Correlation between sodium and potassium excretion in 24- and 12-h urine samples

Low-sodium and high-potassium diets have been recommended as an adjunct to prevention and treatment of hypertension. Analysis of these nutrients in 24-h urine has been considered the reference method to estimate daily intake of these minerals. However, 24-h urine collection is difficult in epidemiological studies, since urine must be collected and stored in job environments. Therefore, strategies for shorter durations of urine collection at home have been proposed. We have previously reported that collecting urine during a 12-h period (overnight) is more feasible and that creatinine clearance correlated strongly with that detected in 24-h samples. In the present study, we collected urine for 24 h divided into two 12-h periods (from 7:00 am to 7:00 pm and from 7:00 pm to 7:00 am next day). A sample of 109 apparently healthy volunteers aged 30 to 74 years of both genders working in a University institution was investigated. Subjects with previous myocardial infarction, stroke, renal insufficiency, and pregnant women were not included. Significant (P < 0.001) Spearman correlation coefficients (r_s) were found between the total amount of sodium and potassium excreted in the urine collected at night and in the 24-h period (r_s = 0.76 and 0.74, respectively). Additionally, the 12-h sodium and potassium excretions (means ± SD, 95% confidence interval) corresponded to 47.3 ± 11.2%, 95%CI = 45.3-49.3, and 39.3 ± 4.6%, 95%CI = 37.3-41.3, respectively, of the 24-h excretion of these ions. Therefore, these findings support the assumption that 12-h urine collected at night can be used as a reliable tool to estimate 24-h intake/excretion of sodium and potassium.     

Effect of restricted potassium intake on its excretion and on physiological responses during heat stress

Summary The effect of low potassium (K⁺) intake on its excretion, concentration in sweat and on physiological responses during heat stress was evaluated on eight Indian male soldiers in winter months at Delhi. After a stabilization period of 3 days on each diet, i.e., 85 mEq of K⁺/d (diet I, normal), 55 mEq of K⁺/d (diet II), and 45 mEq of K⁺/d (diet III), the physiological responses and the sodium and potassium concentrations in sweat, plasma, RBC, and urine were measured when the subjects were exposed to heat for 3 h daily in a climatic chamber maintained at 40 C DB and 32 C WB. The subjects worked in the chamber at the rate of 465 W/h for 20 min periods with 40 min rest between each period of exercise. The whole body sweat was collected after the first spell of work and was analysed for sodium and potassium levels.Throughout the study the subjects remained on positive sodium balance except on day 4 in diet III. Fluid balance also remained positive while potassium balance was negative in subjects on diet II and diet III. There was no significant change in heart rate, sweat volume, oral temperature, sodium, and potassium concentrations in plasma and RBC during the entire period of the study. Even in the subjects with negative potassium balance there was no change in the sodium and potassium concentrations in sweat during exercise in heat. The only evidence of potassium conservation was a reduced excretion in urine. Out of the eight subjects, in one subject there was a flattening of the T wave in the ECG and reduction in amplitude of the T wave in two more subjects. As there is no reduction in sweat potassium concentration and the urine volume is low, the marginal level of reduced excretion of potassium in urine with a high rate of sweating (7–81) in subjects doing work in the tropics, there is every likelihood of potassium deficiency if a liberal intake is not ensured.     

Thermoregulatory adjustments during continuous heat exposure

Summary Body temperature regulation was studied in 6 male subjects during an acclimation procedure involving uninterrupted heat exposure for 5 successive days and nights in a hot dry environment (ambient temperature =35° C, dew-point temperature =7° C; air velocity = 0.2 m·s^–1). Data were obtained at rest and during exercise (relative mechanical workload =35% ). At rest, hourly measurements were made of oesophageal and 4 local skin temperatures, to allow the calculation of mean skin temperature, and of body motility and heart rate. During the working periods these measurements were made at 5 min intervals. Hourly whole-body weight loss was measured at rest on a sensitive platform scale while in the working condition just before starting and immediately after completing the bicycle exercise. The results show that, in both exercise and at rest, the successive heat exposures increased the sweat gland output during the first 3 days. Afterwards, sweat rate decreased without any corresponding change, in body temperature. For the fixed workload, the sweat rate decline was associated with a decrease in circulatory strain. Adjustments in both sweating and circulatory mechanisms occur in the first 3 days of continuous heat exposure. The overall sweat rate decline could involve a redistribution of the regional sweating rates which enhances the sweat gland activities of skin areas with maximal evaporative efficiencies.     

