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Results for “BODY FLUID BALANCE”

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PubMed1998

Recovery after exercise in the heat--factors influencing fluid intake.

The restoration of body fluid balance following dehydration induced by exercise will occur through regulatory responses which stimulate ingestion of water and sodium ions. A number of different afferent signalling systems are necessary to generate appropriate thirst or sodium appetite. The primary sensory information of naturally occurring thirst is derived from receptors sensing cell volume and the volume of the extracellular fluid compartment. Sensory information from the oropharyngeal region is also an important determinant of thirst. The interaction of these various afferent signalling systems within the central nervous system determines the extent of fluid replacement following dehydration.

Afferent Pathways↗

PubMed2002

Circulating relaxin acts on subfornical organ neurons to stimulate water drinking in the rat.

Relaxin, a peptide hormone secreted by the corpus luteum during pregnancy, exerts actions on reproductive tissues such as the pubic symphysis, uterus, and cervix. It may also influence body fluid balance by actions on the brain to stimulate thirst and vasopressin secretion. We mapped the sites in the brain that are activated by i.v. infusion of a dipsogenic dose of relaxin (25 microg/h) by immunohistochemically detecting Fos expression. Relaxin administration resulted in increased Fos expression in the subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus, and magnocellular neurons in the supraoptic and paraventricular nuclei. Ablation of the SFO abolished relaxin-induced water drinking, but did not prevent increased Fos expression in the OVLT, supraoptic or paraventricular nuclei. Although ablation of the OVLT did not inhibit relaxin-induced drinking, it did cause a large reduction in Fos expression in the supraoptic nucleus and posterior magnocellular subdivision of the paraventricular nucleus. In vitro single-unit recording of electrical activity of neurons in isolated slices of the SFO showed that relaxin (10(-7) M) added to the perfusion medium caused marked and prolonged increase in neuronal activity. Most of these neurons also responded to 10(-7) M angiotensin II. The data indicate that blood-borne relaxin can directly stimulate neurons in the SFO to initiate water drinking. It is likely that circulating relaxin also stimulates neurons in the OVLT that influence vasopressin secretion. These two circumventricular organs that lack a blood-brain barrier may have regulatory influences on fluid balance during pregnancy in rats.

Angiotensin II↗

PubMed1977

CNS regulation of salt and water intake.

The brain has evolved a number of mechanisms to maintain body fluid balance. They include the sensation of thirst, which stimulates water intake, the secretion of vasopressin, which helps prevent water loss, and the secretion of aldosterone, which helps prevent sodium depletion. In the research described here, all three mechanisms are shown to be mediated by the actions of angiotensin on the brain.

Aldosterone↗

PubMed2005

Aquaporin-8 is involved in water transport in isolated superficial colonocytes from rat proximal colon.

Water is an essential nutrient because it must be introduced from exogenous sources to satisfy metabolic demand. Under physiologic conditions, the colon can absorb and secrete considerable amounts of water even against osmotic gradients, thus helping to maintain the body fluid balance. Here we describe studies on both aquaporin (AQP) expression and function using cells isolated from the superficial and lower crypt regions of the rat proximal colon. The expression of AQP-3, -4, and -8 in isolated colonocytes was determined by semiquantitative RT-PCR and by immunoblotting. The localization of AQP-8 in the colon was evaluated by immunohistochemistry. A stopped-flow light scattering method was used to examine osmotic water movement in isolated colonocytes. Moreover, the contribution of AQP-8 to overall water movement through isolated colonocytes was studied using RNA interference technology. Colonocytes from the proximal colon express AQP-3, -4, and -8 with increasing concentrations from the lower crypt cells toward those on the surface. Osmotic water permeability was higher in surface than in crypt colonocytes (P < 0.05); it was significantly inhibited by the water channel blocker dimethyl sulfoxide, and reversed by beta-mercaptoethanol (P < 0.05). Immunohistochemistry revealed a strong AQP-8 labeling in the apical membrane of the superficial colonocytes. Inhibition of aquaporin-8 expression by small interfering RNA significantly decreased osmotic water permeability (approximately 38%; P < 0.05). Current results indicate that aquaporin-8 may play a major role in water movement through the colon by acting on the apical side of the superficial cells.

