Isotonic and hypertonic sodium loading in supine humans.

The hypothesis that hypertonic saline infusion induces a greater natriuresis than infusion of the same amount of sodium as isotonic saline was tested in 8 supine subjects on fixed sodium intake of 150 mmol NaCl day(-1). Sodium loads equivalent to the amount of sodium contained in 10% of measured extracellular volume were administered intravenously over 90 min either as isotonic saline or as hypertonic saline (850 mmol L(-1)). A third series without saline infusion served as time control. Experiments lasted 8 h. Water balance and sodium loads were maintained by replacing the excreted amounts every hour. Plasma sodium concentrations only increased following hypertonic saline infusion (by 2.7 +/- 0.3 mmol L(-1)). Oncotic pressure decreased significantly more with isotonic saline (4.1 +/- 0.3 mmHg) than with hypertonic saline (3.2 +/- 0.2 mmHg), indicating that isotonic saline induced a stronger volumetric stimulus. Renal sodium excretion increased more than a factor of four with isotonic and hypertonic saline but also increased during time control (factor of three). Cumulated sodium excretions following isotonic (131 +/- 13 mmol) and hypertonic saline (123 +/- 10 mmol) were statistically identical exceeding that of time control (81 +/- 9 mmol). Plasma angiotensin II decreased in all series but plasma ANP concentrations and urinary excretion rates of endothelin-1 remained unchanged. In conclusion, hypertonic saline did not produce excess natriuresis. However, as the two loading procedures induced similar natriureses during different volumetric stimuli, part of the natriuresis elicited by hypertonic saline could be mediated by stimulation of osmoreceptors involved in renal sodium excretion. The supine position does not provide stable time control conditions with regard to renal excretory function.     

Influence of ruminal water‐loading on renal sodium excretion and water intake following feeding in sheep

We investigated the effect of ruminal water loading before feeding on the natriuretic and drinking responses that follow feeding. Six sheep fed 800 g of chaff drank 1360 ± 150 mL during the 5 h immediately following feeding and increased renal Na excretion. Plasma Na concentration increased by 4 mmol L^–1 and plasma osmolality by 9 mosmol kg^–1 within 1.5 h and remained elevated. A rumen load of water administered before feeding prevented the increases in plasma Na and osmolality without affecting feeding. The natriuresis, water drinking and vasopressin secretion in response to feeding were abolished. Total sodium excreted during the experiment was halved in water‐loaded animals compared with untreated animals (30.4 ± 2.1 mmol^–1 cf. 63.8 ± 2.9 mmol^–1; P < 0.01). Ruminal loading with isotonic saline caused a 33% reduction in postprandial drinking, however, reducing cerebrospinal fluid NaCl concentration abolished postprandial drinking and natriuresis. Intravenous infusion of isotonic dextran appeared to delay the onset of water intake without changing the total volume of water drunk, suggesting a role of plasma volume in initiating drinking. We conclude from the data that central osmoregulatory mechanisms that include increased sodium excretion as well as thirst and vasopressin release are activated following food intake by sheep.     

Saline‐induced natriuresis and renal blood flow in conscious dogs: effects of sodium infusion rate and concentration

Aim: This study focused on static and dynamic changes in total renal blood flow (RBF) during volume expansion and tested whether a change in RBF characteristics is a necessary effector mechanism in saline‐induced natriuresis. Methods: The aortic flow subtraction technique was used to measure RBF continuously. Identical amounts of NaCl (2.4 mmol kg^?1) were given as slow isotonic (Iso, 120 min), slow hypertonic (Hyper, 120 min), and rapid isotonic loads (IsoRapid, 30 min). Results: During Iso and IsoRapid, arterial blood pressure increased slightly (6–7 mmHg), and during Hyper it remained unchanged. Iso and Hyper increased sodium excretion (4 ± 1 to 57 ± 27 and 10 ± 4 to 79 ± 28 μmol min^?1, respectively) and decreased plasma renin activity (by 38% and 29%), angiotensin II (by 56% and 58%) and aldosterone (by 47% and 65%), while RBF remained unchanged. IsoRapid caused a similar increase in sodium excretion (to 72 ± 19 μmol min^?1), a similar decrease in renin system activity, but a 15% elevation of RBF (282 ± 22 to 324 ± 35 mL min^?1). Selected frequency domain parameters of RBF autoregulation did not change in response to any load. Conclusions: In response to slow saline loading simulating daily sodium intake, the rate of sodium excretion may increase 10–20‐fold without any change in mean arterial blood pressure or in RBF. Regulatory responses to changes in total body NaCl levels appears, therefore, to be mediated primarily by neurohumoral mechanisms and may occur independent of changes in arterial pressure or RBF.     