Effects of aldosterone on intralymphocytic sodium and potassium in patients with essential hypertension

Summary In vitro binding of aldosterone to mineralocorticoid receptors on human mononuclear leukocytes (HML) and its effects on the intracellular sodium and potassium concentrations of HML have already been described. In the present paper this easily accessible human cell model was investigated in 13 patients with essential hypertension. In only four patients sodium in HML without incubation was elevated compared with the range for normal persons. A decrease of intracellular sodium or potassium occurred during incubation without aldosterone (P<0.02). The addition of 1.4 nM aldosterone did not prevent this loss of electrolytes as observed in normal persons. Plasma renin activity and aldosterone were not correlated with the electrolyte response and were within the normal limits. The number of mineralocorticoid receptors/cell were within or close to the normal range (n=9). The independence of intracellular electrolytes from aldosterone despite a normal number of mineralocorticoid receptors may reflect an impairment of the mineralocorticoid effector mechanism in the HML of patients with essential hypertension.Abbreviations HML human mononuclear leukocytes - HEPES N-2-hydroxyethylpiperazine-N-2-ethanesulfonic acid - Tris Tris(hydroxymethyl)aminomethane     

The electrical basis for enhanced potassium secretion in rat distal colon during dietary potassium loading

Previous studies in rat distal colon provide evidence for an active absorptive process for potassium under basal conditions, and for active potassium secretion during chronic dietary potassium loading. The present studies were performed with conventional and potassium-selective microelectrodes to determine the electrical basis for the increase in transcellular (active) potassium secretion observed during potassium loading. Compared to control tissues, potassium loading resulted in a 5-fold increase in transepithelial voltage (V _T) and a 52% decrease in total resistance (R _T) in the distal colon. The rise inV _T was due to a decrease in apical membrane resistance and an increase in basolateral membrane voltage from –45±2 mV (cell interior negative) in control to –56±2 mV (P<0.001) in potassium loaded tissues. This difference in basolateral membrane voltage reflected in increase in intracellular potassium activity from 86±4 mM to 153±12 mM (P<0.001). In control tissues, the sequential mucosal addition of the sodium channel blocker amiloride (0.1 mM) and the potassium channel blocker tetraethylammonium chloride (TEA: 30 mM) produced no effect on the electrical measurements. However, in potassium loaded tissues, amiloride and TEA produced transepithelial changes consistent with inhibition of apical membrane conductances for sodium and potassium, respectively, reflected by increases in the resistance ratio, (ratio of apical to basolateral membrane resistances). These data indicate that the decrease in apical membrane resistance during potassium loading was caused by an increase in apical membrane conductance for both potassium and sodium.     

Influence of repeated passive body heating on subsequent night sleep in humans

Summary Experiments were carried out on four healthy male subjects in two separate sessions: (a) A baseline period of two consecutive nights, one spent at thermoneutrality [operative temperature (T _o)=30°C, dew-point temperature (T _dp)=7°C, air velocity (V _a)=0.2 m·s⁻¹] and the other in hot condition (T _o=35°C,T _dp=7°C,V _a=0.2 m·s⁻¹). During the day, the subjects lived in their normal housing and were engaged in their usual activities. (b) An acclimation period of seven consecutive daily heat exposures from 1400 to 1700 hours (T _o=44°C,T _dp=29°C,V _a=0.3 m·s⁻¹). During each night, the subjects slept in thermoneutral or in hot conditions. The sleep measurements were: EEG from two sites, EOG from both eyes, EMG and EKG. Esophageal and ten skin temperatures were recorded continuously during the night. In the nocturnal hot conditions, a sweat collection capsule recorded the sweat gland activity in the different sleep stages. Results showed that passive body heating had no significant effect on the sleep structure of subsequent nights at thermoneutrality. In contrast, during nights atT _o=35°C an effect of daily heat exposure was observed on sleep. During the 2nd night of the heat acclimation period, sleep was more restless and less efficient than during the baseline night. The rapid eye movement sleep duration was reduced, while the rate of transient activation phases observed in sleep stage 2 increased significantly. On the 7th night, stage 4 sleep increased (+68%) over values observed during the baseline night. The sweating adaptive mechanisms of heat acclimation persisted only in stage 4 sleep. The results indicated that body temperature rhythmicity was maintained in the heat by an increase in stage 4 sleep which reduced core temperature during the first part of the night.     