Animals↗

PubMed1999

Modulation of renin secretion by atrial natriuretic factor prohormone fragment 31-67.

BACKGROUND: Earlier studies have indicated that the atrial natriuretic factor prohormone fragment 31-67 (Pro ANF31-67) has important effects for the promotion of sodium excretion and vasodilation in several animal species. However, the mechanisms for the natriuretic actions of Pro ANF31-67 are not completely defined. In the present study, the effects of synthetic Pro ANF31-67 on renin secretion were examined in sodium-depleted, anesthetized dogs with a single intact kidney (n = 5). METHODS: After 3 20-minute control renal clearance periods, synthetic dog Pro ANF31-67 was given intrarenally at a sustained dose of 0.03 microg/kg/min for 3 20-minute experimental intervals, and after discontinuation of the peptide infusion, 3 final 20-minute recovery periods were determined. RESULTS: Sustained intrarenal infusions of the Pro ANF31-67 produced striking decrements (p<0.05) in renin secretion, from a control value of 1418 +/- 243 to 401 +/- 223 ng of angiotensin I/min. This 66% fall in renin secretion was associated with significant (P < 0.05) increases in creatinine clearance (40%), renal blood flow (8%), urine flow (50%), and sodium excretion (17%). CONCLUSIONS: It is suggested that this inhibition of renin secretion was mediated, at least in part, in response to a ProANF31-67-induced increment in the sodium load delivered to the macula densa. An interaction of the peptide with the renal vascular receptor for suppression of renin release is also possible. ProANF31-67 may represent an important hormonal mechanism involved in the regulation of body-fluid balance.

Animals↗

PubMed2000

American College of Sports Medicine roundtable. The physiological and health effects of oral creatine supplementation.

Creatine (Cr) supplementation has become a common practice among professional, elite, collegiate, amateur, and recreational athletes with the expectation of enhancing exercise performance. Research indicates that Cr supplementation can increase muscle phosphocreatine (PCr) content, but not in all individuals. A high dose of 20 g x d(-1) that is common to many research studies is not necessary, as 3 g x d(-1) will achieve the same increase in PCr given time. Coincident ingestion of carbohydrate with Cr may increase muscle uptake; however, the procedure requires a large amount of carbohydrate. Exercise performance involving short periods of extremely powerful activity can be enhanced, especially during repeated bouts of activity. This is in keeping with the theoretical importance of an elevated PCr content in skeletal muscle. Cr supplementation does not increase maximal isometric strength, the rate of maximal force production, nor aerobic exercise performance. Most of the evidence has been obtained from healthy young adult male subjects with mixed athletic ability and training status. Less research information is available related to the alterations due to age and gender. Cr supplementation leads to weight gain within the first few days, likely due to water retention related to Cr uptake in the muscle. Cr supplementation is associated with an enhanced accrual of strength in strength-training programs, a response not independent from the initial weight gain, but may be related to a greater volume and intensity of training that can be achieved. There is no definitive evidence that Cr supplementation causes gastrointestinal, renal, and/or muscle cramping complications. The potential acute effects of high-dose Cr supplementation on body fluid balance has not been fully investigated, and ingestion of Cr before or during exercise is not recommended. There is evidence that medical use of Cr supplementation is warranted in certain patients (e.g.. neuromuscular disease); future research may establish its potential usefulness in other medical applications. Although Cr supplementation exhibits small but significant physiological and performance changes, the increases in performance are realized during very specific exercise conditions. This suggests that the apparent high expectations for performance enhancement, evident by the extensive use of Cr supplementation, are inordinate.

Adult↗

PubMed2004

Expression of the arginine vasopressin gene in response to salt loading in oxytocin gene knockout mice.

