Erythrocyte cations and Na+,K+-ATPase pump activity in athletes and sedentary subjects

Summary The chronic effect of training on intraerythrocyte cationic concentrations and on red cell Na⁺,K⁺-ATPase pump activity was studied by comparing well-trained athletes with sedentary subjects at rest. Also the acute effect of a 50-min cross-country run on these erythrocyte measurements was studied in the athletes. At rest the intraerythrocyte potassium concentration was increased (P<0.01) in the athletes compared to that of the control subjects. The intraerythrocyte concentrations of sodium and magnesium and red cell Na⁺, K⁺-ATPase pump activity were, however, similar in the trained and the untrained subjects.As compared with the resting condition, the intraerythrocyte potassium concentration was decreased (P<0.05) after exercise in the athletes, and this was accompanied by a minor increase in the intraerythrocyte sodium concentration. Red cell Na⁺,K⁺-ATPase pump activity was slightly increased (P<0.05) after exercise.     

Effects of Lanthanum on Pinocytosis Induced by Cations in Amoeba proteus

Lanthanum chloride (≥ 10^-5 M) induced pinocytosis in normal and at ≥10^-4 M in Ca⁺⁺-deficient amoeba. With respect to the Ca⁺⁺-requirement of the pinocytotic response low and high concentrations of La⁺⁺⁺ had effects like Na⁺ and K.⁺, respectively. The concentration of La⁺⁺⁺ and the concentration and species of inducing monovalent cation determined whether La⁺⁺⁺ stimulated or inhibited other types of pinocytosis. Thus all concentrations of La⁺⁺⁺ inhibited sodium induced pinocytosis while high concentrations (> 10^-3 M) stimulated and low concentrations diminished potassium induced pinocytosis. Only the latter effect required the presence of Ca⁺⁺. In the presence of La⁺⁺⁺ other inducers acted either like K⁺ or Na⁺. Inducers may cause channel formation by opening a pore for Ca⁺⁺ in the plasma membrane, Na⁺-like inducers being less effective than K⁺-like inducers, and by releasing Ca⁺⁺ into the cytoplasm from the glycocalyx (Na⁺-like inducers) or from the entire cell membrane (K⁺-like inducers). La⁺⁺⁺ may diminish the effect of Na⁺-like inducers and vice versa by direct competition for sites in the glycocalyx and the effect of K⁺-like inducers by redistribution of Ca⁺⁺ in the cell surface. At high concentrations or in the presence of a K⁺-like inducer La⁺⁺⁺ may enter the Ca⁺⁺ pore, release Ca⁺⁺ from the interior of the membrane and so induce or stimulate pinocytosis.     

Effect of acetyl choline on ion transport in sheep tracheal epithelium

The action of acetylcholine (ACh) on sheep tracheal epithelium has been investigated. ACh increases transiently the short-circuit current (I_SC). The same response is obtained in tissues in which the apical membrane has been permeabilized with amphotericin B in the presence of a potassium gradient. Microelectrode studies show that the majority of tracheal epithelial cells depolarize as the apical fractional resistance decreases on application of ACh. These results, together with the finding that bumetanide decreases the initial ACh-induced I_SC increase, are consistent with an initial activation by ACh of apical Cl^– channels and basolateral K⁺ channels. Following the initial increase, I_SC declines to values lower than in control conditions both in untreated and in amphotericin-permeabilized tissues, suggesting that the basolateral K⁺ conductance falls during this phase. The late decrease in I_SC induced by ACh is significantly reduced in tissues pretreated with amiloride, suggesting that the apical Na⁺ channels are also involved in this response. ACh abolishes the net Na⁺ absorption by decreasing the mucosal to serosal Na⁺ flux. This effect is possibly a result of a down-regulation of apical Na⁺ channels and basolateral K⁺ channels.     