Central and peripheral contributions to control of heart rate during heat acclimation

The contributions of the autonomic nervous system and the cardiac pacing cells in the development of heat-acclimation-induced bradycardia were analyzed, and the effect of heat acclimation on the chronotropic response of the heart to heat stress (40° C) was studied. Rats were acclimated at 34° C for 0, 5, 14, 30 and 60 days. Heart rate (HR) was measured in conscious animals, using chronic subcutaneous electrodes. Sympathetic and parasympathetic influences were studied by IP administration of 0.1 and 1 mg/100 g body weight atropine and propranolol respectively, while intrinsic HR (HR_i) was measured following administration of both drugs simultaneously. The effects of carbamylcholine and norepinephrine on the beating rate of isolated rat atria were investigated to study pacemaker responsiveness to neutrotransmitters. Up to day 14 of heat acclimation, bradycardia was attained by tonic parasympathetic acceleration (18%) and temporal sympathetic withdrawal (0.8% on day 14), to compensate for the gradually augmented HR_i (2.5% and 8% on days 5 and 14, respectively). Following long-term acclimation HR_i declined below pre-acclimation rate. This was associated with resumed sympathetic activity (16% and 10% on days 30 and 60 respectively) while parasympathetic activity continued to be high (18%). Tachycardia, known to occur with severe uncontrolled body hyperthermia, was attenuated following heat acclimation by 42%. It was concluded that during the initial phase of heat acclimation bradycardia is achieved primarily by changes in autonomic influences, while following long-term acclimation, changes in the intrinsic properties of the pacing cells (HR_i) and the autonomic system both play a role.     

Renal handling of sodium and potassium during hypochloremic alkalosis in the rat

Summary Sodium and potassium excretion was evaluated by micropuncture methods in rats with experimental hypochloremic alkalosis (HA). Inulin, sodium and potassium concentrations were measured in cortical nephron segments. Split-drop half-times of isotonic saline reabsorption and transit times were measured in the proximal tubule. These data were compared with those obtained in control and 5% NaHCO₃ infused rats. GFR was reduced in HA; fluid reabsorption was not altered significantly in the proximal tubule, but was reduced with respect to controls along distal tubule and collecting duct. It was, however, greater than that found in acutely alkalotic rats. In spite of the alterations in bicarbonate concentrations and reabsorption rates found in HA, sodium reabsorption along the nephron was not significantly altered, as evaluated by TF/P Na⁺/In ratios or by the split-drop method. Fractional urinary potassium excretion and distal nephron secretion were increased inspite of low plasma potassium concentrations and absence of changes in distal PD.Extracellular volume was not significantly altered in HA rats with respect to controls. It is concluded that sodium is reabsorbed at a rate sufficient to maintain this volume, irrespective of the accompanying anion, thus maintaining volume at the cost of acid-base equilibrium.Supported by Fundação de Amparo à Pesquisa de ESP.     

