We began by briefly reviewing the historical background of neurophysiological studies of the somato-autonomic reflexes and then discussed recent studies on somatic-visceral reflexes in combination with autonomic efferent nerve activity and effector organ responses. Most of the studies that have advanced our knowledge in this area have been carried out on anesthetized animals, thus eliminating emotional factors. We would like to emphasize again that the functions of many, or perhaps all visceral organs can be modulated by somato-sympathetic or somato-parasympathetic reflex activity induced by a appropriate somatic afferent stimulation in anesthetized animals. As mentioned previously, some autonomic nervous outflow, e.g. the adrenal sympathetic nerve activity, is involved in the control of hormonal secretion. John F. Fulton wrote in his famous textbook "Physiology of the Nervous System" (1949) [18] that the posterior pituitary neurosecretion system (i.e. for oxytocin and vasopressin) could be considered a part of the parasympathetic nervous system. In the study of body homeostasis and environmental adaptation it would seem very important to furthar analyze the contribution of somatic afferent input to the autonomic nervous and hormonal regulation of visceral organ activity. Also, some immunological functions have been found to be influenced by autonomic nerves or hormones (e.g. adrenal cortical hormone and catecholamines). Finally, we must take into account, as we have briefly discussed, that visceral functions can be modulated by somatic afferent input via various degrees of integration of autonomic nerves, hormones, and immunological processes. We trust that such research will be expanded to higher species of mammals, and that ultimately this knowledge of somato-visceral reflexes obtained in the physiological laboratory will become clinically useful in influencing visceral functions.

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The contracture produced by removal of the external Na was studied in the pregnant rat myometrium and this was compared with that of the non-pregnant myometrium. The Na-free contracture was small compared with spontaneous phasic contractions in the circular muscle of non-pregnant rat, but the contracture increased during pregnancy. On the other hand, in the longitudinal muscle, the contracture was large in both non-pregnant and pregnant myometria. The change in circular muscle did not seem to result from an increased sensitivity to the external Ca. Since the contracture induced by 40mM K had properties similar to those of the Na-free contracture, it is likely that weak tension development in non-pregnant circular muscle is either due to a limited Ca influx or due to a low efficiency of the excitation-contraction coupling for the sustained contraction compared with the phasic contraction. A small contraction which was independent of the external Ca was observed in Na-free solution in the both layers of non-pregnant myometrium, but this was not observed in the longitudinal muscle of pregnant myometrium.

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Active K⁺ secretion in guinea pig distal colon was studied in vitro in Ussing chambers. Changes in short-circuit current (I_sc), transepithelial conductance (G_t), and the unidirectional flux of ⁴²K from serosa to mucosa (J^K_sm) were determined under a variety of physiological and pharmacological conditions. Mucosal tetraethylammonium (TEA) (10 or 30mM) increased I_sc, while it decreased G_t and J^K_sm. Seroal bumetanide (10^-4M) also caused an increase in I_sc and decreases in G_t and J^K_sm. The effects produced by TEA were abolished in the presence of bumetanide. The increase in I_sc caused by bumetanide was greatly reduced by mucosal high-K⁺ conditions. Isoproterenol (10^-6M), a β-adrenergic agonist, elicited a decrease in I_sc and an increase in G_t. Responses to isoproterenol (10^-6M) were reduced or abolished by mucosal TEA, serosal bumetanide, serosal ouabain (10^-4M), and serosal Na⁺- or Cl^--free conditions. Mucosal high K⁺ also reduced the isoproterenol-induced decrease in I_sc. These results suggest that K⁺ secretion is electrogenic and dependent on the bumetanide-sensitive cotransport in the basolateral membrane. K⁺ exit across the apical membrane might be conductive and sensitive to TEA. In addition, β-adrenergic agonists might stimulate K⁺ secretion.

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Changes in blood flow in the carotid, superior mesenteric, or renal artery or terminal aorta during grooming were measured in the conscious rat with a chronically implanted electromagnetic flow probe. Arterial pressure was measured simultaneously with an indwelling catheter. During grooming, carotid flow almost doubled and arterial pressure rose slightly, while hindquarter (terminal aortic) flow decreased by an average of about 20%. Superior mesenteric flow decreased occasionally and renal flow remained almost unchanged. Heart rate increased by an average of about 10%. An increase in carotid flow during grooming was similarly observed after cervical sympathectomy. After ganglion blockade with hexamethonium, grooming did not decrease hindquarter flow any more. These findings suggest that during grooming a substantial amount of blood flow is switched from the hindquarters to the carotid areas, to achieve a redistribution of cardiac output largely by excitation of the respective regional sympathetic and parasympathetic fibers and that sympathetic vasoconstrictor fibers supplying different vascular areas are controlled by separate pathways from separate neuron groups.