Effects of dietary sodium on body and muscle potassium content during heat acclimation

Summary It has been suggested that renal conversion of sodium (Na⁺) during training in hot environments results in potassium (K⁺) deficiencies. This investigation examined the influence of two levels of dietary Na⁺ intake (399 vs 98 mmol · d⁻¹) on intramuscular, urinary, sweat, and whole body K⁺ homeostasis. Nine unacclimated, untrained males underwent heat acclimation during two 8 day dietary-exercise regimens (40.1±0.1‡ C, 23.5±0.4%RH). Both diets resulted in depressed urinary K⁺ excretion. Sweat K⁺ and muscle K⁺ concentrations were not altered by diets or acclimation. The whole body stores of Na⁺ increased 31.1% (+ 916.8 mmol) during the high Na⁺ diet and decreased 7.8% (−230.4 mmol) during the low Na⁺ diet; whole body stores of K⁺ increased 4.1% (+ 137.6 mmol) during the high Na⁺ diet and increased 3.4% (+ 113.6 mmol) during the low Na⁺ diet. This dietary-acclimation protocol did not result in whole-body or intramuscular K⁺ deficits and offers no evidence to support previous claims that dietary sodium levels affect K⁺ balance.     

Expression of a renal Na+-nucleoside cotransport system (N2) in Xenopus laevis oocytes

Xenopus laevis oocytes have been used for the expression of a renal, pyrimidine-selective, Na⁺-nucleoside cotransporter (N2). As compared to its uptake in water-injected oocytes, Na⁺-dependent thymidine uptake was enhanced in a time- and dose- dependent manner in oocytes injected with rat renal cortex total poly(A)⁺ RNA. An increased uptake was also observed after injection of size fractionated rat renal cortex poly(A)⁺ RNA (2–3 kb). Consistent with the selectivity of the N2 nucleoside transporter, cytidine significantly inhibited Na⁺-dependent thymidine uptake in oocytes injected with total poly(A)⁺ RNA whereas guanosine and formycin B did not. Na⁺-dependent thymidine uptake was also enhanced in oocytes injected with size fractionated human renal cortex poly(A)⁺ RNA (2–3 kb). The above data demonstrate functional expression of renal cortex, Na⁺-nucleoside cotransporters in Xenopus laevis oocytes.     

Intracellular sodium modulates the state of protein kinase C phosphorylation of rat proximal tubule Na+,K+‐ATPase

The natriuretic hormone dopamine and the antinatriuretic hormone noradrenaline, acting on α‐adrenergic receptors, have been shown to bidirectionally modulate the activity of renal tubular Na⁺,K⁺‐adenosine triphosphate (ATPase). Here we have examined whether intracellular sodium concentration influences the effects of these bidirectional forces on the state of phosphorylation of Na⁺,K⁺‐ATPase. Proximal tubules dissected from rat kidney were incubated with dopamine or the α‐adrenergic agonist, oxymetazoline, and transiently permeabilized in a medium where sodium concentration ranged between 5 and 70 mM . The variations of sodium concentration in the medium had a proportional effect on intracellular sodium. Dopamine and protein kinase C (PKC) phosphorylate the catalytic subunit of rat Na⁺,K⁺‐ATPase on the Ser23 residue. The level of PKC induced Na⁺,K⁺‐ATPase phosphorylation was determined using an antibody that only recognizes Na⁺,K⁺‐ATPase, which is not phosphorylated on its PKC site. Under basal conditions Na⁺,K⁺‐ATPase was predominantly in its phosphorylated state. When intracellular sodium was increased, Na⁺,K⁺‐ATPase was predominantly in its dephosphorylated state. Phosphorylation of Na⁺,K⁺‐ATPase by dopamine was most pronounced when intracellular sodium was high, and dephosphorylation by oxymetazoline was most pronounced when intracellular sodium was low. The oxymetazoline effect was mimicked by the calcium ionophore A23187. An inhibitor of the calcium‐dependent protein phosphatase, calcineurin, increased the state of Na⁺,K⁺‐ATPase phosphorylation. The results imply that phosphorylation of renal Na⁺,K⁺‐ATPase activity is modulated by the level of intracellular sodium and that this effect involves PKC and calcium signalling pathways. The findings may have implication for the regulation of salt excretion and sodium homeostasis.     