Accumulating evidence suggests that both oxytocin and arginine vasopressin (AVP) are vital components in the regulation of body fluid balance. However, the physiological role of oxytocin and possible cooperative interactions between oxytocin and AVP in sodium balance remain obscure, even though recent studies using oxytocin knockout (OTKO) mice suggested that oxytocin may contribute to the regulation of salt appetite. In the present study, we examined the effects of salt loading (drinking 2% NaCl for 5 days) on the expression of the AVP gene in the paraventricular (PVN) and supraoptic nuclei (SON) of wild-type, OTKO and heterozygous littermates using in situ hybridization histochemistry. In addition, the effects of salt loading on the expression of the oxytocin gene were also examined in wild-type and heterozygous mice. Under the non salt-loaded condition, the levels of AVP mRNA in the PVN and SON of OTKO mice were significantly decreased compared to those in wild-type mice. Nevertheless, the up-regulation of the expression of the AVP gene in response to salt loading was preserved in OTKO mice. The degree of the up-regulation in OTKO mice tended to be greater compared to those in wild-type mice, suggesting compensatory up-regulation of the expression of the AVP gene in OTKO mice after salt loading. The basal levels of oxytocin mRNA in the PVN and SON of heterozygous mice were significantly lower than those in wild-type mice. Salt loading caused an increase of oxytocin mRNA levels in the PVN and SON of both wild-type and heterozygous mice. The ratios of increase of oxytocin mRNA levels were very similar between wild-type and heterozygous mice, suggesting that the single remaining oxytocin gene in heterozygous mice responds normally to an osmotic cue. Finally, salt loading tended to increase the serum concentration of sodium regardless of genotype, and there were no genotype differences in both the control and salt-loaded groups. These results suggest ways in which oxytocin may play a cooperative role together with AVP in the regulation of sodium balance.

Animals↗

PubMedDate not supplied

Differential neural control of glomerular ultrafiltration.

The renal nerves constrict the renal vasculature, causing decreases in renal blood flow (RBF) and glomerular filtration rate (GFR). Whether renal haemodynamics are influenced by changes in renal nerve activity within the physiological range is a matter of debate. We have identified two morphologically distinct populations of nerves within the kidney, which are differentially distributed to the renal afferent and efferent arterioles. Type I nerves almost exclusively innervate the afferent arteriole whereas type II nerves are distributed equally on the afferent and efferent arterioles. We have also demonstrated that type II nerves are immunoreactive for neuropeptide Y, whereas type I nerves are not. This led us to hypothesize that, in the kidney, distinct populations of nerves innervate specific effector tissues and that these nerves may be selectively activated, setting the basis for the differential neural control of GFR. In physiological studies, we demonstrated that differential changes in glomerular capillary pressure occurred in response to graded reflex activation of the renal nerves, compatible with our hypothesis. Thus, sympathetic outflow may be capable of selectively increasing or decreasing glomerular capillary pressure and, hence, GFR by differentially activating separate populations of renal nerves. This has important implications for our understanding of the neural control of body fluid balance in health and disease.

Animals↗

PubMed1998

Properties and glial origin of osmotic-dependent release of taurine from the rat supraoptic nucleus.

1. Taurine, prominently concentrated in glial cells in the supraoptic nucleus (SON), is probably involved in the inhibition of SON vasopressin neurones by peripheral hypotonic stimulus, via activation of neuronal glycine receptors. We report here the properties and origin of the osmolarity-dependent release of preloaded [3H]taurine from isolated whole SO nuclei. 2. Hyposmotic medium induced a rapid, reversible and dose-dependent increase in taurine release. Release showed a high sensitivity to osmotic change, with a significant enhancement with less than a 5% decrease in osmolarity. Hyperosmotic stimulus decreased basal release. 3. Evoked release was independent of extracellular Ca2+ and Na+, and was blocked by the Cl- channel blockers DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid) and DPC (N-phenylanthranilic acid), suggesting a diffusion process through volume-sensitive Cl- channels. 4. Evoked release was transient for large osmotic reductions (> or = 15%), probably reflecting regulatory volume decrease (RVD). However, it was sustained for smaller changes, suggesting that taurine release induced by physiological variations in osmolarity is not linked to RVD. 5. Basal and evoked release were strongly inhibited by an incubation of the tissue with the glia-specific toxin fluorocitrate, but were unaffected by a neurotoxic-treatment with NMDA, demonstrating the glial origin of the release of taurine in the SON. 6. The high osmosensitivity of taurine release suggests an important role in the osmoregulation of the SON function. These results strengthen the notion of an implication of taurine and glial cells in the regulation of the whole-body fluid balance through the modulation of vasopressin release.