Increase in plasma sodium enhances natriuresis in response to a sodium load unable to change plasma atrial peptide concentration

The influence of plasma sodium concentration in the control of sodium excretion was investigated in conscious, water-diuretic dogs. NaCl was infused for 60 min as a hypertonic or isotonic solution at a rate of 60 mumol NaCl min-1 kg-1 body wt. Plasma sodium concentration rose only during hypertonic infusion (P less than 0.05). Sodium excretion increased markedly with both infusions (hypertonic, from 2.4 +/- 0.6 to 105 +/- 27 mumol min-1; isotonic, from 3.9 +/- 1.3 to 58 +/- 17 mumol min-1). Fractional sodium excretion increased more during hypertonic than during isotonic infusion. Hypertonic infusion decreased diuresis from 3.1 +/- 0.5 to 1.3 +/- 0.6 ml min-1, while isotonic infusion elicited an increase from 3.9 +/- 0.5 to 7.2 +/- 0.7 ml min-1. Plasma renin activity and plasma aldosterone decreased markedly in both series (P less than 0.05), the relative changes in the two series being very similar. Central venous pressure increased (2.8 +/- 0.7 to 4.5 +/- 1.0 mmHg) during isotonic infusion but not significantly during hypertonic infusion. Arterial pressure, heart rate and plasma levels of atrial natriuretic peptide and catecholamines did not change measurably in either series. It is concluded that simultaneous increases in extracellular volume and sodium concentration cause a larger natriuretic response than a change in volume alone, and that a 40-fold increase in sodium excretion may occur without measurable changes in plasma atrial natriuretic peptide concentration.     

Sodium balance and the natriuresis of hypertonic saline infusion in dogs.

Recently, a paradoxical effect of dietary salt intake on the natriuresis following hypertonic saline infusion was observed in rats. In these experiments the effects of alterations in dietary sodium on the natriuretic response to a hypertonic saline load was studied in dogs. Dogs maintained on a high-sodium diet did not have a significantly different natriuresis than those on a low-sodium diet. When differences in sodium balance were amplified by the use of deoxycorticosterone, furosemide, and manipulation of dietary sodium, dogs in positive sodium balance showed a significantly enhanced initial excretion of sodium followed by a reversal of the pattern. Consequently, the cumulative sodium excretion was not different between low- and high-sodium groups. Since the cumulative natriuretic response to isotonic saline infusion was larger in dogs in positive sodium balance compared to those in negative sodium balance, the failure to detect a difference following hypertonic saline infusion was probably because of the increased plasma sodium concentration.     

Natriuresis in conscious dogs caused by increased carotid [Na+] during angiotensin II and aldosterone blockade

The renal response to a selective increase in the Na⁺ concentration of the blood perfusing the central nervous system was investigated in conscious dogs treated with the converting enzyme inhibitor enalaprilat and the aldosterone antagonist canrenoate. In split-infusion experiments the plasma [Na⁺] of carotid blood was increased (approx. 6 mM) by bilateral infusion of hypertonic NaCl. Concomitantly distilled water was infused into the v. cava making the sum of the infusions isotonic. In control experiments isotonic saline was infused at identical rates into all three catheters. Na⁺ excretion increased markedly in both series, 103 ± 14 to 678± 84 μmol min^-1 during split-infusion and 90 ± 14 to 496 ± 74 μmol min^-1 during the isotonic volume expansion. Peak rate of excretion, peak fractional sodium excretion, and cumulative sodium excretion were all significantly higher (P < 0.05) during split-infusion than during control experiments. Plasma vasopressin increased only during split-infusion (0.68 ± 0.11 to 2.4 ± 0.8 pg ml^-1) while the increases in plasma atrial natriuretic peptide were similar in the two series. Urinary excretion of urodilatin (ANP95-126) increased significantly more during split-infusion (46 ±11 to 152 ±28 fmol min^-1) than during the isotonic volume expansion (45 ± 14 to 84 ± 16 fmol min^-1) (P < 0.05). It is concluded that the natriuretic mechanisms activated by a selective increase in the Na⁺ concentration of carotid blood and associated with increased excretion of urodilatin cannot be eliminated by blockade of the renin-angiotensin-aldosterone system.     