Characterization of ouabain-induced noradrenaline and acetylcholine release from in situ cardiac autonomic nerve endings

Aim: Although ouabain modulates autonomic nerve ending function, it is uncertain whether ouabain‐induced releasing mechanism differs between in vivo sympathetic and parasympathetic nerve endings. Using cardiac dialysis, we examined how ouabain induces neurotransmitter release from autonomic nerve ending. Methods: Dialysis probe was implanted in left ventricle, and dialysate noradrenaline (NA) or acetylcholine (ACh) levels in the anaesthetized cats were measured as indices of neurotransmitter release from post‐ganglionic autonomic nerve endings. Results: Locally applied ouabain (100 μm ) increased in dialysate NA or ACh levels. The ouabain‐induced increases in NA levels remained unaffected by cardiac sympathetic denervation and tetrodotoxin (Na⁺ channel blocker, TTX), but the ouabain‐induced increases in ACh levels were attenuated by TTX. The ouabain‐induced increases in NA levels were suppressed by pretreatment with desipramine (NA transport blocker) and augmented by reserpine (vesicle NA transport blocker). In contrast, the ouabain‐induced increases in ACh levels remained unaffected by pretreatment with hemicholinium‐3 (choline transport blocker) but suppressed by vesamicol (vesicle ACh transport blocker). The ouabain‐induced increases in NA levels were suppressed by pretreatment with ω‐conotoxin GVIA (N‐type Ca²⁺ channel blocker), verapamil (L‐type Ca²⁺ channel blocker) and TMB‐8 (intracellular Ca²⁺ antagonist). The ouabain‐induced increases in ACh levels were suppressed by pretreatment with ω‐conotoxin MVIIC (P/Q‐type Ca²⁺ channel blocker), and TMB‐8. Conclusions: Ouabain‐induced NA release is attributable to the mechanisms of regional exocytosis and/or carrier‐mediated outward transport of NA, from stored NA vesicle and/or axoplasma, respectively, while the ouabain‐induced ACh release is attributable to the mechanism of exocytosis, which is triggered by regional depolarization. At both sympathetic and parasympathetic nerve endings, the regional exocytosis is because of opening of calcium channels and intracellular calcium mobilization.     

Microdialysis studies on cortical noradrenaline release: basic characteristics, significance of extracellular calcium and massive post-mortem increase

Extracellular noradrenaline was measured on-line in the cerebral cortex of the freely moving rat by microdialysis coupled to high performance liquid chromatography and electrochemical detection. High potassium concentrations in the perfusion fluid led to a strong increase, whereas tetrodotoxin led to almost undetectable levels of noradrenaline. This shows that noradrenaline in the dialysate was directly derived from active neuronal release. Noradrenaline levels were sensitive to calcium concentrations in the perfusion fluid: from 10% in calcium-free medium to 200% for 10 mM calcium. An overdose of anesthetic caused a 60-fold increase of noradrenaline post-mortem.     

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.     

Local administration of l-DOPA in the chicken ventromedial hypothalamus increases dopamine release in a dose-dependent manner

l-DOPA induced extracellular dopamine (DA), norepinephrine (NE) and serotonin (5-HT) in the ventromedial hypothalamus (VMH) of chickens were measured by in vivo microdialysis. Several doses of 3,4-dihydroxy-l-phenylalanine (l-DOPA) were administered locally through the microdialysis probe into the VMH of chickens for 10 min. Local perfusion of l-DOPA increased the extracellular levels of DA. The increased DA was dose-related and was significantly higher compared to the baseline and control group. The maximal level of DA was 212% and 254%, respectively, of the baseline following administration of 1 and 2 μg/ml l-DOPA. There were no changes in NE and 5-HT levels from baseline after l-DOPA perfusion. l-DOPA (1 μg/ml) was mixed with Ca²⁺-free Ringer, tetrodotoxin (TTX) (2 μM) and high K⁺ and was perfused for 30 min into the chicken VMH. TTX and Ca²⁺-free Ringer's solution inhibited the effectiveness of l-DOPA in increasing DA release. The NE and 5-HT levels were significantly lower than the baseline. After administration of K⁺ a significant increase of DA, NE and 5-HT was observed. The microdialysis results are consistent with our objective that l-DOPA induced extracellular DA increases in the VMH in a dose-dependent manner and the released DA, NE and 5-HT within the dialysate were related to neuronal activity.     