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Aconitine will induce arrhythmias after the fiber has been completely repolarized. This arrhythmia is generally facilitated in the presence of high Ca²⁺ solution, yet the aconitine-induced arrhythmia occurs even in the presence of low Ca²⁺ solutions. We studied aconitine-induced arrhythmia (particularly the ampliitude of delayed afterdepolarization) in the frog atrium or guinea-pig papillary muscles in Ca²⁺-free solution, in the presence or absence of Ca²⁺ channel blocking agents. In Ca²⁺-free solution, aconitine (10^-5g/ml) decreased the resting potential, overshoot, V_max, and shortened the duration of the 90% action potential, before the onset of delayed afterdepolarization in frog atrial preparations. Tetrodotoxin (TTX) (2×10^-7g/ml) blocked these aconitine-induced electrical changes. Verapamil (10^-6g/ml) in nominally Ca²⁺-free solution blocked neither the generation of delayed afterdepolarization nor the triggered activity, while LaCl₃ (0.5mM) or TTX halted it. Delayed afterdepolarization appeared following the aconitine-induced transient increase in twitch tension. This transient increase in twitch tension was blocked by LaCl₃ and TTX but not by verapamil. Delayed afterdepolarization in Ca²⁺-free solution demonstrated the voltage dependence of a U shape between -40 and -80mV and was inhibited by low Na⁺ and high K⁺. Under the influence of aconitine in the guinea pig papillary muscle exposed to the Ca²⁺-free solution, depolarizing clamp pulses produced a transient inward current, and here the sigmoid time- and voltage-dependent characteristics were similar to those seen in the case of digitalis intoxication. These results suggest that intracellular Na⁺ loading plays an important role in the aconitine-induced delayed afterdepolarization and transient inward currents in low Ca²⁺ solution.

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To assess a possible direct tubular action of α-human atrial natriuretic peptide (α-hANP), we studied the effects of α-hANP on volume reabsorption (J_V), transepithelial voltage (V_T), and p-aminohippuric acid (PAH) secretion in the rabbit proximal straight tubules (PST) by in vitro microperfusion technique. In superficial PST (SFPST), addition of α-hANP at various concentrations (10^-7, 10^-9, 10^-11M) to the bath solution did not alter J_V significantly. Bath α-hANP (10^-7M) did not change V_T in SFPST, either. In juxtamedullary PST (JMPST), addition of α-hANP (10^-7M) to the bath solution changed neither V_T nor J_V significantly. The α-hANP (10^-7M) in the luminal fluid caused no changes in either V_T or J_V in SFPST. Furthermore, α-hANP (10^-7M) in the bath did not change the rate of PAH secretion in SFPST. Thus, we could not obtain any evidence for direct tubular action of α-hANP in rabbit PST. Accordingly, α-hANP may increase solute excretion without directly affecting solutes transport in PST of the rabbit kidney.

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Effects of a Ca channel blocker, nicardipine, on excitation-contraction (E-C) coupling were investigated in single twitch fibers dissected from short skeletal muscles of the frog, Rana japonica. The treatment with 20μM nicardipine at 25°C evoked a reversiblé twitch potentiation. By contrast, the treatment at the same concentration at 5°C for 30min evoked an intense twitch inhibition. The inhibition was irreversible. This paralyzed fiber remained at nearly normal resting and propagated action potentials. The treatment with 30μM nicardipine for 14min at 6°C completely inhibited a potassium contracture by 190mEq/l potassium ion for 1.5h after the removal of nicardipine despite the retention of normal resting potentials. The paralyzed fiber which was previously treated with 20μM nicardipine for 30min at 6°C, also remained at normal action potential and at partial potassium contracture, and responded to 3mM caffeine stimulation with a normal contracture. Dose-dependence curves obtained from the data on the treatments with nicardipine at various concentrations for 30min at 6°C consisted of an opposite sigmoidal shape with both threshold and half maximum inhibition at 1 and 1.5μM for twitch and similarly at 5 and 12μM for potassium contracture. Temperature-dependence curves obtained from the data on the treatments with 20μM nicardipine for 30min at various temperatures consisted of a sigmoidal shape with half maximum inhibition at 15°C for twitch and at 12°C for potassium contracture. A working hypothesis "two component-three state model" for E-C coupling was proposed based on the interpreted mechanism of nicardipine action.