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

PubMed2001

Regulation of sympathetic nervous system function after cardiovascular deconditioning.

Humans subjected to prolonged periods of bed rest or microgravity undergo deconditioning of the cardiovascular system, characterized by resting tachycardia, reduced exercise capability, and a predisposition for orthostatic intolerance. These changes in cardiovascular function are likely due to a combination of factors, including changes in control of body fluid balance or cardiac alterations resulting in inadequate maintenance of stroke volume, altered arterial or venous vascular function, reduced activation of cardiovascular hormones, and diminished autonomic reflex function. There is evidence indicating a role for each of these mechanisms. Diminished reflex activation of the sympathetic nervous system and subsequent vasoconstriction appear to play an important role. Studies utilizing the hindlimb-unloaded (HU) rat, an animal model of deconditioning, evaluated the potential role of altered arterial baroreflex control of the sympathetic nervous system. These studies indicate that HU results in blunted baroreflex-mediated activation of both renal and lumbar sympathetic nerve activity in response to a hypotensive stimulus. HU rats are less able to maintain arterial pressure during hemorrhage, suggesting that diminished ability to increase sympathetic activity has functional consequences for the animal. Reflex control of vasopressin secretion appears to be enhanced following HU. Blunted baroreflex-mediated sympathoexcitation appears to involve altered central nervous system function. Baroreceptor afferent activity in response to changes in arterial pressure is unaltered in HU rats. However, increases in efferent sympathetic nerve activity for a given decrease in afferent input are blunted after HU. This altered central nervous system processing of baroreceptor inputs appears to involve an effect at the rostral ventrolateral medulla (RVLM). Specifically, it appears that tonic GABAA-mediated inhibition of the RVLM is enhanced after HU. Augmented inhibition apparently arises from sources other than the caudal ventrolateral medulla. If similar alterations in control of the sympathetic nervous system occur in humans in response to cardiovascular deconditioning, it is likely that they play an important role in the observed tendency for orthostatic intolerance. Combined with potential changes in vascular function, cardiac function, and hypovolemia, the predisposition for orthostatic intolerance following cardiovascular deconditioning would be markedly enhanced by blunted ability to reflexly activate the sympathetic nervous system.

Animals↗

PubMed1983

The hypothalamic slice approach to neuroendocrinology.

The magnocellular peptidergic cells of the supraoptic and paraventricular nuclei comprise much of what is known as the hypothalamo-neurohypophysial system and is involved in several functions, including body fluid balance, parturition and lactation. While we have learned much from experiments in vivo, they have not produced a clear understanding of some of the crucial features associated with the functioning of this system. In particular, questions relating to the osmosensitivity of magnocellular neurones and the mechanism(s) by which their characteristic firing patterns are generated have not been answered using the older approaches. Electrophysiological studies with brain slices present direct evidence for osmosensitivity, and perhaps even osmoreceptivity, of magnocellular neurones. Other evidence indicates that the phasic bursting patterns of activity associated with vasopressin-releasing neurones (a) occur in the absence of patterned chemical synaptic input, (b) may be modulated by electrotonic conduction across gap junctions connecting magnocellular neurones and (c) are likely to be generated by endogenous membrane currents. These results make untenable the formerly held idea that phasic bursting activity is dependent upon recurrent synaptic inhibition.

Animals↗

PubMed2003

Effect of charge on interstitial distribution of albumin in rat dermis in vitro.

At physiological pH, negatively charged glycosaminoglycans in the extracellular matrix may influence distribution volume of a probe. We hypothesized that by varying the probe charge we would be able to observe a graded response of available volume fraction. Human serum albumin (HSA) (isoelectric point (pI) 5.0) was made more positive by cationization. Using reaction times of 10, 45 and 60 min, cationized HSA (cHSA) with respective pIs of 6.5, 7.3 and 8.0 were made. After eight days of equilibration in a buffer containing labelled native HSA and cHSA, the distribution volumes were calculated relative to that of 51Cr-EDTA, an extracellular tracer. The available volume in fully swollen dermis for native albumin relative to that of the extracellular tracer averaged 0.485+/-0.008 (n=49), with corresponding volumes for cHSA-10 min, cHSA-45 min and cHSA-60 min of 0.554+/-0.012 (n=17), 0.647+/-0.026 (n=17) and 0.718+/-0.021 (n=12), respectively. Increasing the ionic strength of the bathing solution to 1 M NaCl, thereby screening the fixed charges of tissue elements and probes alike, resulted in similar available and thereby excluded volumes of native HSA and neutral cHSA-45 min. These experiments suggest that fixed negative charges, most likely glycosaminoglycans, contribute significantly to interstitial exclusion of charged macromolecules, a phenomenon of importance for hydration of the interstitial fluid phase and therefore for body fluid balance. Moreover, the data indicate that previous findings of similar excluded volumes for the two differently sized major plasma proteins albumin (molecular mass 66 kDa) and IgG (molecular mass 160 kDa) may be explained by a more pronounced electrostatic repulsion of the former by the extracellular matrix.

