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At least 127 records · Page 7Linked to original sources
PubMed1999

Vascular, renal, and endocrine responses to low-dose atrial natriuretic peptide in the fluid-balanced New Zealand genetically hypertensive rats with and without endogenous arginine vasopressin.

In hypertension, the relationship between atrial natriuretic peptide (ANP) and vasopressin (AVP) is not yet clear, although their renal actions are effectively autoregulation. To examine the possible interaction further, the responses to ANP infusion (75 ng x min (-1), i.v.) have been investigated in both hypertensive and normotensive AVP-replete (HT and NT) and AVP-deficient (HTDI and NTDI) rats. This study aimed to assess the renal function and the plasma hormone concentrations of AVP, angiotensin II (AII), ANP, aldosterone, and corticosterone in the conscious, chronically catheterized, fluid-balanced rats, and to examine the cardiovascular, renal, and endocrine responses to a constant infusion of a low-dose ANP. Data gained from the present study showed, for the first time, the hormone profile, plasma electrolyte composition, and detailed renal function of the servo-controlled, fluid-balanced rats. The similarities of plasma electrolyte composition between servo-controlled and untreated rats indicated that the servo-controlled fluid replacement technique maintained the differences between the strains and maintained body fluid balance during the experimental periods. Following ANP administration, there were no changes in glomerular filtration rate (GFR) in all groups, but an enduring diuresis and natriuresis were observed in HT and NT, which were milder in HTDI rats. However, the hypotensive effect of ANP was of a similar magnitude in all rat strains. HTDI rats exhibited an inhibition of the renin-angiotensin system (RAS), which may have participated in the reduced mean arterial blood pressure (MAP) and natriuresis observed in these rats. The renal actions of ANP appear to rely upon renal tubular events, as indicated by increased fractional electrolyte excretions in the AVP-replete rats. This study highlights the importance of AVP to the profile of the renal actions of ANP in normal rats.

Animals↗
PubMed1997

Water deprivation increases the expression of pituitary adenylate cyclase-activating polypeptide gene in the rat subfornical organ.

The effect of water deprivation on the expression of pituitary adenylate cyclase-activating polypeptide (PACAP) was examined in the rat subfornical organ (SFO), using a combination of immunohistochemistry and in situ hybridization histochemistry. In the euhydrated condition, PACAP-immunoreactivity (PACAP-IR) and the expression of PACAP gene was observed in the SFO. Water deprivation for 24 h and 48 h caused a significant increase in PACAP gene transcripts in the SFO, compared with euhydrated animals. Additionally, water deprivation for 48 h caused an increase in PACAP-IR. This increase of PACAP-IR was demonstrated in both nerve fibers and cell bodies. High correlation was found between the localization of PACAP-IR cell bodies and PACAP messenger RNA synthesizing cell bodies in the peripheral part of the SFO. These results suggest that PACAP in the SFO may play a role in the humoral and neural changes associated with the regulation of body fluid balance after water deprivation.

Analysis of Variance↗
PubMed1979

Pathophysiological studies on hypertension induced in rats by kidney extract and salt.

The renin-angiotensin-aldosterone system, electrolyte and water balance, body fluid, and neurogenic tone and reactivity of the vasculature were studied in hypertension induced in uninephrectomized rats by repeated injection of renin-rich kidney extract and 1% saline drinking. The control rats were injected with physiological saline. Various measurements were made in conscious rats on the 10th day of the treatment. As compared with the control, plasma renin concentration and serum sodium increased significantly, while plasma aldosterone and renal excretory function did not differ. Blood volume (BV) expressed as per body weight increased significantly, but absolute BV, absolute or body weight-related plasma volume and hematocrit were not significantly different. The hypotensive effect of 1-Sar-8-Ile-angiotensin II was negligible 12 hours after the preceding injection of kidney extract. It was small but significant 1 hour after the injection. Increase in water turn-over and fractional sodium excretion occurred during the development of hypertension. Spironolactone did not significantly modify the developmental course. We observed increased depressor response to hexamethonium and increased reactivities to noradrenaline and angiotensin II (A II); these response curves relatively resembled those of spontaneously hypertensive rats. Hypertensive vascular changes were seen in the kidney and heart by histology. Thus, it was suggested that a direct vascular action of A II played a partial role in this hypertensive process while aldosterone played little role. The significance of BV increase and possible contribution of A II's other actions were discussed.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed2003

[Physical activity in the heat: physiology of hydration recommendations].