Renal and hormonal responses to isotonic saline infusion after 3 days' head‐down tilt vs. supine and seated positions

Aim: The study aimed to determine whether prolonged exposure to simulated microgravity produces a level of thoracic volume receptor loading similar to that seen in the upright position or immediately after lying down. Methods: We used a cross‐over design to compare responses to a saline infusion in eight healthy subjects during a 4‐day, ?6° head‐down tilt (HDT) and in the acute seated and acute supine positions. Results: The first 24 h of HDT were associated with greater urinary excretion of water and sodium (UV, UNaV) than seated and acute supine [cumulative UV, 3035 ± 219, 2311 ± 156 (P < 0.05), and 2448 ± 182 mL (P < 0.05), respectively; cumulative UNaV, 256 ± 19, 180 ± 11 (P < 0.05), and 189 ± 15 mmol (P < 0.05), respectively]. Haemoglobin and haematocrit were increased after 24 h and plasma volume decreased after 48 h of HDT (P < 0.05). With prolongation of HDT, UV and UNaV returned near the baseline values, and plasma atrial natriuretic factor (ANF) and renin values returned to acute seated levels; in acute supine, ANF values were higher and renin lower than in the two other positions. After a 30‐min infusion of 20 mL kg^?1 isotonic saline on the fourth HDT day or during acute seated or acute supine, sodium excretion within 4 h was similar during HDT and acute seated (83 ± 6 and 84 ± 9 mmol, respectively) and greater during supine (104 ± 8 mmol, P < 0.05). The renin decrease was greater in HDT and seated than in supine. The plasma ANF increase was greater during HDT than during supine; during seated, plasma ANF was unchanged. Conclusion: These data suggest that, after 4 days of HDT, thoracic volume receptor loading returns to the same level as in the seated position, leading to blunted responses to volume expansion as compared with the acute supine position.     

Influence of volume expansion,serum sodium,and fractional excretion of sodium on urate excretion

The relative contributions of volume expansion and increased fractional excretion of sodium to the uricosuria of saline infusion were assessed in 19 subjects by volume expansion with rapid infusion of 21 of hypertonic saline (3%), isotonic saline (0.9%), or hypotonic saline (0.45%). Urate excretion increased 385 mug/min (P less than 0.01) with hypertonic, 145 mug/min (P less than 0.05) with isotonic saline, and 294 mug/min (P less than 0.001) with hyptonic saline. When 150 meq of sodium chloride was administered as appropriate volumes of hypertonic, isotonic of hypotonic saline, the magnitude or uricosuria was correlated with volume load (r = 0.66, P less than 0.002). fractional excretion of sodium correlated with infusion volumes for all studies taken together (r = 0.35, P greater than 0.1). The relationship between fractional excretion of sodium and fractional excretion of urate was entirely attributed to their correlation with infusion volume. Both post-pyrazinamide urate excretion and pyrazinamide suppressible urate excretion increased with volume expansion.     

Plasma Renin Activity Following Central Infusion of Angiotensin II and Altered CSF Sodium Concentration in the Conscious Goat

To study central influences on the renal release of renin, angiotensin II was infused into the lateral cerebral ventricle of conscious hydrated goats. CSF sodium concentration was increased or lowered by similar infusions of hypertonic NaCl or of isotonic fructose solution. Infusion of anglotensin II in doses from 0.5 to 1 μg caused a drop in plasma renin activity (PRA) and elicited a rise in blood pressure, antidiuresis, natriuresis, and thirst. Intraventricular infusion of hypertonic NaCl also suppressed PRA, induced anti-diuresis, natriuresis, and an inconsistent rise in blood pressure. Lowering of CSF [Na⁺] by infusion of isotonic fructose caused a rise in PRA and was followed by a water diuresis in the non-hydrated animal. The fructose infusions caused some decrease in renal K⁺ excretion but no consistent change in renal Na⁺ excretion. The results indicate that angiotensin II and changes in sodium balance modulate renal renin release also via the central nervous system.     