Effects of temperature,ouabain and diuretics on the cell sodium and potassium contents of isolated rat kidney tubules

Cell Na⁺ and K⁺ contents were measured by flame photometry in single pieces of rat medullary thick ascending limb (MAL) and medullary collecting tubules (MCT) after an overnight incubation at various temperatures. Below 8°C, MCT samples were no more able to sustain high-K⁺, low-Na⁺ cell concentrations, and sodium progressively replaced cell potassium as the temperature decreased. The loss of potassium and the accompanying accumulation of sodium by MCT cells occurred at lower or higher temperature when amiloride (20 mol/l) or ouabain (1 mmol/l) was present respectively in the incubation medium compared to that observed on control non-treated MCT. In contrast, MAL samples maintained normal cation gradients across their membrane at all temperatures, including 0°C, even in the presence of ouabain. However, MAL cells lost nearly all their potassium which was replaced by sodium when they were incubated in K⁺-free solution. These Na⁺-loaded, K⁺-depleted MAL cells restored high-K⁺ and low-Na⁺ contents similar to those of control samples when they were further incubated for 1 h at 0°C in presence of 5 mmol/l external potassium. Even in the presence of 1 mmol/l ouabain and at 0°C, a restoration of almost normal cation gradients occured provided that Na⁺-loaded MAL were incubated for 24 h after potassium addition to the external medium. The results are discussed in relation to the respective effects of low temperatures on the passive and active components of the cation balance in the cells of the two nephron segments.     

Changes in extracellular potassium and calcium in rat cerebellar cortex related to local inhibition of the sodium pump

Extracellular K⁺, Ca²⁺, and Na⁺ ([K⁺]_e, [Ca²⁺]_e, [Na⁺]_e) were recorded with ion selective microelectrodes in the cerebellar cortex of urethane-anesthetized rats. Superfusion of the cerebellum with artificial cerebrospinal fluid containing K-strophanthidin (10^–6–10^–4 mol/l) or other cardioactive steroids, known to be inhibitors of the sodium/potassium pump, had the following effects: elevation of resting [K⁺]₃, reduction of poststimulus K⁺-undershoots, decrease of resting [Ca²⁺]_e and [Na⁺]_e. For instance, at 3×10^–5 mol/l K-strophanthidin within the superfusion solution (the unknown intracerebellar concentration being certainly much smaller), [K⁺]_e was elevated up to 130% and [Ca²⁺]_e reduced to 70% of their resting values. Iontophoretic K⁺-pulses were enhanced in amplitude at the same time. Control experiments with iontophoretic TMA application demonstrated that the glycoside effects were not due (or in higher concentrations only partly due) to shrinkage of the extracellular fluid volume. When tetrodotoxin (10^–7 mol/l) or Mn²⁺ (1–3 mmol/l) were additionally superfused, K-strophanthidin effects were qualitatively similar, though quantitatively smaller. This indicates that part of the effects were indirect via neuronal activity evoked by the blockade of the sodium pump. The experiments show that reduction of sodium pump activity in cerebellar cortex has rapid and serious consequences on the distribution of potassium and calcium in the extracellular space, resulting in an alteration of neuronal circuit excitability.     

Ionic mechanisms of alpha-autoinhibition of [3H]noradrenaline secretion in guinea-pig vas deferens: possible role of extracellular sodium

Guinea-pig isolated vas deferens, in which the neuronal transmitter stores were labelled by preincubation with [³H](?)-noradrenaline was used to study ionic mechanisms of α-autoinhibition of the secretion of [³H]noradrenaline evoked by transmural electrical stimulation or by depolarizing concentrations of K⁺. Replacement of Na⁺ in the medium markedly enhanced K⁺-evoked secretion, and thus probably improved depolarization-secretion coupling. It had a dual effect on the tetrodotoxinsensitive electrically-evoked secretion: at sufficiently low Na⁺ levels the secretory response was severely depressed, presumably because of failure of impulses to invade the varicosities. At intermediate Na⁺ concentrations the secretory response was greater than at normal Na⁺ levels. It is concluded that extracellular Na⁺ depresses depolarization-secretion coupling in invaded varicosities. The depressing effect of extracellular Na⁺ did not appear to be due to lowering of the affinity of the secretory mechanism for external Ca²⁺. The inhibitory effect of exogenous or endogenous noradrenaline, or of prostaglandin E₂, on electrically or K⁺-evoked secretion, was reduced or abolished at low concentrations of Na⁺.It is suggested that the α-adrenoceptor mediated inhibition of depolarization-secretion coupling might involve the same mechanism by which extracellular sodium ions inhibit the secretion of noradrenaline.     