Physical exercise in the heat causes severe disturbances in homeostasis. The need for evaporative thermolysis is increased due to the combination of endogenous and exogenous heat production. Despite a marked increase in cardiac output, muscles and skin must compete for sufficient blood flow. In addition progressive dehydration can impair the ability of the cardiocirculatory to adjust adequately. The most serious risk associated with exercise in a hot environment is heat stroke. Although deleterious effects of dehydration occur only if large amounts of water and electrolytes are lost without being replaced, even moderate fluid depletion can reduce both physical and cognitive performance. Another mechanism by which heat exposure directly affects performance involves core temperature elevation which can induce profound changes in muscular activity and energy consumption, thereby accelerating exhaustion. Prevention of deleterious effects on health and performance requires an effective rehydration strategy to maintain body fluid balance. This strategy must optimize all three potentially limiting factors for fluid replacement, i.e., fluid intake, gastric emptying, and intestinal absorption. Practical guidelines are given to answer the questions of when, what and how much to drink.

Body Temperature Regulation↗
PubMed2001

Brain angiotensin and body fluid homeostasis.

Angiotensinogen, the precursor molecule of the peptides angiotensin I, II, and III, is synthesized in the brain and the liver. Evidence is reviewed that angiotensin II, and possibly angiotensin III, that are generated within the brain act within neural circuits of the central nervous system to regulate body fluid balance. Immunohistochemical studies in the rat brain have provided evidence of angiotensin-containing neurons, especially in the hypothalamic paraventricular nucleus, subfornical organ, periventricular region, and nucleus of the solitary tract, as well as in extensive angiotensin-containing fiber pathways. Angiotensin immunoreactivity is observed by electron microscope in synaptic vesicles in several brain regions, the most prominent of these being the central nucleus of the amygdala. Neurons in many parts of the brain (lamina terminalis, paraventricular and parabrachial nuclei, ventrolateral medulla, and nucleus of the solitary tract) known to be involved in the regulation of body fluid homeostasis exhibit angiotensin receptors of the AT(1) subtype. Pharmacological studies in several species show that intracerebroventricular administration of AT(1) receptor antagonist drugs inhibit homeostatic responses to the central administration of hypertonic saline, intravenous infusion of the hormone relaxin, or thermal dehydration. Responses affected by centrally administered AT(1) antagonists are water drinking, vasopressin secretion, natriuresis, increased arterial pressure, reduced renal renin release, salt hunger, and thermoregulatory adjustments. We conclude that angiotensinergic neural pathways in the brain probably have an important homeostatic function, especially in regard to osmoregulation and thermoregulation, and the maintenance of arterial pressure.

Angiotensin II↗
PubMed1991

Comparative quantitative ultrastructural studies of the choroidal epithelium of hydrocephalic (hpy/hpy) and normal mice, and the effect of stress induced by water deprivation.