Decay of heat acclimation during exercise in cold and exposure to cold environment

Sixteen male students exercised for 14 days (1 h/day) in the heat for heat acclimation (HA). During deacclimation (DA) one group exercised in the cold (EXG, n=8) for 60 min/day (morning) and was exposed to the cold for another hour (afternoon) for 14 days. The other group was exposed to the cold (EPG, n=8) for 1 h each in the morning and afternoon (Ta: 18.0°C, RH: 58%) over the same period. All returned to exercise in the heat for reacclimation (RA) for 10 days. Subjects were tested on days 1, 16, 21, 32, 36 and 44 on a bicycle ergometer for 60 min at 60% of VO_2max in the heat (Ta: 31.1°C, RH: 70%). Rectal temperature (T _re) and heart rate (HR) at 40 min of exercise were used to determine the decay/gain of HA, which was calculated using the formula described by Pandolf et al. (Ergonomics, 20:399–408, 1977). After HA (day 16) T _re and HR decreased significantly. During DA, EXG showed decay in T _re of 24 and 35% and HR of 29 and 35% on days 21 and 32, respectively. For EPG the corresponding decay was of 2 and 9% for T _re and 17 and 17% for HR. After 10 days of RA, EXG showed gains of 11% in T _re and 12% in HR, while EPG showed gains of 47% in T _re and 38% in HR. In conclusion, EXG had greater decay during DA and lower gains in RA compared to EPG. However, the differences between groups were significant only for T _re after 4 days of DA.     

The discrepancy between thermometry and calorimetry during exercise

Summary During prolonged exercise in a hot and dry environment one may observe that a man seems to maintain a caloric equilibrium for about one hour. When the man dehydrates, however, a continuous rise in rectal temperature may be observed simultaneously. This discrepancy between calorimetry and thermometry was investigated by measuring calorimetrically the body heat storage during exercise. In a series of experiments work and heat load were kept constant throughout (M=7.5 kcal/min; 35°C; RH 15%), but the exposure time was increased in steps of 18 min up to 144 min. The heat storage did not alter between the 54th and the 108th min. In the same period the rectal temperature rose steadily.This article was prepared while holding a research fellowship from the Anglo-American Corporation of South Africa.     

Plasma potassium and ventilation during incremental exercise in humans: modulation by sodium bicarbonate and substrate availability

Summary It has recently been demonstrated that, compared to normal conditions, ventilation ( ) was increased during exercise after glycogen depletion, in spite of a marked increase in plasma pH (pH_P). It was further demonstrated that in patients with McArdle's syndrome was reduced when substrate availability was improved. In the present experiments, six endurance trained men performed two successive cyclo-ergometric incremental exercise tests (tests A, B) after normal nutrition (N) and after a fatty meal in conjunction with a sodium bicarbonate (NaHCO₃) solution (F_SB) or without NaHCO₃ (F), and the relationship between , plasma potassium concentration ([K⁺]P), and pHP was checked. Plasma free fatty acid concentration ([FFA]_P) was markedly increased in the F and FSB trials (P<0.001). In F_SB pH_P was significantly increased, compared to N and F (P<0.001). In all the B tests, pH_P increased during moderate and intense exercise and in F_SB, remained alkalotic even during maximal exercise intensity. In contrast, and [K⁺]_P changes were almost equal in all the trials and in tests A and B. It was found that exercise-induced changes of and [K⁺]_P in the present experiments were not markedly affected by [FFA]_P or pH_P values and that these changes also occurred independently of changes in pHP or plasma bicarbonate concentration. The often used glycogen depletion strategy may have slightly increased but apparently did not overcompensate for a possible decrease in due to increased pH_P. The close relationship between and [K⁺]_P was not affected by acid-base or substrate changes; this would further confirm the hypothesis that K⁺ may act as a stimulus for exercise .     

Evaluation of a temperate-environment test of heat tolerance in prior heatstroke patients and controls