Influence of ruminal water-loading on renal sodium excretion and water intake following feeding in sheep.

We investigated the effect of ruminal water loading before feeding on the natriuretic and drinking responses that follow feeding. Six sheep fed 800 g of chaff drank 1360 +/- 150 mL during the 5 h immediately following feeding and increased renal Na excretion. Plasma Na concentration increased by 4 mmol L (-1) and plasma osmolality by 9 mosmol kg (-1) within 1.5 h and remained elevated. A rumen load of water administered before feeding prevented the increases in plasma Na and osmolality without affecting feeding. The natriuresis, water drinking and vasopressin secretion in response to feeding were abolished. Total sodium excreted during the experiment was halved in water-loaded animals compared with untreated animals (30.4 +/- 2.1 mmol (-1) cf. 63.8 +/- 2.9 mmol-1; P < 0.01). Ruminal loading with isotonic saline caused a 33% reduction in postprandial drinking, however, reducing cerebrospinal fluid NaCl concentration abolished postprandial drinking and natriuresis. Intravenous infusion of isotonic dextran appeared to delay the onset of water intake without changing the total volume of water drunk, suggesting a role of plasma volume in initiating drinking. We conclude from the data that central osmoregulatory mechanisms that include increased sodium excretion as well as thirst and vasopressin release are activated following food intake by sheep.     

Saline-induced natriuresis and renal blood flow in conscious dogs: effects of sodium infusion rate and concentration

AIM: This study focused on static and dynamic changes in total renal blood flow (RBF) during volume expansion and tested whether a change in RBF characteristics is a necessary effector mechanism in saline-induced natriuresis. METHODS: The aortic flow subtraction technique was used to measure RBF continuously. Identical amounts of NaCl (2.4 mmol kg(-1)) were given as slow isotonic (Iso, 120 min), slow hypertonic (Hyper, 120 min), and rapid isotonic loads (IsoRapid, 30 min). RESULTS: During Iso and IsoRapid, arterial blood pressure increased slightly (6-7 mmHg), and during Hyper it remained unchanged. Iso and Hyper increased sodium excretion (4 +/- 1 to 57 +/- 27 and 10 +/- 4 to 79 +/- 28 micromol min(-1), respectively) and decreased plasma renin activity (by 38% and 29%), angiotensin II (by 56% and 58%) and aldosterone (by 47% and 65%), while RBF remained unchanged. IsoRapid caused a similar increase in sodium excretion (to 72 +/- 19 micromol min(-1)), a similar decrease in renin system activity, but a 15% elevation of RBF (282 +/- 22 to 324 +/- 35 mL min(-1)). Selected frequency domain parameters of RBF autoregulation did not change in response to any load. CONCLUSIONS: In response to slow saline loading simulating daily sodium intake, the rate of sodium excretion may increase 10-20-fold without any change in mean arterial blood pressure or in RBF. Regulatory responses to changes in total body NaCl levels appears, therefore, to be mediated primarily by neurohumoral mechanisms and may occur independent of changes in arterial pressure or RBF.     