Animals homozygous for the recessive, pleiotropic, mutation hpy(hydrocephalic-polydactyl) develop hydrocephalus early in the postnatal period. The condition develops in the apparent absence of any overt indications of obstruction in the cerebrospinal fluid (CSF) drainage system suggesting a continued, inappropriate, secretion of CSF. Electron microscope investigations were undertaken to both characterize and quantify the cell types present in the choroidal epithelium of mutants and their wild-type littermates and to gauge their response to a prolonged (24 h) deprivation of water, which has severe adverse effects on the general body fluid balance. Collectively, the findings indicate that the cellular makeup of the choroidal epithelium of normal animals and the manner of its response to changing fluid conditions is more complex than formerly anticipated. Also that inferences derived from a simple extrapolation of findings from other fluid-transporting epithelia to choroidal cells are misleading and erroneous. In wild-type animals allowed free access to water light cells with clavate microvilli (secretory cells) predominated whereas, following water deprivation there was a preponderance of dark cells with filiform microvilli, abundant mitochondria, multivesicular bodies and osmiophilic droplets (resorptive cells). In hydrocephalic mutants, the makeup of the choroidal epithelium of non-water-deprived animals resembled that of water-deprived wild-type mice and showed little change following water deprivation. These findings suggest that while the choroidal cells of mutants are capable of mounting a response to conditions having adverse effects on water balance (i.e., hydrocephalus) their response falls short of the level needed to fully redress the imbalance and is not materially increased by imposition of further, stringent, conditions (e.g., water deprivation). Thus, the findings lend support to the view that the mutational event affects the regulation of solute transport rather than effecting abrogation of the membrane pump itself.

Animals↗
PubMed1995

Atrial natriuretic peptide fragments in dogs with experimental heart failure.

1. This study in the canine arteriovenous (AV) fistula model of high-output heart failure (HOHF) evaluated the chronic temporal changes in plasma ANF and pro ANF 31-67 and their relationship to body-fluid balance and the renin-aldosterone axis. In addition, the haemodynamic, hormonal and renal excretory effects of synthetic pro ANF 31-67 infusions were examined in normal and AV fistula dogs with compensated HOHF. 2. Following the construction of the AV fistula, the dogs exhibited chronic parallel elevations in right atrial pressure and the plasma concentrations of ANF and pro ANF 31-67. The gradual increases in the two peptides were associated with a gradual decrease in plasma renin activity and the re-establishment of sodium balance. 3. In normal and compensated AV fistula dogs, synthetic pro ANF 31-67 produced similar significant reductions in arterial blood pressure, right atrial pressure and elevations in urinary sodium excretion. These effects were not associated with increases in plasma or urinary cyclic GMP (cGMP). 4. These results suggest that the elevation in the endogenous circulating levels of pro ANF 31-67 in the AV fistula dogs may represent one chronic adaptive mechanism to achieve body fluid homeostasis. Furthermore, via potentially different mechanisms of action, ANF and pro ANF 31-67 may coordinate and contribute to the regulation of haemodynamic and renal function during physiological and pathophysiological situations.

Animals↗
PubMed2003

Drinking decreases the noradrenaline release in the median preoptic area caused by hypovolemia in the rat.

Previous observations have suggested that the noradrenergic system in the median preoptic nucleus (MnPO) is implicated in the regulation of body fluid balance and cardiovascular function. The present study was carried out to investigate whether water intake alters the release of noradrenaline (NA) in the MnPO area caused by hypovolemia in freely moving rats. Nonhypotensive hypovolemia was induced by subcutaneous polyethylene glycol (PEG), and extracellular levels of NA were measured using intracerebral microdialysis techniques. Subcutaneous injections of PEG (30%, 5 ml) significantly enhanced the NA release in the MnPO area. Water ingestion significantly attenuated the elevation in the NA release in the MnPO area induced by the PEG treatment. These results show the involvement of the noradrenergic system in the MnPO in the maintenance of body fluid volume, and suggest that the system may play an important role in the elicitation of hypovolemia-induced dipsogenic response.

Animals↗
PubMed1997

Comparison of the effects of selective endothelin ETA and ETB receptor antagonists in congestive heart failure.

