Skin vessels of the human finger and toe can constrict in response to local skin heating. This vascular response is, therefore, not confined only to the skin of animals, such as the sheep's leg, rat's tail, rabbit's ear, and kangaroo's tail. The target of this response appears to be arteriovenous anastomoses of the glabrous side of hand and foot. This "heat-induced" vasoconstriction appears to retard heat input from hot exterior environment.

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In order to evaluate the role of glucagon in brown adipose tissue (BAT) function under cold or stress, the changes in immunoreactive glucagon of BAT and plasma as well as uptake and metabolism of radioactive glucagon (¹²⁵I-G) in this tissue were studied in rats. Glucagon per g fresh tissue was higher in the dorso-cervical BAT than in the interscapular BAT. In warm controls (WC), acute cold exposure (-5°C, 15min) (CE) or stress (immobilization, 30min) (AS) elevated glucagon of both sites of BAT as well as plasma. In cold-acclimated animals (CA), the resting levels of BAT glucagon, but not plasma glucagon, were higher than WC. CE caused elevation of plasma glucagon, but not BAT glucagon in CA. AS did not affect glucagon levels in both plasma and BAT in CA. Cold acclimation did not influence ¹²⁵I-G uptake by BAT, but resulted in a rather lower ¹²⁵I-G level in plasma and liver. The present results suggest that BAT is a target tissue for glucagon to cause nonshivering thermogenesis in response to cold or stress and that turnover of glucagon is enhanced by cold acclimation.

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Effects of cold acclimation and cold exposure for 25 generations on triglyceride (TG)-, total phospholipid (PL)-, and cardiolipin (CL)-fatty acid (FA) compositions were studied in the different types of skeletal muscles (red and white muscles from quadriceps, and soleus) as well as brown adipose tissue (BAT) in rats. TG: in cold-acclimated rats (CA) and rats reared in cold for 25 generations (25G) white muscle showed the decreased saturated FA (SA) and increased polyunsaturated FA (PU). In soleus of 25G, monounsaturated FA (MU) and PU increased, and SA decreased. In BAT, SA increased and MU decreased in CA, and SA and PU decreased, and MU increased in 25G. PL: in red muscle of CA, SA increased and PU decreased. In red muscle of 25G the similar but more marked changes were found accompanied by lowered arachidonic acid and unsaturation index (UI). In BAT, SA, PU, arachidonic acid, and UI increased in CA, and arachidonic acid increased in 25G. CL: in red and white muscles of 25G, oleic acid and MU increased. In BAT, arachidonic acid increased in CA and 25G, and UI increased in 25G. These results suggest that FA unsaturation of CL in the muscles as well as BAT is involved in an enhanced thermogenesis in cold-exposed rats.

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We measured changes in membrane potential (MP), extra- and intracellular potassium and intracellular sodium ion activities (a^o_K, aⁱ_K, and aⁱ_Na) in papillary muscle of the guinea-pig heart induced by repetitive stimulation at various frequencies and periods in vitro, using double-barrelled ion-selective microelectrodes. Stimulation (2-4Hz) depolarized the cells, and termination of stimulation induced hyperpolarization. The aⁱ_K and aⁱ_Na (stimulated at 0.20Hz) were 92.3±4.6 and 7.8±2.0mM (mean±S.D.), respectively. Prolongation of the stimulation period (0.5-2min) increased aⁱ_Na time-dependently, but there was no further increase by stimulation for longer than 3min. The increase in aⁱ_Na was dependent on stimulus frequency. After termination of the stimulation, aⁱ_Na declined exponentially. aⁱ_K slightly decreased by the stimulation (3-4Hz). a^o_K increased during the stimulation period, and decreased below the initial level after termination of the stimulation. Results suggest that in guinea-pig papillary muscle, the. contribution of an electrogenic component of Na-K pump to the hyperpolarization after stimulation would be small, since the hyperpolarization could be explained mostly by depletion of a^o_K induced by Na-K pump activity.

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A small tonic contraction could be evoked by 3mM adenosine triphosphate (ATP) in the longitudinal muscle of pregnant rat myometrium which was incubated with the Ca-, Mg-free solution containing 2mM EGTA (40mM K). The amplitude of the tonic contraction was decreased by exposure to the solution within a few hours, but was again increased when 1-10mM Mg was added to the Ca-free solution. The ATP-induced contraction was increased for more than 7h during exposure to the Ca- free solution containing Mg ions. The ATP-induced contraction in the Ca- free (Mg-free) solution was also produced when the solution contained 1mM Mn or 1.5mM La. On the other hand, the tonic contraction evoked by 1mM Ca or Ba in the presence of 40mM K was depressed by ATP. The above results led us to propose that the ATP-induced contraction evoked in the Ca-free solution containing Mg was mediated by a process independent of Ca, and possibly mediated by a translocation of Mg in the cell. La and Mn could take the place of Mg in producing a tonic contraction caused by ATP application.