Animals↗

PubMed2005

Effect of hydration on interstitial distribution of charged albumin in rat dermis in vitro.

At physiological pH, negatively charged glycosaminoglycans in the extracellular matrix may influence distribution volume of macromolecular probes, a phenomenon of importance for hydration of the interstitium and therefore for body fluid balance. We hypothesized that such charge effect was dependent on hydration. Human serum albumin (HSA) (the pH value for the isoelectric point (pI) = 4.9) was made neutral by cationization (cHSA) (pI = 7.6). Rat dermis was studied in vitro in a specially designed equilibration cell allowing control of hydration. Using a buffer containing labelled native HSA and cHSA, the distribution volumes were calculated relative to that of 51Cr-EDTA, an extracellular tracer. During changes in hydration (H), defined as (wet weight - dry weight) (dry weight)(-1)), the slope of the equation describing the relationship between extracellular fluid volume (V(x)) (in g H2O (g dry weight)(-1)) and H (V(x) = 0.925 H + 0.105) differed significantly from that for available volumes of cHSA (V(a,cHSA) = 0.624 H - 0.538) and HSA (V(a,HSA) = 0.518 H - 0.518). A gradual reduction in H led to a reduction in difference between available volumes for the two albumin species. Screening the fixed charges by 1 m NaCl resulted in similar available and excluded volumes of native HSA and neutral cHSA. We conclude that during gradual dehydration, there is a reduced effect of fixed negative charges on interstitial exclusion of charged macromolecules. This effect may be explained by a reduced hydration domain surrounding tissue and probe macromolecules in conditions of increased electrostatic interactions. Furthermore, screening of negative charges suggested that hyaluronan associated with collagen may influence intrafibrillar volume of collagen and thereby available and excluded volume fraction.

Animals↗

PubMed1981

Altered concentration of catecholamines in the hypothalamus of the rat after renal denervation.

Concentrations of noradrenaline, adrenaline, and dopamine were measured using a sensitive radioenzymatic assay in hypothalamic nuclei of rats 4 days after bilateral renal denervation. After renal denervation, catecholamine levels in several hypothalamic nuclei were found to be different from those of sham-operated animals. Noradrenaline was found to be increased in the supraoptic nucleus, adrenaline was increased in the paraventricular nucleus and lateral hypothalamic area, and dopamine was decreased in the supraoptic nucleus, medial preoptic nucleus and lateral hypothalamic area. These data suggest that afferent renal fibers influence the metabolism of hypothalamic catecholamines and that neural information originating in the kidney and transmitted to the hypothalamus is probably involved in physiological responses related to cardiovascular adjustments and body fluid balance.

Animals↗

PubMed2003

Intravenous angiotensin induces brain c-fos expression and vasopressin release in the near-term ovine fetus.

The effect of intravenous angiotensin II (ANG II) on fetal brain c-fos expression and arginine vasopressin (AVP) release was studied in the near-term ovine fetus. Fetuses with chronically implanted catheters received an intravenous infusion of ANG II or saline. Fetal plasma AVP concentrations were significantly increased after the peripheral administration of ANG II, with peak levels (3-fold) at 30 min after the intravenous infusion. There was no change in fetal plasma osmolality, sodium, and hematocrit levels between the control and experimental groups or between the periods before and after the infusion of ANG II. Intravenous ANG II administration induced Fos immunoreactivity (Fos-IR) in the circumventricular organs and the median preoptic nucleus of the fetal brain. Fos-IR was also demonstrated in the fetal supraoptic nuclei (SON). Double labeling demonstrated that the AVP-containing neurons in the SON were expressing c-fos in response to intravenous ANG II. These results indicate that the peripheral ANG II in the fetus may play a significant role in stimulating the central hypothalamic-neurohypophysial system during late gestation. It supports the hypothesis that circulating ANG II may act at the fetal AVP neurons in the hypothalamus in body fluid balance via the circumventricular organs, which are situated outside the blood-brain barrier, and the central neural pathway between these two brain structures has been relatively established in utero, at least at near-term.