Summary It has been reported that scores from a temperate-environment step test describe the heat-tolerance status of prior heatstroke patients (HP). This investigation evaluated the ability of this temperate-environment heat-tolerance test (HTT) to indicate altered heart rate (HR) and rectal temperature (T _re )responses of HP, after 7 days of heat acclimation. On day 1, ten male HP (61 ± 7 days post-heatstroke) and five control subjects (C) bench-stepped (0.30 m high, 27 steps · min^–1) for 15 min (25.8° C dry bulb, 16.2° C wet bulb). On days 2–8, subjects underwent heat acclimation (40.1° C dry bulb, 23.8°C wet bulb; treadmill, 90 min · day^–1). Heat acclimation resulted in significant decreases in final HR (152±5 vs 130±3 beats·min^–1 P<0.025) and finalT _re (38.62±0.11 vs 38.13±0.07°C,p < 0.01) in HP. One HP but no C was defined heat intolerant, exhibiting inability to adapt to daily exercise in the heat. On day 9, HP repeated HTT, exactly as performed on day 1; mean group HTT scores did not change (day 1=39±6; day 9=48±6,P>0.05). All physical characteristics and physiological responses of HP (days 1, 2, 7, 9) were statistically similar (P>0.05) to those of C. In contrast to heat-acclimation data, HTT scores (score 30) indicated that four HP were heat intolerant on day 1 and two HP were heat intolerant on day 9. It was concluded that HTT was not a substitute for lengthier tests of heat tolerance conducted in hot environments, because HTT scores (at 25.8°C did not reflect HR andT _re responses (at 40.1° C) in 33% of heat-acclimated (e.g., heat-tolerant) HP. In addition, HTT scores did not validly discriminate between heat tolerant and heat-intolerant HP.     

Effects of a synthetic cationic polymer on sodium and potassium currents of frog nerve fibres

(1) Voltage-clamped nerve fibres of the frogRana esculenta were treated with the synthetic cationic polymer hexadimethrine bromide (HDM) [Polybrene]. (2) 1 M HDM irreversibly reducedI _Na to about 65% of its original size. The time to peak remained almost unaffected, while the decaying phase of the currents (for pulse potentials <–10 mV) became accelerated. The size ofI _Na was hardly reduced further even with a 1,000-fold higher concentration of HDM. (3) The cationic polymer HDM was without effect on the voltage-dependence of activation and there was only a small shift (–4.5 mV) of the voltage dependence of steadystate inactivation. (4) Variation of [Ca²⁺] in the Ringer solution shifted the voltage-dependence of activation and of steady-state inactivation to the same extent before and after treatment with HDM. By contrast, 0.5 mM La³⁺ markedly decreased the Ca²⁺-induced shifts. (5) The decrease of the size ofI _Na by increasing [Ca²⁺] was strongly reduced by HDM, as well as by the presence of La³⁺. (6) These results suggest, that HDM is bound irreversibly to Ca²⁺ and La³⁺ binding sites of the membrane that affect the size ofI _Na. These sites are different from Ca²⁺ (or La³⁺ binding sites acting on the gating mechanism. (7) The potassium currents were also irreversibly reduced by HDM-treatment. This effect, however, was different for inward and outward currents; for inward currents theI _K remaining was about 20% of its original size, while for outward currentsI _K was reduced only to about 65%. The time course of activation ofI _K was not affected by HDM-treatment. Analysis of the K⁺ tail currents revealed that HDM-treatment nearly abolished one of the two fast components ofI _K (g_Kf1) while g_Kf2 remained nearly unaffected.     

Effects of heat acclimation of distance runners in a moderately hot environment

Summary Five distance runners (H group) performed a 60 min bicycle exercise at a load of 60–70% VO_{2 max} in a moderately hot environment (T _a: 33.5 C, 60% RH). Following a period of heat acclimation with bench-stepping at a load equal to about 25–30% VO_{2 max}, in a hot environment (T _a: 45–50 C, 30–40% RH) for 9 days, the work test was repeated. Two control subjects (R) performed the same work tests with no heat acclimation. Heat acclimation increased performance time. Rectal temperature, mean skin temperature, heart rate, and Na⁺ concentrations in sweat were lower in H and, with one exception, sweat rate was higher after heat acclimation. All H subjects demonstrated that the linear relationship between sweat rate and rectal temperature was shifted to a lower temperature (threshold shift). This shift correlated with a lowering of resting rectal temperature. The magnitude of the reduction in those two temperatures due to heat acclimation was identical. The observed improvement of work performance in moderate heat following heat acclimation to a higher temperature is attributed to a more efficient thermoregulatory mechanism.     