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Eighty-four healthy asymptomatic sedentary smokers and 92 healthy sedentary non-smokers of the age range 20-59 years were investigated for their maximum oxygen uptake capacity (V_O2max) and related cardiorespiratory parameters at the level of maximal exercise by bicycle ergometry. The subjects were blocked into four age decades of 20-29, 30-39, 40-49, and 50-59 years to show the effect of smoking on V_O2max of smokes of different age groups. The physical characteristics of smokers and non-smokers of comparable age groups did not show any significant difference. The smokers of each subsequent age group consumed 5.9±4.1, 6.3±5.7, 12.7±7.1, and 11.5±9.1 pack years of cigarettes, respectively (pack year=number of packets of cigarettes per day ×number of years of smoking). VO2max of smokers (38.9±4.6 ml•kg^-1•min^-1) was significantly lower (p<0.05) than that of nonsmokers (42.1±3.2ml•kg^-1•min^-1) only in the young age group of 20-29 years. V_O2max expressed in per kg of the body weight (V_O2max/BW) was found to be significantly (p<0.01) and negatively correlated with number of cigarettes smoked per day (-0.36, p<0.01), number of years through which smoked (-0.38, p<0.01), and pack years (-0.42, p<0.01). In other age groups, though non-smokers predominated over smokers in V_O2max, the differences were not statistically significant. Also, in these age groups, smoking histories failed to reveal any significant correlation with V_O2max. This suggests that smoking impairs V_O2max only in the young ages. By increasing age, V_O2max was diminished by 13% from 20 to 59years in non-smokers and 15.5% from 20 to 59years in smokers. Age also diminished HRmax and VEmax of smokers in the same manner as in the case of non-smokers. The V_O2max of Indian sedentary non-smokers was found to be lower than those of Caucasians, Kurds, Yemenites, Europeans, and Africans. Values reported on Asians were found to be comparable with those of the present study.

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Electrical activity was recorded intracellularly from the uterine longitudinal muscle of estrogen-treated rat. Membrane potential was -59mV. Action potential consisted of initial spike and the following plateau potential on which repetitive spike discharge rode. Tetracaine (0.1, 0.2mM) reduced the maximum rates of rise and fall of initial spike and increased the duration of plateau potential. Sustained depolarization at -33mV was produced by the application of 0.8mM tetracaine. The membrane depolarization was accompanied with the increase in membrane resistance. Reduction of initial spike by tetracaine in the maximum rates of rise and fall was prevented by increasing the external Ca concentration and accelerated by decreasing it. In low K (1.2mM) or isoprenaline (10^-8M)-containing solution, tetracaine-induced prolongation of plateau potential was inhibited. Plateau potential was reduced in amplitude and was prolonged only slightly by tetracaine in low Na solution (sucrose substitution). Both the initial spike and plateau potentials were blocked completely by 0.2mM tetracaine in the presence of Mn (0.5mM) or verapamil (0.5μM). It is speculated that tetracaine suppresses the K conductances responsible for resting membrane potential and the repolarizations of spike and plateau potentials. Ca influx during the generation of action potential is also supposed to be inhibited by tetracaine.

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Using the radioimmunoassay technique, we studied androgenic regulations of proteinase F in the submandibular salivary glands (SMG) of various mouse strains (ICR, BALB/CA, C3H/HeN, C57BL/10N, and DBA/2N). The proteinase contents in BALB/CA and DBA/2N mice were almost the same between males and females. However, prominent sex differences in enzyme content were seen in all other strains; i.e., male glands of C3H/HeN and C57BL/10N contained more proteinase F than female glands did. On the contrary, the enzyme level in the ICR was exceedingly higher in females than in males. The enzyme contents in ICR SMG increased in males following castration and decreased after androgen injection in both castrated males and normal females. On the contrary, the enzyme level in C3H/HeN was decreased by castration and increased by androgen injection. Therefore, these sex differences in ICR and C3H/HeN mice depend on androgen, though the direction of the response is opposite.

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It was found that phenylephrine and methoxamine had two effects (one was inhibitory and the other was augmentative) on isoproterenol-stimulated cyclic AMP in rat parotid slices. The augmentation was abolished by α-adrenergic antagonists or by omission of calcium in the medium. Cyclic AMP accumulation by norepinephrine (NE) was significantly decreased by omission of calcium in the medium. Calmodulin antagonists, trifluoperazine and W-7, decreased NE-induced cyclic AMP accumulation, but another Calmodulin antagonist, carmidazolium, did not. Phorbol ester such as 4β-phorbol 12-myristate, 13-acetate, and phorbol 12, 13-dibutyrate, did not augment the effect of isoproterenol. These results suggest that although the influx of calcium is required in the α-adrenergic agonists-induced augmentation, calmodulin and protein kinase C may not be intermediates in this process. Calcium ions (10^-7 and 10^-6M) slightly increased the activity of adenylate cyclase, but calcium (10^-6-10^-4M) dose-dependently inhibited the effect of isoproterenol. Therefore, calcium ions do not participate in the augmentation by directly modulating the activity of adenylate cyclase. The inhibitory effect was not affected by α-adrenergic antagonists. The activation of adenylate cyclase by isoproterenol was inhibited by phenylephrine with higher inhibition being obtained in lower concentrations of isoproterenol. Phenylephrine in the presence of isobutylmethylxanthine increased the amount of cyclic AMP and this effect was inhibited by propranolol, but not by phentolamine. [³H]-CGP 12177 binding of the parotid membrane was inhibited by α-adrenergic antagonists. These results suggest that the inhibitory effect of phenylephrine and methoxamine may be mediated by β-adrenergic receptor.

