) on fluid secretion and intracellular messengers in interlobular ducts isolated from the rat pancreas and maintained in short-term tissue culture. 2. Ductal fluid secretion was measured using micropuncture techniques. Intracellular free calcium ([Ca2+]i) and cyclic AMP concentrations were measured in single ducts using fura-2 microspectrofluorimetry and radioimmunoassay techniques respectively. Changes in the levels of these intracellular messengers were correlated with fluid secretion. 3. ACh stimulated ductal fluid secretion. The dose required for a half-maximal response was about 0.4 microM and maximal secretion was achieved with 10 microM ACh. These effects of ACh were blocked by atropine and by removal of extracellular Ca2+. 4. ACh was about four orders of magnitude less potent as an activator of ductal fluid transport than the hormone secretin; however, the maximal rates of fluid secretion evoked by these two agonists were similar. 5. ACh caused a dose-dependent rise in duct cell [Ca2+]i, but had no effect on cyclic AMP. In contrast, secretin increased duct cell cyclic AMP, but had no effect on [Ca2+]i. 6. The [Ca2+]i response evoked by ACh resulted from both mobilization of intracellular Ca2+ stores and influx of Ca2+ from the extracellular space. 7. The Ca2+ ionophore, ionomycin, mimicked the effect of ACh on ductal [Ca2+]i and fluid secretion. 8. We conclude that ACh stimulates fluid secretion from rat pancreatic duct cells by activating a 'Ca2+ pathway' which is distinct from the well documented 'cyclic AMP pathway' utilized by secretin.

Acetylcholine↗
PubMed1992

Comparison between acetate and bicarbonate dialysis for the treatment of lithium intoxication.

Lithium is used to treat manic-depressive disorders, but toxic side effects commonly occur. The preferred treatment of severe lithium intoxication is hemodialysis. No data, however, exist comparing the effectiveness of acetate to bicarbonate dialysis for the removal of lithium. We present a case of lithium intoxication treated with both. During acetate dialysis, lithium removal occurred exclusively from the extracellular fluid space, while during bicarbonate dialysis, lithium removal occurred equally from both the extracellular and intracellular fluid spaces. We hypothesize that acetate but not bicarbonate activates the sodium-hydrogen antiporter on cell membranes, and that lithium, substituting for sodium, is driven into cells. This may explain the rebound in lithium levels commonly noted after conventional dialysis. We recommend bicarbonate hemodialysis as the therapy of choice for severe lithium intoxication.

Acetates↗
PubMed1995

Neuroendocrine mechanisms during reversible hypovolaemic shock in humans with emphasis on the histaminergic and serotonergic system.

In humans, the head-up tilted position results in central hypovolaemia which mimicks haemorrhage and is associated with cardiovascular changes that can be divided into two stages. 1) One stage with increase in HR and vascular resistance and a slight increase in MAP. 2) Another stage with decrease in HR, vascular resistance and MAP and appearance of presyncopal symptoms (hypovolaemic shock). The first stage is "sympathoexcitatory" as plasma NA originating from postganglionic vasoconstrictory sympathetic neurons increase. Limb vascular resistance contributes to the increase in TPR at this time. The second stage is "sympathoinhibitory" in nature as plasma NA slightly decreases, or remains unchanged, while plasma A, originating from the adrenal medulla, raises. This pattern is a reflection of a differentiated sympathetic response as an increase in the activity of the nerves innervating the adrenals and decrease in renal sympathetic nerves has been reported by others. There is a decrease in limb as well as total vascular resistance. The secretion of potent vasoactive peptides may contribute to the circulatory changes taken place during head-up tilt. The head-up tilted position is associated with central hypovolaemia which is reliably monitored by electrical impedance. There is a close relation between the increase in thoracic electrical impedance and the decrease in plasma ANP which is regulated by atrial stretch. Also, from recording of technetium labeled red blood cells and measurements of haematocrite the decrease in CBV is reflected by thoracic electrical impedance. In contrast, CVP reflects changes in CBV during the initial head-up tilt only, whereafter CVP usually is unchanged or may even increase. After the initial head-up tilt the decrease in the CBV is caused by further reduction in plasma volume as shown by increase in haematocrite and unchanged distribution of labeled red blood cells. This mechanism is reflected by application of regional electrical impedance measurements at a low and high frequency current. The low frequency current, passing extracellular fluid only, changing more than the high frequency current that passes extra as well as intracellular fluid. Central hypovolaemia was found to stimulate the pituitary-adrenal axis, and the development of hypotension strongly increases plasma ACTH, beta-END, cortisol and PRL. Blocking histaminergic receptors did not change the pituitary-adrenal response to central hypovolaemia, while the sympathoadrenal response was affected by histaminergic receptor blockade. The H2-receptor antagonist cimetidine inhibited plasma A, while the H1-receptor antagonist mepyramine attenuated plasma NA and reduced cardiovascular tolerance, and also induced some sedation. A possible effect of sedation and anxiolysis was investigated by administration of the GABAergic drug diazepam. This drug did not change the cardiovascular response to head-up tilt, but reduced the increase in plasma cortisol. This indicates that the appearance of presyncopal symptoms is not related to "stress" but associated with the cardiovascular effects of central hypovolaemia. Another endogenous substance, serotonin (5-HT), may be also involved in cardiovascular as well as endocrine regulation. We investigated the effect of blocking three main receptors on the development and effects of hypovolaemic shock. Methysergide (5-Ht1+2-receptor antagonist) attenuated plasma NA, beta-END, PRL and PRA during tilt with a slight reduction of cardiovascular tolerance. The 5-HT2-receptor antagonist ketanserin reduced cardiovascular tolerance without significant effects on the hormonal responses. The 5-HT3-receptor antagonist ondansetron inhibited the plasma CGRP and adrenalin response to central hypovolaemia without influencing cardiovascular tolerance. It is concluded that the head-up tilted model in humans can be applied to study cardiovascular and endocrine mechanisms until the development of hypovolaemic shock.(ABSTRACT TRUNCATED)