Antidiuretic hormone and evaporative weight loss during heat stress

Summary In order to investigate the effects of vasopressin (ADH) on evaporative weight loss during heat exposure, four modifications of a single experiment were used. In all experiments the subjects (co-authors) initially ingested an amount of tap water equal to 2% of their body weight. During 3 out of 4 experiments urinary and evaporative weight loss was replenished at 15 min intervals while no further water was ingested in the 4th experiment. Following a 2 hr period at room temperature (25–27.8°C), the subjects entered the heat chamber maintained at 43–44°C D. B., 28–29°C W. B. Heat exposure for 3 experiments lasted 2 hrs, while for a 4th exposure the time lapse was 4 hrs. Vasopressin (5 units) was injected intramuscularly at the beginning of the last hour of heat exposure in two experiments wherein water replacement took place. Vasopressin injection had no apparent effect on rates of evaporative weight loss. For these experiments the effects of exercise, hypohydration and probably subject anxiety could be ruled out as influencing these results.This work was supported by N. I. H. grants 5 RO1 HE-07075 and 1K3 HE 25,110     

孕酮对脑缺血再灌注大鼠纹状体水、钠、钾及钙含量的影响

目的:孕酮(PROG)已被证明是一种"神经活性甾体",本文探讨PROG对缺血脑的神经保护作用。方法:采用大鼠局灶性脑缺血再灌注模型,测定大脑中动脉阻塞(MCAO)2h再灌注22h后纹状体水、钠、钾、钙含量。结果:①I/R和DMSO组MCAO侧纹状体的水、钠、钙明显高于、钾显著低于非MCAO侧,I/R和DMSO组之间相比无显著差异;②与I/R和DMSO组相比,PROG预防及防治组MCAO侧纹状体的水、钠、钙明显减少,钾明显增加(P＜0.01);PROG治疗组则水、钠明显减少,但钾和钙无显著差异(P＞0.05);③PROG各组与阳性对照DEXA组相比,MCAO侧纹状体水、钠、钙、钾的差别均无显著(P＞0.05)。结论:PROG可减轻脑缺血/再灌注大鼠纹状体的损伤。     

The role of extracellular sodium on heart muscle energetics

A study has been made of changing external sodium concentration [Na]_e, over the range 75 to 200 mmol · l^–1, on contractile parameters and heat production in isolated, arterially perfused, interventricular rabbit septa.-The observed changes in maximum rate of contraction with [Na]_e, either in the presence of a constant external Ca concentration [Ca]_e or in the presence of a constant [Na] _e ² /[Ca]_e ratio, paralleled those observed for tension development (T). On the other hand the maximal rate of relaxation and the ratio increased. While the ratio between active heat production and developed tension remained unaltered (0.111±0.003 mJ · mN^–1 · g^–1 dry weight), resting heat production increased with [Na] _e ² with a slope of 95±18 mW · g^–1 · mol^–2 · l². Under resting conditions, a decrease in [Na]_e of 50 mmol · l^–1 induced a fall in⁴²K uptake of about 16 nmol · s^–1 · g^–1 without changes in⁴²K efflux, suggesting that such an intervention depresses K influx. If the depressed K influx, induced by a decrease in [Na]_e of 50 mmol · l^–1 is associated with a decrease in Na–K pump activity, a fall in resting heat production of about 0.64 mW · g^–1 would be expected. This represent 56% of the calculated change in the resting heat production, 1.14±0.22 mW · g^–1 (mean ± one confidence interval), suggesting that some process in addition to a depressed Na-K pump activity may be altered by changes in [Na]_e.Supported by the Consejo Nacional de Investigaciones Cientificas y Técnicas (CONICET), Argentina     

Effect of dietary sodium content on renal handling of lithium

Previous studies have shown that the clearance of lithium (C_Li) is a quantitative measure of the delivery of tubular fluid to Henle's loop in rats given food with an ordinary or high sodium content but not in rats given food with a low sodium content, because under these circumstances lithium is also reabsorbed to some extent in the distal nephron segment. The present study examines C_Li, C_Na and urine flow in diabetes insipidus rats at various dietary sodium contents. The results showed that C_Li was 120 l/min/100 g b.w. when no distal reabsorption took place at a dietary sodium content of 300 mmol/kg. At a dietary sodium content of 5 mmol/kg the calculated distal lithium reabsorption reduced C_Li by 55 l/min/100 g b.w.; at 25 mmol/kg distal reabsorption was reduced to half this value; at 50 mmol/kg distal reabsorption was slight and barely significant, and at 75–300 mmol/kg there was no distal reabsorption of lithium. It is concluded that C_Li can be used as a quantitative measure of the delivery of tubular fluid to the loop of Henle at dietary sodium contents higher than 50–75 mmol/kg in the rat.     