Role of prostaglandin cyclooxygenase and cytochrome P450 pathways in the mechanism of natriuresis which follows hypertonic saline infusion in the rat

AIM: The prostaglandin cyclooxygenase (COX) and P450 cytochrome (CYP450) pathways of arachidonic acid metabolism are functionally interrelated and both engaged in control of sodium excretion; the study focused on their contribution to the natriuresis which follows hypertonic saline infusion in the rat. METHODS: In anaesthetized rats, clearance studies were conducted, supplemented with laser-Doppler measurements of the cortical and medullary blood flow (CBF, MBF), and measurement of medullary tissue admittance (Y), an index of interstitial ion concentration. RESULTS: Indomethacin (Indo), 5 mg kg(-1) i.v. paradoxically enhanced the natriuresis secondary to intra-aortic suprarenal 5% saline load, further increasing sodium excretion by 385 +/- 73% (P < 0.01). After acute clotrimazole, 10 mg kg(-1) i.v. an inhibitor of CYP450 epoxygenase, the increase in natriuresis was smaller and did not differ from that observed after the drug's ethanol solvent. In rats pre-treated with clotrimazole for 3 days, hypertonic saline loading increased sodium excretion (U(Na)V) to 0.94 +/- 0.22 micromol min(-1) , compared with a significantly greater (P < 0.05) increase to 2.76 +/- 0.48 micromol min(-1) measured in untreated controls. Indo increased U(Na)V twofold, similarly in the clotrimazole and in the control group; in the absence or presence of clotrimazole treatment, COX blockade significantly decreased MBF and increased Y. CONCLUSION: The data indicate that blockade of the CYP450 epoxygenase significantly impairs excretion of sodium in rats acutely loaded with hypertonic NaCl solution. The paradoxical post-Indo natriuresis is preserved in clotrimazole treated rats, which speaks against the role of CYP450 pathway in the response.     

Elevated renal perfusion pressure does not contribute to natriuresis induced by isotonic saline infusion in freely moving dogs

The study was designed to determine to what extent moderate elevation of renal perfusion pressure (RPP) via the mechanism of 'pressure natriuresis' contributes to the natriuresis induced by acute i.v. saline loading. Nine Beagle dogs maintained on ample sodium intake (5.5 mmol (kg body mass)⁻¹ day⁻¹) were chronically equipped with an aortic occluder to servocontrol RPP, a bladder catheter to measure renal function, and catheters for measurement of RPP and mean arterial blood pressure (MABP). A swivel system allowed free movement in the kennel during experiments. Isotonic saline loading (500 ml in 100 min) was studied as follows: with and without servocontrol of RPP, and these two protocols repeated in the presence of angiotensin-converting enzyme inhibition (ACEI, Enalapril, 2 mg (kg body mass)⁻¹). Saline loading increased MABP by about 12 mmHg and sodium excretion from about 28 μmol min⁻¹ up to about 350 μmol min⁻¹. Without ACEI, servocontrol of RPP at 10% below control 24 h MABP slightly delayed the onset of the saline-induced natriuresis, but did not reduce peak sodium excretion or cumulative sodium excretion. The slight delay most probably resulted from pressure-controlled renin release because, with ACEI, servocontrol of RPP did not delay or reduce the saline-induced natriuresis. In conclusion, pressure natriuresis does not contribute to the natriuresis following acute saline loading.     

Mechanisms of acute natriuresis in normal humans on low sodium diet

This study evaluates the relative importance of several mechanisms possibly involved in the natriuresis elicited by slow sodium loading, i.e. the renin-angiotensin-aldosterone system (RAAS), mean arterial blood pressure (MAP), glomerular filtration rate (GFR), atrial natriuretic peptide (ANP), oxytocin and nitric oxide (NO). Eight seated subjects on standardised sodium intake (30 mmol NaCl day⁻¹) received isotonic saline intravenously (NaLoading: 20 μmol Na⁺ kg⁻¹ min⁻¹ or ≈11 ml min⁻¹ for 240 min). NaLoading did not change MAP or GFR (by clearance of ⁵¹Cr-EDTA). Significant natriuresis occurred within 1 h (from 9 ± 3 to 13 ± 2 μmol min⁻¹). A 6-fold increase was found during the last hour of infusion as plasma renin activity, angiotensin II (ANGII) and aldosterone decreased markedly. Sodium excretion continued to increase after NaLoading. During NaLoading, plasma renin activity and ANGII were linearly related ( R = 0.997) as were ANGII and aldosterone ( R = 0.999). The slopes were 0.40 p m ANGII (mi.u. renin activity)⁻¹ and 22 p m aldosterone (p m ANGII)⁻¹. Plasma ANP and oxytocin remained unchanged, as did the urinary excretion rates of cGMP and NO metabolites (NO_x). In conclusion, sodium excretion may increase 7-fold without changes in MAP, GFR, plasma ANP, plasma oxytocin, and cGMP- and NO_x excretion, but concomitant with marked decreases in circulating RAAS components. The immediate renal response to sodium excess appears to be fading of ANGII-mediated tubular sodium reabsorption. Subsequently the decrease in aldosterone may become important.     