Haemolymph ionic concentration in freshwater gastropods: A comparative study

Haeomolymph ionic concentrations were determined in three freshwater gastropods, Indoplanorbis exustus (Deshayes), Lymnaea acuminata (Lamarck) f. rufescens (Gray), and Pila virens (Lamarck). The influence of age (shell size) on the haemolymph concentrations of Na⁺, K⁺, Ca²⁺ and Cl^–, as well as haemolymph osmolality was studied in groups of small, intermediate and large-sized snails of the three species. Sodium -and chloride were found to be the dominant ions in all the three species. In I. exustus and L. acuminata f. rufescens the concentrations of Na⁺ and K⁺ ions showed progressive decrease with increase in shell size. In I. exustus calcium concentration was higher in the small size-group snails whereas in L. acuminata f. rufescens it was in the large size-group snails. In P. virens also sodium, potassium and calcium ions showed age-dependent variations in concentration, sodium and calcium concentrations being higher in the large size-group snails, and potassium being higher in the small size-group snails. There was no statistically significant difference in haemolymph concentration of chloride, as in the osmolality among the three sizegroup snails of the three species.     

Inhibition of transcellular NaCI reabsorption in dog kidneys during hypercalcemia

Reduced concentrating and diluting capacity of the kidney in acute and chronic hypercalcemia may partly be due to inhibition of transcellular sodium reabsorption (R_Na) in the thick ascending limb of Henle's loop. To examine this hypothesis, local heat production and R_Na were measured during normo-and hypercalcemia at comparable glomerular filtration rate (GFR) in volume expanded, anesthetized dogs. Changes in proximal R_Na which might occur during CaCl₂ infusion, were minimized by infusing acetazolamide (75 mg/kg body wt iv). When ultrafiltrable calcium was increased from 1.12±0.09 to 2.95±0.10 mmol/1, cortical heat production was unchanged, whereas outer medullary heat production fell by 32±4%. R_Na was reduced by 32±6%. Bicarbonate reabsorption did not change but calcium reabsorption and potassium excretion increased significantly. The potassium content of cortex and outer medulla increased during hypercalcemia, whereas ouabain, an inhibitor of Na⁺ K⁺-ATPase reduces the potassium content. We conclude that hypercalcemia does not inhibit transcellular R_Na in the diluting segment by a direct effect on the Na⁺ K⁺-ATPase or the mitochondria, but by interfering with the coupled NaCI transport across the luminal cell membrane.     

Regulation of voltage-gated sodium current by endogenous Src family kinases in cochlear spiral ganglion neurons in culture

Voltage-gated sodium (Na⁺) and potassium (K⁺) channels have been found to be regulated by Src family kinases (SFKs). However, how these channels are regulated by SFKs in cochlear spiral ganglion neurons (SGNs) remains unknown. Here, we report that altering the activity of endogenous SFKs modulated voltage-gated Na⁺, but not K⁺, currents recorded in embryonic SGNs in culture. Voltage-gated Na⁺ current was suppressed by inhibition of endogenous SFKs or just Src and potentiated by the activation of these enzymes. Detailed investigations showed that under basal conditions, SFK inhibitor application did not significantly affect the voltage-dependent activation, but shifted the steady-state inactivation curves of Na⁺ currents and delayed the recovery of Na⁺ currents from inactivation. Application of Src specific inhibitor, Src40–58, not only shifted the inactivation curve but also delayed the recovery of Na⁺ currents and moved the voltage-dependent activation curve towards the left. The pre-inhibition of SFKs occluded all the effects induced by Src40–58 application, except the left shift of the activation curve. The activation of SFKs did not change either steady-state inactivation or recovery of Na⁺ currents, but caused the left shift of the activation curve. SFK inhibitor application effectively prevented all the effects induced by SFK activation, suggesting that both the voltage-dependent activation and steady-state inactivation of Na⁺ current are subjects of SFK regulation. The different effects induced by activation versus inhibition of SFKs implied that under basal conditions, endogenously active and inactive SFKs might be differentially involved in the regulation of voltage-gated Na⁺ channels in SGNs.     