Effects of calcium and sodium on contracture tension in the smooth muscle of the rat portal vein

Summary The purpose of the present study was to determine the quantitative relationship between membrane potential (or [K⁺]₀) and contracture tension in the smooth muscle of the rat portal vein, and to examine the influence of Ca⁺⁺ and Na⁺ on this relationship. However, electrical all-or-none responses were successfully abolished only in Na⁺-free sucrose-Krebs due to hyperpolarization and in K⁺-high Krebs due to depolarization. It did not seem possible to eliminate spike discharge at intermediate levels of membrane potential without the simultaneous loss of contractility. In the hyperpolarized state the muscle remained relaxed despite the very low levels of [Na⁺]₀ and despite increases in [Ca⁺⁺]₀ up to 20 mM. The depolarized portal vein developed a contracture which was intimately dependent on [Ca⁺⁺]₀, the threshold concentration being of the order of 0.1 to 0.3 mM. Spike-induced, phasic contractions showed a similar Ca⁺⁺-dependence. Variations in [Na⁺]₀ had only a slight and irregular influence on the Ca⁺⁺ dose-response curve of the depolarized muscles.Differences in the effects of Na⁺ on the rate of rise and the rate of fall of the contracture tension, respectively, suggested that Na⁺ is more important for the removal of Ca⁺⁺ from the contractile system than for the supply of Ca⁺⁺ to the system. With regard to the interaction of Ca⁺⁺ and Na⁺ in the excitation-contraction coupling the vascular smooth muscle seemed to differ from both heart muscle and skeletal muscle.The present study was supported by grants from the Swedish Medical Research Council (B 70-14x-28-06 A), from Air Force Office of Scientific Research through the European Office of Aerospace Research, OAR, United States Air Force under Contract F 1052-68-C-0044, from U.S. Public Health Service (HE-05678-08), from AB Hässle, Göteborg, and from the Deutsche Forschungsgemeinschaft (Bi 122/1).     

The topography of eccrine sweating in humans during exercise

The purpose of this study was to investigate the distribution of steady-state sweating rates (m _sw), during stressful exercise and heat exposures. Six men completed 42-min trials: 2-min rest and 40-min cycling at 40% peak power in 36.6° C (relative humidity 46.0%). The m _sw, was monitored using ventilated capsules at the forehead, and at three additional sites. Repeat trials allowed monitoring from eleven skin surfaces. Auditory canal temperature (T_ac) and 11 skin temperatures were measured. After normalising m _sw to the forehead response within subjects, differences in T _ac and onset time thresholds, and transient and steady-state m _sw were examined. The pooled, lower torso m _sw onset [mean 45.5 (SEM 42.0) s] preceded that of the head [mean 126.5 (SEM 34.8) s, P<0.05], but was not significantly different from the legs [mean 66.6 (SEM 25.7) s], upper torso [mean 80.2 (SEM 36.8) s] or arms [mean 108.6 (SEM 31.2) s]. Transient m _sw did not differ among regions (P=0.16). Mean, steady-state forehead m _sw [3.20 (SEM 0.51) mg · cm^–2 · min^–1]was not significantly greater than the scapula, forearm, hand, stomach and lower back m _sw (in descending order), but was greater than the chest [1.6 (SEM 0.2)], upperarm [1.6 (SEM 0.2)], calf [1.5 (SEM 0.3)] and thigh m _sw [1.0 (SEM 0.2), P<0.05 for all comparisons]. The results did not support the caudal-to-rostral sweat onset evident during supine, resting heat stress. Equivalent T _ac sweat thresholds existed between sites, while steady-state m _sw topography varied among subjects and was not dominated by central regions.