Renal sodium excretion after oral or intravenous sodium loading in sodium-deprived normotensive and spontaneously hypertensive rats

Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats that had been on a low sodium diet for 3 days were given 1.5 mmol sodium chloride kg^-1 body weight either orally or intravenously. The rats receiving an oral sodium load showed a greater natriuresis than those receiving the same saline load intravenously. No increase of renal sodium excretion was observed when the rats received a hypertonic mannitol solution orally. The cumulative sodium excretion during the 8 h following oral loading was two to three times larger in SHR than in WKY, whereas no difference between strains could be demonstrated after giving saline intravenously. Furthermore, after switching from normal to low sodium diet the rate of decrease of renal sodium excretion was greater in SHR than in WKY rats. It is proposed that there exists a gastrointestinal sensory mechanism for sodium controlling the renal sodium excretion. Furthermore, it is suggested that the function of this mechanism differs between SHR and WKY.     

Canjoint Action of Sodium and Angiotensin on Brain Mechanisms Controlling Water and Salt Balances

Andersson , B. and L. Eriksson , Conjoint action of sodium and angiotensin on brain mechanisms controlling water and salt balances. Acta physiol. scand. 1971. 81. 18–29. The effects on water and salt balances of a simultaneous infusion of angiotensin and hypertonic NaCl into the 3rd brain ventricle were studied in goats in normal water balance and in hydrated animals. For comparison similar infusions of angiotensin alone (solved in slightly hypotonic saline) and of hypertonic NaCl were made. Like the hypertonic NaCl, 30 min infusions of angiotensin alone induced drinking in animals in normal water balance, and an inhibition of the water diuresis in the hydrated goat. The simultaneous infusion of both substances resulted in a marked potentiation of the dipsogenic and the antidiuretic effects. A possible explanation may be that angiotensin facilitates the transport of Na⁺ into brain cells regulating thirst and ADH release, and that the intracellular Na⁺ concentration rather than strictly osmotic factors determines the activity of these cells. In the hydrated goat a central effect of angiotensin strongly enhanced the natriuretic response to intraventricular infusions of hypertonic NaCl, and extreme natriuresis developed as result of the combined infusions in hydrated, salt-supplemented animals. During normal water balance this sodium-angiotensin synergism was less obvious, which suggests that both an expanded fluid volume and an elevated intracellular Na⁺ concentration are needed for optimal activation of a brain mechanism which stimulates renal Na' excretion, The time course of the centrally induced natriuresis indicates that the effect on the kidney may be mediated by a humoral agent.     

Substantial effect of acute hydration on blood pressure in patients with autonomic failure

The effect of acute hydration on arterial blood pressure levels was investigated in ten patients with severe postural hypotension due to autonomic failure. Blood pressure and heart rate were determined in the supine and 60-degree head-up tilted position. Plasma volume and left ventricular ejection fraction were measured in the supine position. Measurements were repeated after rapid infusion of 11 of isotonic saline. Acute hydration resulted in increased supine mean blood pressure levels (P less than 0.01) despite normal plasma volumes in all patients. The postural reductions in mean blood pressure were reduced from 40 mmHg before to 20 mmHg after saline (median values, P less than 0.01). The results indicate that normal plasma volumes do not ensure optimal circulatory status in patients with autonomic failure. Acute hydration with isotonic saline may be used for immediate corrections of blood pressure levels in patients with autonomic failure and the response to acute hydration may be used as an indicator of the circulatory status in these patients.     