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Differential distribution of synaptic terminals on the soma and dendrites of lamprey (Lampetra japonica) giant interneurons were investigated with electron microscope after marking them intracellularly with Procion scarlet. Synaptic terminals were classified by the morphology of their synaptic vesicles as S (spherical) or F (flat). The ratio of F- terminals to S-terminals (F/S) on the somata was 2.62 from 5 neurons (number of terminals observed, n=527), and that on the dendrites from 3 neurons was 0.71 (n=348). The physiological meanings of differential distribution of synaptic terminals were discussed.

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The effects of ammonia on lung stretch receptor activity and respiration were studied in the rabbit. This chemical agent caused rapid and shallow breathings or augmented breaths or their combination. The majority of slowly adapting pulmonary stretch receptors (SRs) following ammonia inhalation increased their activity during both inspiration and expiration. At 30s after ammonia inhalation, the responses of SR activity in both respiratory phases were grouped into four different types: an increase, no effect, a decrease, and no activity. In the time course of ammonia inhalation, the occurrence of a tonic firing pattern of SR activity preceded by a silent phase of the activity was observed in some SRs. In comparison with the findings of a previous report in the rabbit concerning the discharge pattern of SR activity after ammonia inhalation, the results obtained in this study suggest that some SRs in the rabbit are probably located peripheral to the site of the obstruction in the lung unit.

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The diffusivities of creatine phosphate and ATP were measured in an aqueous solution by pulsed field gradient ³¹P NMR. The diffusion coefficient of creatine phosphate was 1.4 times larger than that of ATP, suggesting the advantage of creatine phosphate in the energy transport in muscle cells.

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Physiological significance of vasoactive intestinal polypeptide (VIP), a putative co-transmitter of the cholinergic neuron innervating sweat glands, was investigated by its local effect on drug-induced sweating. VIP, methacholine chloride (MCH), or VIP plus MCH dissolved in 0.1ml of 0.9% NaCl solution to a specified concentration was injected intradermally at the center of a forearm test area of 15cm² and the sweat rate was recorded continuously by capacitance hygrometry. In a cool environment (Ta, 23°C), VIP failed to cause sweat secretion, but increased the rate of MCH-induced sweating, most markedly at a concentration of 10^-5g/ml, where the rise in local skin temperature was the greatest. On an area anesthetized by nerve block in a hot environment (Ta, 35°C), the effect was less obvious and less consistent, indicating that the sweat-facilitatory effect of VIP is reduced under the condition of passive cutaneous vasodilation. It may be postulated that VIP plays a role in securing ample oxygen supply to functioning sweat glands, especially with a relatively high cutaneous vasoconstrictor tone.

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CERRETELLI et al. (1982) proposed a model to estimate pH changes due to lactate production in exercise. This model was modified in the present study so as to express the relationship between CO₂ excess and lactate production. The modified model fitted to the data reported on endurance-trained men.

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When female analbuminemic rats were injected with 0.8mg uric acid every 3h, their survival time at 5°C increased from 14h to 28h, but uric acid had no effect on analbuminemic male rats. When female rats were oophorectomized 1week before cold exposure, the injection of uric acid had no effect on their survival. Furthermore, uric acid did not increase the survival of the female rats that were administered a pellet containing 5mg testosterone 1 week before the cold exposure. When the male rats were castrated 1week before cold exposure, their survival time decreased from 20h to 14h, and administrations of 5mg estradiol pellet at the time of castration and 0.8mg uric acid every 3h during cold exposure increased their survival time to 23h.

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Mechanical responses such as twitch and tetanus were markedly reduced in Xenopus single twitch fibers which were previously treated with either 125mM NaCl or 250mM sucrose hypertonic Ringer despite the retention of nearly normal action potential and caffeine contracture. This inhibition of excitation-contraction coupling was accompanied by a large reduction in membrane capacity to approximately 2μF/cm² during and after immersion in the hypertonic Ringer and can possibly be attributed to the same origin of disruption of the transverse tubular system as "glycerol effect."

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The effects of implantation of γ-aminobutyric acid (GABA) and serotonin (5-HT) into the arcuate nucleus (ARC) on serum luteinizing hormone (LH) and prolactin (PRL) were examined in the conscious ovariectomized rat. Following implantation of 5-HT, but not GABA, serum PRL was significantly increased. While 5-HT did not affect pulsatile LH secretion, GABA significantly decreased the mean LH concentration and pulse frequency, but not amplitude.

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A method for isolating rabbit sinoatrial cells is described. This gives long, thin cells (length from 40 to 150μm) which retain their elongated shape in normal calcium concentration. Round cells are also seen, many of which come from the rounding up of elongated cells.

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