OBJECTIVES: This study was designed 1) to determine the extent to which endogenous endothelin (ET) affects hemodynamic, hormonal and body fluid balance through ETA and ETB receptors in congestive heart failure (CHF); and 2) to assess the therapeutic benefits and adverse effects of ET receptor antagonists for ETA and ETB on cardiorenal and neurohormonal variables. BACKGROUND: ET has two receptors, ETA and ETB, both of which are distributed in various tissues and cells. In vascular beds, ETA receptors mediate vasoconstriction, whereas ETB receptors mediate vasorelaxation. However, ETB receptors also exist in smooth muscle and mediate vasoconstriction. METHODS: We administered either the ETA receptor antagonist FR139317 (FR [n = 8], 1 and 10 mg/kg body weight) or the ETB receptor antagonist RES-701-1 (RES [n = 8], 0.2 and 1.5 mg/kg) to dogs with CHF induced by rapid ventricular pacing. The effects of both antagonists on cardiorenal and hormonal functions were studied. RESULTS: FR decreased cardiac pressures and the plasma atrial natriuretic peptide (ANP) level and increased cardiac output (CO). Urinary flow rate and urinary sodium excretion increased in association with an increase in the glomerular filtration rate and renal plasma flow (RPF). In contrast, RES increased cardiac pressures and decreased CO. It also decreased the plasma aldosterone level and RPF. Neither antagonist affected plasma norepinephrine levels. CONCLUSIONS: Endogenous ETs increase cardiac pressures and the retention of body fluid through ETA receptors in CHF. The vasodilative action through ETB receptors is overall functionally more important than the constrictive action through ETB receptors. ETs may regulate the secretion of ANP and aldosterone. Our findings suggest that selective ETA receptor antagonists have potential therapeutic benefits affecting both hemodynamic variables and diuresis, whereas ETB receptor antagonists have adverse hemodynamic effects, with the possibility of preventing fluid retention through suppression of aldosterone secretion in dogs with CHF.

Analysis of Variance↗
PubMed1993

Nutrition considerations in the management of ventilator-dependent patients.

Nutrition support of the patient with ventilatory failure is an important adjunct to recovery. Malnutrition and respiratory failure are frequently interrelated. Ventilator dependence occurs when the patient cannot independently sustain oxygenation, carbon dioxide removal, or acid-base balance. Nutrition assessment, determination of energy requirements, and provision of nutrient solutions utilizing the most appropriate route of administration should be initiated early in the ventilator-dependent patient's hospital course. Careful assessment will identify patients needing repletion along with maintenance calories, as well as special macronutrient and micronutrient needs. The nutrient prescription is designed to provide carbohydrate, protein, and fat in amounts for optimal substrate utilization. Body fluid balance, micronutrient needs, electrolyte homeostasis, and acid-base balance affect respiratory muscle function and must also be considered in developing the nutrition regimen. Properly constructed enteral or parenteral nutrition plans begun early offer the best support for ventilator-dependent patients.

Enteral Nutrition↗
PubMed1975

Relationships of the renin-angiotensin-aldosterone system and sodium balance to blood pressure regulation in chronic renal failure of polycystic kidney disease.

In 5 patients with polycystic kidney disease and creatinine clearances ranging from 4 to 40 ml/min, relationships between changes in blood pressure, sodium balance, body fluid compartments, plasma renin activity (PRA), urinary aldosterone excretion, and plasma aldosterone concentrations were studied during periods of low, medium, and high sodium intake. Total body water (TBW), total exchangeable body sodium (TEBS), and extracellular volume (ECV) were measured by isotope dilution techniques, plasma volume with Evan's blue dye, and PRA and aldosterone by radioimmunoassay. Low sodium intake reduced kidney function, blood pressure, and serum sodium, while PRA reached its highest levels. Subsequent increases in sodium intake improved kidney function and increased blood pressure. Plasma volume increased slightly and ECV markedly, while PRA dropped to 15 percent of the value noted after the low sodium intake. TBW and TEBS showed inconsistent changes. Aldosterone changes correlated closely with PRA. Blood pressure showed a negative correlation with PRA, but a positive one with body weight and cumulative sodium balance, and with plasma and extracellular volumes.it is suggested that whereas renin and aldosterone are involved in the maintenance of circulatory homeostasis during sodium loss, sodium retention causes an increase in blood pressure by concomitant changes in body fluids.