The effect of renal arterial infusion of albumin on renal function in the rat

Summary An infusion of an isotonic saline solution or of the same solution to which human serum albumin had been added in a concentration of 6 and 25% was administered into the renal artery of rats. The sodium and water excretion and the inulin and PAH clearances were not different when isotonic saline solution or 6% albumin were applied. After an infusion of 25% albumin solution a transient natriuresis and diuresis, accompanied by an increase of blood pressure, was observed. These experiments do not support the hypothesis which suggests the importance of peritubular oncotic pressure for the reabsorption of fluid and sodium in the rat renal tubules.     

Effects of experimental pain on jaw muscle activity during goal-directed jaw movements in humans

To study the effects of masseter muscle pain on jaw muscle electromyographic (EMG) activity during goal-directed tasks. Mandibular movement was tracked and EMG activity was recorded from bilateral masseter, and right posterior temporalis, anterior digastric, and inferior head of lateral pterygoid muscles in 22 asymptomatic subjects at postural jaw position, and during three tasks: (a) protrusion, (b) contralateral (left), (c) open jaw movement. Tasks were performed during three conditions: control (no infusion), test 1 [continuous infusion into right masseter of 4.5% hypertonic saline to achieve 30–60 mm pain intensity on 100-mm visual analog scale (VAS)], and test 2 (isotonic saline infusion; in 16 subjects only); the sequence of hypertonic and isotonic saline was randomized. The average EMG root-mean-square values at 0.5 mm increments of mid-incisor-point displacement were analysed using linear mixed effects model statistics (significance: P < 0.05). Right masseter hypertonic saline infusion resulted in significantly (P < 0.0005) more pain (mean ± SD VAS 47.3 ± 14.3 mm) than isotonic infusion (12.2 ± 17.3 mm). Although there was evidence of inter-subject variation, the principal EMG findings were that the significant effects of hypertonic saline-induced pain on EMG activity varied with the task in which the muscle participated irrespective of whether the muscle was an agonist or an antagonist in the tasks. The direction of the hypertonic saline-induced pain effect on EMG activity (i.e., whether the hypertonic saline-induced EMG activity was less than or greater than control EMG activity) could change with the magnitude of jaw displacement. Hypertonic saline infusion had no significant effect on postural EMG activity in any of the recorded jaw muscles. The data suggest that under constrained goal-directed tasks, the pattern of pain-induced changes in jaw muscle EMG activity is not clear cut, but can vary with the task performed, jaw displacement magnitude, and the subject being studied.     

Renal and hormonal responses to isotonic saline infusion after 3 days' head-down tilt vs. supine and seated positions

AIM: The study aimed to determine whether prolonged exposure to simulated microgravity produces a level of thoracic volume receptor loading similar to that seen in the upright position or immediately after lying down. METHODS: We used a cross-over design to compare responses to a saline infusion in eight healthy subjects during a 4-day, -6 degree head-down tilt (HDT) and in the acute seated and acute supine positions. RESULTS: The first 24 h of HDT were associated with greater urinary excretion of water and sodium (UV, UNaV) than seated and acute supine [cumulative UV, 3035 +/- 219, 2311 +/- 156 (P < 0.05), and 2448 +/- 182 mL (P < 0.05), respectively; cumulative UNaV, 256 +/- 19, 180 +/- 11 (P < 0.05), and 189 +/- 15 mmol (P < 0.05), respectively]. Haemoglobin and haematocrit were increased after 24 h and plasma volume decreased after 48 h of HDT (P < 0.05). With prolongation of HDT, UV and UNaV returned near the baseline values, and plasma atrial natriuretic factor (ANF) and renin values returned to acute seated levels; in acute supine, ANF values were higher and renin lower than in the two other positions. After a 30-min infusion of 20 mL kg(-1) isotonic saline on the fourth HDT day or during acute seated or acute supine, sodium excretion within 4 h was similar during HDT and acute seated (83 +/- 6 and 84 +/- 9 mmol, respectively) and greater during supine (104 +/- 8 mmol, P < 0.05). The renin decrease was greater in HDT and seated than in supine. The plasma ANF increase was greater during HDT than during supine; during seated, plasma ANF was unchanged. CONCLUSION: These data suggest that, after 4 days of HDT, thoracic volume receptor loading returns to the same level as in the seated position, leading to blunted responses to volume expansion as compared with the acute supine position.