The effect of sodium ions on the light-induced86Rb release from the isolated crayfish retina

The effect of low external Na⁺ concentrations on the light-induced K⁺ release from crayfish photoreceptor cells was tested by labelling intracellular K⁺ with the isotope⁸⁶Rb. The amount of isotope released per light stimulus is roughly proportional to the external Na⁺ concentration if the osmolarity is kept constant by replacing Na⁺ with Tris, choline or sucrose. When sucrose is used to replace the depleted Na⁺ the light-induced K⁺ release is a linear function of the external Na⁺ concentration and is reduced by approx. 95% at an external Na⁺ concentration of 5 mmol/l. For choline and Tris substitutions the relationships are less clear but at Na⁺ concentrations 56 mmol/l it seems that in comparison with sucrose the light-induced K⁺ release is smaller in a Tris solution and larger in a choline solution. It is suggested that the light-induced K⁺ release is due mainly to an activation of voltage sensitive K⁺ channels.     

Ionic regulation of human basophil releasability. II. Non-releasing basophils are converted into releasing basophils in a low-Na+ medium

The effects of different extracellular Na⁺ and CV²⁺ concentrations on histamine release from human basophils were investigated. Isosmotic replacement of extracellular Na ⁺ either with choline ⁺, a non-permeant Na ⁺ analogue, or glucose significantly increased spontaneous and anti-IgE-induced histamine release. Basophils from 12 of 49 normal subjects, which were found not to release histamine upon challenge with an optimal dose of anti-IgE in a 135 mM NaCl buffer, were converted into releasing basophils when stimulation with anti-IgE was performed in a low-Na⁺ medium. The increase in Na ⁺ concentration in the extracellular medium was accompanied by a reduction in the magnitude of basophil response to anti-IgE, which was significantly more pronounced in non-releasers than in releasers (per cent inhibition by 70 mM NaCl 75.5 + 3.2 vs 43.5 + 9.0, P < 0.01). At higher Na⁺ concentrations a progressive and almost complete abrogation of histamine release was observed in non-releasers, but not in releasers (maximal per cent inhibition at 140 mM NaCl 97.3+1.3 vs 50.4 + 8.6). The Na⁺/H⁺ exchanger monensin had a dose-dependent inhibitory effect on anti-IgE-induced histamine release, and the concentration inhibiting 50% of histamine release was l.5 × 10^?7M. When basophils were challenged in the presence of different Na⁺ and C²⁺ concentrations, it was shown that the two cations have antagonistic effects, which is to say that they down-regulate and upregulate histamine release, respectively. Moreover, the requirement of extracellular Ca²⁺ was lowered in a low-Na⁺ medium. These results suggest that Na⁺ and Ca⁺ ions contribute with opposite effects to the modulation of basophil response to anti-IgE and that non-releasing basophils are converted into releasing basophils in a low-Na ⁺ medium.     

Regional difference in lipolysis caused by a β-adrenergic agonist as determined by the microdialysis technique

We have investigated the difference in lipolysis caused by a β-adrenergic agent between visceral and abdominal subcutaneous adipose tissues in vivo. Glycerol levels (lipolysis index) were continuously monitored in mesenteric and abdominal subcutaneous adipose tissues of anaesthetized Wistar rats using the microdialysis technique. During microdialysis, increasing concentrations of the lipolytic agent, isoproterenol (10^?8, 10^?7, 10^?6, 10^?5 mol L^?1), were added to the perfusion. Glycerol concentrations in dialysate at each isoproterenol concentration, blood glucose concentrations during the experiment, and plasma insulin concentrations before and immediately after the experiment were measured. The effect of isoproterenol on local blood flow was investigated using the ethanol technique. The clearance rate of ethanol from the perfusion medium was used as the index of local blood flow. There was no significant change in blood glucose or plasma insulin concentrations during the study. Glycerol levels in dialysate were significantly higher in mesenteric than in abdominal subcutaneous adipose tissues at all isoproterenol concentrations. The percentage change of baseline ethanol ratio was not altered by increasing isoproterenol concentrations in both mesenteric and subcutaneous adipose tissues. There was also no significant difference in percentage change of the baseline ethanol ratio between mesenteric and abdominal subcutaneous adipose tissues. These results suggest that mesenteric adipose tissue is characterized by an even higher β-adrenergic agonist-induced lipolysis than abdominal subcutaneous adipose tissue.