Adult↗
PubMed1985

B. W. Zweifach Award lecture. Regulation of the microcirculation.

Microcirculatory blood flow and transport are controlled to meet local and systemic demands for material exchange and body fluid balance. Control mechanisms act through effectors (smooth muscle cells) at many sites within the microvascular bed. Responses at different sites are not uniform, resulting in a broadly heterogeneous distribution of pressures and flows which is constantly changing. Simplified, uniform models of microvascular networks have made it possible to identify the principles governing blood circulation and blood-tissue transport. However, knowledge of how these principles are integrated at the microcirculatory level requires the variability and heterogeneity to be taken into account. Indeed, there is much reason to believe that heterogeneity is an important part of microcirculatory control.

Arterioles↗
PubMed2002

Adenosine type 1 receptor antagonists in fluid retaining disorders.

Adenosine is a vasoactive hormone whose action is mediated through at least four receptors. The most prevalent receptors are type 1, which promote vasoconstriction, and type 2, comprised of 2 subtypes (a,b) that promote vasodilation. In the kidney, type 1 receptors located on preglomerular vessels and in the tubule are involved in the regulation of glomerular filtration. Whole body fluid balance is strongly dependent on the ability of the kidney to maintain stable glomerular filtration. Several antagonists to adenosine type 1 receptors have been developed. These agents generate excess fluid (diuresis) and sodium (natriuresis) excretion in control animals and animal models of fluid retention, as well as in normal and oedematous humans. In both animals and humans, these effects are generally achieved without major changes in glomerular filtration. Animal studies have confirmed the location of adenosine type 1 receptors in relevant tissue sites in the kidney. More highly selective antagonists for adenosine type 1 receptors are regularly developed, improving their use in fluid retaining disorders. Clinical trials with these agents have commenced for the treatment of hypertension, renal failure and congestive heart failure, all disorders that include varying levels of fluid retention. The clinical trial results have been mixed. The early results with congestive heart failure suggest great promise for these agents, whereas trials in hypertension and renal failure have been equivocal.

Animals↗
PubMed1996

Integrative role of the lamina terminalis in the regulation of cardiovascular and body fluid homeostasis.

1. Cardiovascular and body fluid homeostasis depends upon the activation and co-ordination of reflexes and behavioural responses. In order to accomplish this, the brain receives and processes both neural and chemical input. Once in the brain, information from sources signalling the status of the cardiovascular system and body fluid balance travels, and is integrated, throughout a widely distributed neural network. Recent studies using neuroanatomical and functional techniques have identified several key areas within this neural network. One major processing node is comprised of structures located along the lamina terminalis. 2. Structures associated with the lamina terminalis include the median preoptic nucleus (MePO) and two sensory circumventricular organs (SCVO), the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT). Current evidence indicates that blood-borne signals, such as angiotensin II (AngII), reach SCVO (e.g. SFO) where they are transduced. This information is then carried via neural pathways to brain nuclei (e.g. MePO) where it is integrated with other inputs, such as those derived from systemic arterial blood pressure and volume receptors. 3. Because of their receptive and integrative functions, lamina terminalis structures are essential for the normal control of hormone release (e.g. vasopressin), sympathetic activation and behaviours (thirst and salt appetite), which collectively contribute to maintenance of cardiovascular and body fluid homeostasis.

Adrenergic Fibers↗
PubMed1994

[Variations of body composition by bioelectric impedancemetry after major surgery].