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To simplify the rebreathing method to obtain the pulmonary diffusing capacity for CO (DL_CO), a one-sampling method was developed, combined with a simulation technique. The change in CO fraction in rebreathing air depends on the rebreathing volume (VRB), the dead space volume (VD), the gas volume in the lung-bag-system (VS) as well as the DL_CO: Using the measured VRB, VD, and Vs, the changes in CO fraction in bag and alveolar air were simulated by varying the DL_CO, where the expired and inspired gas volumes Were represented by a sinusoidal function of time. The DL_CO was determined by checking the similarity between the simulated and measured CO fractions at the 7th expiratory period. To confirm the validity of the simulation method, two-sampling rebreathing and single breath methods were additionally carried out in 6 normal subjects in the sitting position. The DL_CO measured by the simulation agreed well with that measured simultaneously by the two-sampling method. The DL_CO measured by this method was also compatible with that obtained from the single breath method, when the dead space was excluded from the measured lung gas volume.

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The mechanism by which Ag⁺ induces muscle contracture was elucidated by investigating the effect of external Ca²⁺ concentration and Ca²⁺ channel blocker on the maximum tension amplitude in single fibers from frog toe skeletal muscle. Five μ_M Ag⁺ induced two different types of contracture in the presence of external Ca²⁺ more than 0.1mM, i.e., a phasic and a subsequent tonic contracture. The phasic contracture appeared only in fibers with intact T-tubules immersed in a solution with or without Ca²⁺ after a lag time of 5.71±0.9s (N=5). The maximum amplitude was 58% of the tetanus tension observed in the same fiber immediately before Ag⁺ exposure. Diltiazem at high-concentration (100μ_M) inhibited the Ag⁺-induced phasic contracture only to a small extent (17%). The contracture was not affected by 1μM TTX or 1mM DAP at all. These results indicate that Na⁺, K⁺, and Ca²⁺ channels on the T-tubular membrane would not be attributed to the phasic tension development induced by Ag⁺. On the contrary, a tonic contracture did not require intact T-tubules. The amplitude and the rate of rise of the contracture depended on external Ca²⁺ concentrations and were inhibited by a high concentration of diltiazem. Neither 1μ_M TTX nor 1m_M DAP affected them. Therefore, the tonic contracture seems to be triggered by Ca²⁺ which entered the muscle fiber through the surface but not T-tubular membranes.

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Ten healthy young males were studied with a double-blind, cross-over trial to determine whether or not chlormadinone acetate (CMA), a potent synthetic progesterone, augments hypoxic chemosensitivity.Seven days after CMA administration, inspiratory minute volume (VI) and tidal volume (VT) significantly increased. Pa_CO2 decreased by 3.0±2.6 (S.D.) Torr (p<0.05) and plasma bicarbonate decreased by 2.9±1.1mM (p<0.01). During CMA administration, the atmospheric hypoxic ventilatory response (HVR), assessed by minute ventilatory (ΔVI/ΔSa_O2), and occlusion pressure responses (ΔP.₂/ΔSa_O2), significantly increased about 1.9 (p<0.05) and 1.6 times (p<0.01) compared to the placebo response, respectively. The calculated normocapnic HVR (ΔVI/ΔSa_O2) increased about 2.3 times the placebo run. Hypoxic response evaluated by the withdrawal test, which represents the peripheral chemosensitivity without involving the influence due to secondary hypoxic depression, was about 1.7 times the placebo response (p<0.05). We conclude that CMA augments hypoxic respiratory chemosensitivity.

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Arsenazo III calcium transients during twitches of frog skeletal muscle fibers were recorded in H₂O Ringer (control) and deuterium oxide Ringer (test). In ten fibers, the amplitude of the test at a sarcomere length of 2.5μm was reduced to 57% of the control and accompanied by extremely diminished tension responses. The latency was also increased to 158%.

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Hypercapnic blood was injected into the vertebral artery in anesthetized and paralyzed cats. The stimulating effect on the phrenic nerve activity was dependent on the injection rate, duration, and P_CO2 level of the injected blood. The time delay from the start of injection to the onset of increase in phrenic nerve activity was inversely proportional to both the injection rate and the P_CO2 of injected blood.

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Noradrenaline-elicited accumulation of cyclic AMP and effects of an α-, β-adrenoceptor, or adenosine receptor antagonist on the accumulation were examined in slices of different areas of rat cerebral cortex in which ferrous chloride solution was injected unilaterally into the sensorimotor cortex to induce epileptiform activity. The cyclic AMP accumulation was altered regionally in relation to both lateral dominance of electrographic isolated spike activity and variance of the epileptic process. Involvement of a β-adrenergic, and possibly α-adrenergic, mechanism in the alterations in the cyclic AMP accumulation was indicated.

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