Animals↗
PubMed1986

Renal handling of magnesium: drug and hormone interactions.

Magnesium is the fourth most abundant cation in the human body and the second most common cation in the intracellular fluid. The abundance and distribution of this divalent cation implies an essential role of magnesium in intracellular metabolism. Although no single homeostatic control has been demonstrated for magnesium, the cellular availability of this cation is closely regulated by the gastrointestinal tract, kidney and bone. The purpose of this review is to survey some of the events involved in renal magnesium handling. The excretory side of magnesium balance involves appropriate changes in renal magnesium handling. Present evidence suggests that the renal handling of magnesium is normally a filtration-reabsorption process. Experimental support for secretion remains unconvincing. Renal magnesium reabsorption has distinctive features when compared with that of sodium and calcium. The concentration of magnesium in the proximal tubule rises 1.5 times greater than the glomerular filtrate. Some 20-30% of the filtered magnesium is reabsorbed in the proximal tubule compared to the fractional absorption of sodium or calcium of 50-60%. Although the fractional reabsorption of magnesium is only half that of sodium, it changes in parallel with that of sodium in response to changes in extracellular fluid volume. The major portion of filtered magnesium (some 65%) is reabsorbed in the loop of Henle, mainly in the thick ascending limb. Recent evidence suggests that magnesium reabsorption in the ascending limb may be voltage-dependent and secondary to active sodium chloride reabsorption. Evidence also suggests an important competition between magnesium and calcium for transport at the basolateral surface of the ascending limb cell. The loop of Henle appears to be the major nephron site where magnesium reabsorption is controlled. The principal factors which alter magnesium reabsorption in the loop include parathyroid hormone, changes in plasma magnesium and calcium concentration and the loop diuretics. About 10% of the filtered magnesium is delivered into the distal nephron where only a small fraction of the filtered magnesium is reabsorbed and the transport capacity is readily exceeded with increased magnesium delivery. A number of drugs have been shown to alter magnesium handling; these include antibiotics such as gentamicin, antineoplastic agents such as cisplatin and immunological suppressive drugs such as cyclosporin. The cellular alterations of these diverse drugs leading to renal magnesium wasting are not well understood.

Animals↗
PubMed2003

Regulation of salt gland, gut and kidney interactions.

Marine birds can drink seawater because their cephalic 'salt' glands secrete a sodium chloride (NaCl) solution more concentrated than seawater. Salt gland secretion generates osmotically free water that sustains their other physiological processes. Acclimation to saline induces interstitial water and Na move into cells. When the bird drinks seawater, Na enters the plasma from the gut and plasma osmolality (Osm(pl)) increases. This induces water to move out cells expanding the extracellular fluid volume (ECFV). Both increases in Osm(pl) and ECFV stimulate salt gland secretion. The augmented intracellular fluid content should allow more rapid expansion of ECFV in response to elevated Osm(pl) and facilitate activation of salt gland secretion. To fully utilize the potential of the salt glands, intestinally absorbed NaCl must be reabsorbed by the kidneys. Thus, Na uptake at gut and renal levels may constrain extrarenal NaCl secretion. High NaCl intake elevates plasma aldosterone concentration of Pekin ducks and aldosterone stimulates intestinal and renal water and sodium uptake. High NaCl intake induces lengthening of the small intestine of adult Mallards, especially males. High NaCl intake has little effect on glomerular filtration rate or tubular sodium Na uptake of birds with competent salt glands. Relative to body mass, kidney mass and glomerular filtration rate (GFR) are greater in birds with salt glands than in birds that do not have them. Birds with salt glands do not change GFR, when they drink saline. Thus, their renal filtrate contains excess Na that is, in some species, almost completely renally reabsorbed and excreted in a more concentrated salt gland secretion. Na reabsorption by kidneys of other species, like mallards is less complete and their salt glands make less concentrated secretion. Such species may reflux urine into the hindgut, where additional Na may also be reabsorbed for extrarenal secretion. During exposure to saline, marine birds maintain elevated aldosterone levels despite high Na intake. Marine birds are excellent examples of physiological plasticity.

Animals↗