Body water variations are traditionally measured postoperatively by fluid balance and body weight. Bioelectrical impedance assessment permits the evaluation of body composition, i.e., lean body mass, body fat and total body water. We compared the traditional method (body weight and fluid balance) with bioelectrical impedance assessment while estimating body water. Body weight, fluid balance, resistance, reactance, lean body mass, body fat, total body water, triceps skinfold and total protein blood level were measured prospectively (preop, and on days 1, 3 and 5 postop) in 30 patients admitted for major surgery (thoracic, abdominal or vascular). The results suggest that body composition changed significantly with time (p < .05); in all 3 surgical groups. There was a low correlation between total body water measured by bioelectrical Impedance and fluid balance. Bioelectrical impedance assessment is sensitive to body water changes but appears to overestimate these variations compared to the traditional method.

Blood Proteins↗
PubMed1999

Preventing dehydration in children with cystic fibrosis who exercise in the heat.

PURPOSE: In healthy children who exercise in the heat, the addition of flavor, carbohydrate, and 18 mmol x L(-1) NaCl to water induced a major increase in voluntary drink intake compared with the intake of unflavored water. This increase was sufficient to prevent voluntary dehydration. We hypothesized that, to achieve a similar effect in children with cystic fibrosis (CF), whose NaCl losses in sweat are markedly excessive, the drink should include an NaCl concentration higher than 18 mmol x L(-1). METHODS: Eleven subjects with CF (6 girls, 5 boys, ages 10.9-19.5 yr) attended three 3-h sessions of intermittent exercise of moderate intensity (four 20-min bouts), at 35 degrees C, 50% relative humidity. Either water (W), flavored water (FW), or a 30 mmol x L(-1) NaCl plus 6% carbohydrate solution (Na30) was offered ad libitum, in a counterbalanced sequence. Six subjects performed an additional session in which they drank a 50 mmol x L(-1) NaCl-6% CHO solution (Na50). RESULTS: There was no significant drink effect on body fluid balance, core temperature, heart rate, or serum electrolytes with W, FW, or Na30. Serum osmolality decreased throughout the sessions from 290.6 +/- 1.1 (mean +/- SEM) to 281.3 +/- 1.2 mmol x kg(-1) (P < 0.0005), serum sodium from 143.1 +/- 0.5 to 141.1 +/- 0.7 mmol x L(-1) (P = 0.01) and serum chloride from 109.1 +/- 0.5 to 107.5 +/- 0.5 mmol X L(-1) (P < 0.001). In contrast, the 50 mmol x L(-1) NaCl drink induced a near significant (P = 0.08) higher fluid intake, and it significantly ameliorated the rate of progressive dehydration. CONCLUSIONS: The marked loss of NaCl in the sweat of CF patients may induce an hypo-osmolar state in the serum, even when the drink contains 30 mmol x L(-1) NaCl. This may diminish the thirst drive triggered by hypothalamic osmoreceptors and may lead to voluntary dehydration. A flavored drink with an even higher salt content (50 mmol X L(-1)), however, enhances drinking and attenuates the voluntary dehydration.

Adolescent↗
PubMed1997

[The influence of ACE inhibitors on urinary electrolyte secretion and the response to transitory hypovolemia in chronic heart failure].