Angiotensin II↗

PubMed1985

Afferent renal nerve stimulation excites supraoptic vasopressin neurons.

Single-unit recording experiments were performed in pentobarbital-anesthetized rats to investigate the effects of afferent renal nerve (ARN) stimulation on the activity of neurosecretory vasopressin cells of the supraoptic nucleus (SON). Neurosecretory SON cells were identified by antidromic invasion from the neurohypophysis and classified either as vasopressin (AVP) or oxytocin (OXY) secreting on the basis of their spontaneous activity patterns and response to activation of arterial baroreceptors. Fifty-three spontaneously active units were identified bilaterally in the SON: 40 putative AVP and 13 putative OXY neurons. Most putative AVP neurons (14/14 contralateral, 18/26 ipsilateral) were excited by ARN stimulation (mean onset latency 189 +/- 5 ms, mean response duration 237 +/- 17 ms). In contrast, ARN stimulation had no effect on the firing frequency of the 13 putative OXY neurons. These data indicate that sensory information originating in the kidney selectively alters the activity of SON AVP neurons and suggest that afferent information from the kidney is important in the coordination of neural and hormonal activity concerned with body fluid balance and the regulation of arterial pressure.

Afferent Pathways↗

PubMed1986

Changes in forebrain hexokinase activity after aortic baroreceptor denervation.

Although forebrain structures have been implicated in both the development and maintenance of the elevated arterial pressure (AP) after aortic baroreceptor denervation, little is known about the location of central structures involved in the hypertensive process. In the present study, regions of the forebrain whose metabolic activity was altered after aortic baroreceptor denervation were functionally identified using hexokinase (HK) histochemistry in the rat. Three days after bilateral aortic depressor nerve (ADN) transection AP was significantly elevated compared with sham ADN-transected animals (143 +/- 1 and 122 +/- 2 mmHg, respectively). Significant increases in HK activity were observed in the magno- and parvocellular components of the paraventricular nucleus of the hypothalamus, supraoptic nucleus, nucleus circularis, median preoptic nucleus, subfornical organ, and central nucleus of the amygdala in the ADN-transected animals. These data have demonstrated that removal of aortic baroreceptor afferent inputs alters the activity of forebrain structures previously implicated in regulation of body fluid balance and AP and suggest that these structures are involved in the hypertensive process after ADN transection.

Animals↗

PubMed1990

Electrophysiological evidence that systemic angiotensin influences rat area postrema neurons.

Extracellular single-unit recordings from neurons in the area postrema (AP) and the nucleus tractus solitarius (NTS) in anesthetized male rats demonstrated that most cells in these regions have spontaneous activities of 5 Hz or less. Systemic angiotensin (ANG II) (50-500 ng) enhanced the activity of 55% of AP cells tested (n = 76), whereas 53% of tested NTS neurons (n = 62) were inhibited by ANG II. To determine whether these neurons were influenced specifically by circulating ANG II or by the accompanying increase in mean arterial blood pressure (BP), the effects of adrenergic agonists given intravenously on ANG II influenced neurons were also examined. Subsequently two cell types were characterized: cells responding to iv ANG II but not to the adrenergic agonist ("ANG II sensitive") and cells responding in a similar way to both agents ("BP sensitive"). Most ANG II-responsive neurons in the AP (53.5%) and the NTS (65%) were determined to be BP sensitive. These data demonstrate that ANG II influences the activity of AP neurons. In addition, there exists a second population of AP neurons apparently responsive to perturbations of the cardiovascular system. These studies further emphasize the potential roles of the AP in the regulation of body fluid balance.

Angiotensin II↗