Renin-angiotensin system promotes sodium and chloride retention, participates in the defense response to hypovolemia and, in congestive heart failure, contributes to edema formation and progression of the disease. We investigated whether ACE-inhibitors interfere with the action of the renin-angiotensin system on the nephron, and therefore with water and urinary electrolytes excretion. The interaction among renin-angiotensin system, diuretic treatment and urinary electrolytes was evaluated both during chronic treatment and in response to acute renin-angiotensin system activation as that observed after extracorporeal ultrafiltration-induced transient hypovolemia. Plasma renin activity and aldosterone, body fluid balance and urinary sodium, chloride and potassium concentrations were evaluated in 30 patients with congestive heart failure in NYHA II-III functional class, grouped according to whether long-term therapy did not include (Group I, n = 15) or included (Group II, n = 18) ACE-inhibitors. All parameters were evaluated at baseline and after a single session of extracorporeal ultrafiltration. At baseline, urinary output and urinary sodium and chloride concentrations were similar in the two groups, while urinary potassium concentration was lower in patients assuming ACE-inhibitors (Group II). Plasma renin activity was higher and aldosterone was lower in Group II than in Group I. After removal of similar amounts of plasma water by extracorporeal ultrafiltration, body weight decreased in both groups but the decrease was maintained in the following days only in Group II patients. A transient reduction (48 hours) of both plasma volume and urinary output was observed after ultrafiltration in both groups. Despite plasma renin activity and aldosterone increase, urinary electrolytes response to ultrafiltration was different in the two groups: sodium and chloride were reduced, and potassium did not change in Group 1 while, in Group II, sodium and chloride did not change and potassium excretion was significantly increased. In conclusion, chronic treatment with ACE-inhibitors does not enhance the excretion of sodium in congestive heart failure but just mitigates potassium loss. The role of these drugs becomes particularly relevant during acute renin-angiotensin system activation due to hypovolemia; in this setting ACE-inhibitors counteract sodium and chloride retention resulting in a potential hazard due to interference with the defence mechanisms toward hypovolemia, and an amplification of extracorporeal ultrafiltration efficacy by preventing edema recovery after its mechanical removal.

Aged↗
PubMed1998

Dual facets of hyponatraemia and arginine vasopressin in patients with ACTH deficiency.

OBJECTIVE: Hyponatraemia is often observed in patients with ACTH deficiency who are thought not to suffer from volume depletion. Their high plasma AVP levels relative to plasma osmolality are presumed to be maintained by non-osmotic mechanisms. We attempted to assess volume status from changes in selected clinical measurements related to body fluid balance in the course of i.v. fluid supplementation and following glucocorticoid (GC) replacement in ACTH-deficient patients, and to interpret plasma AVP levels in the context of the estimated volume status. PATIENTS AND DESIGN: This report consists of three parts. First, an ACTH-deficient patient with hyponatraemia and volume depletion who was followed through volume replacement to recovery after GC replacement is described (case report). Secondly, medical records of five ACTH-deficient patients with hypovolaemia and hyponatraemia were surveyed retrospectively to observe changes in serum levels of sodium, uric acid (UA) and haematocrit (Hct) following i.v. fluid supplementation of low sodium content (retrospective study). Thirdly, five ACTH-deficient patients with or without overt dehydration were studied with regard to body weight, blood pressure, serum sodium, total proteins, Hct and blood urea nitrogen before and after GC replacement (prospective study). Plasma AVP levels were measured after i.v. fluid supplementation without GC replacement in the patients of the retrospective study, and before and after GC replacement in the patients of the prospective study. RESULTS: The first patient became more hyponatraemic after i.v. fluid supplementation and recovered ultimately from hyponatraemia after GC replacement. In five patients studied retrospectively, the serum sodium levels fell progressively following i.v. fluid supplementation, concurrent with reduction in UA levels and Hct, which indicated the dilutional nature of the hyponatraemia. In the patients observed prospectively, the accumulation of fluid and sodium was indicated by a rise in body weight, blood pressure and serum sodium levels and a decline in Hct and total proteins after GC replacement. Plasma AVP levels rose similarly in patients with dilutional hyponatraemia and in patients with borderline hyponatraemia before GC replacement. CONCLUSION: Patients with untreated ACTH deficiency may have either of two kinds of hyponatraemia--i.e. borderline hyponatraemia associated with subclinical hypovolaemia, or dilutional hyponatraemia. Similarity of plasma AVP levels in two hyponatraemic states suggests their AVP secretion is regulated by non-osmotic, non-volume mechanisms, possibly released from GC suppression at low plasma osmolality.

Adrenocorticotropic Hormone↗