Application of the patch-clamp technique on smooth muscle has started only a few years ago, but many publications are already emerging. The Ca and K channels so far found in smooth muscles seem to be fundamentally similar to those in other tissues. However, it is likely that Ca channel in smooth muscle is not controlled by cyclic AMP, in contrast to the cardiac muscle. There are at least two different ("fast" and "slow") types of Ca channel, but their relative distribution in different smooth muscles and their physiological significance are not yet fully analyzed. Furthermore, analysis of the receptor-operated Ca channels is still very limited, although these channels are very important for the smooth muscle function. Further careful studies are necessary to examine regulatory mechanisms involved in different types of Ca channel and to clarify the receptor-operated channel. There are also different (voltage- and Ca-activated) types of K channel. The Ca-activated K channel seems predominant in many smooth muscles and regulating their excitability However, K channels responsible for the resting potential or for spontaneous activity should be defined and also contribution of K (and other ionic) channels to receptor-mediated responses remains to be investigated.

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In order to determine whether oxytocin release is controlled by an osmoreceptor mechanism identical with that for vasopressin release, the plasma oxytocin concentration and plasma osmolality were measured during intraatrial infusion and after intraventricular injection of various osmotic solutions in unanesthetized rats. Intraatrial infusion of 0.6M NaCl Locke solution (LS.) or 1.2M mannitol L.S. elevated plasma oxytocin significantly, while 1.2M urea L.S. caused only a small increase and isotonic L.S. did not change in plasma oxytocin. All hypertonic solutions produced significant and similar increases in the plasma osmolality. Plasma oxytocin was positively correlated with plasma osmolality in the animals infused with hypertonic NaCl or mannitol but not in the animals infused with hypertonic urea. The injection of 2μl of 0.6M NaCl artificial cerebrospinal fluid (CSF) or 1.2M mannitol CSF into the third ventricle caused a significant increase in plasma oxytocin immediately (5min after injection) without changing plasma osmolality, while the intraventricular injection of 1.2M urea CSF or isotonic CSF produced no significant change in plasma oxytocin. These results indicate that oxytocin release is controlled by osmoreceptors rather than Na receptors, that the adequate stimulus for the osmoreceptors is one which produces cellular dehydration and that the osmoreceptors are located in the brain region which is accessible to osmotic agents from both the outside and inside of the blood-brain barrier. Since the organum vasculosum of the lamina terminalis (OVLT) lacks a blood-brain barrier and is known to be involved in osmotic control of vasopressin release, a lesion was made in the anteroventral region of the third ventricle which encompasses the OVLT and the effect of hypertonic NaCl infusion on oxytocin release was examined. No significant increase in plasma oxytocin was observed after intraatrial infusion of 0.6M NaCl L.S. in the lesioned rats. All of these findings lead to the conclusion that oxytocin release is under the control of osomoreceptors identical to those for vasopressin release.

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Effects of removal of the external sodium on the contractility of the frog's skeletal muscle were studied. Sodium-free solution, replaced by choline, strongly augmented the twitch tension before it abolished the action potential. A similar marked potentiation was also observed in the sustained contracture induced by a small depolarization under the current-clamped condition where generation of conductive action potential was blocked. On the other hand, the maximum contracture induced either by electrical stimulation or by high potassium solution was not modified by lowering the external sodium concentration. Furthermore, contraction threshold measured on the electrically induced contracture was shifted to more negative value of the membrane potential. Caffeine contracture, examined by a short-term application of 5mM caffeine, was first inhibited by sodium-free solution but afterwards restored or even augmented during the sodium-free perfusion. From these observations it is concluded that a removal of external sodium lowered the mechanical threshold of the muscle by affecting some step of the coupling process at the T-SR junction without affecting the contractile machinery.

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Three regional blood flows were measured in one-kidney, one-clip renovascular hypertensive (one-kidney hypertensive) rats with chronically implanted electromagnetic flow probe. One-kidney hypertensive rats showed about 30% greater superior mesenteric flow, about 20% greater hindquarter flow at the terminal aorta, and an almost unchanged renal flow at the clipped renal artery when compared with control rats, but the sum of the mean values of these three regional blood flows in one-kidney hypertensive rats was almost the same as that of control rats. One-kidney hypertensive rats had a higher peripheral resistance in all the investigated vascular areas. The increase in peripheral resistance of the renal area including the clipped and removed arteries was greater than that in peripheral resistance of the superior mesenteric area or hindquarter area. These findings suggest that the remaining renal area which failed to compensate for the flow deprived by uni-nephrectomy plays a role in the etiology of this kind of hypertension.

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In order to estimate to what extent the stimulatory action of CO₂ on ventilation is mediated by the formation of H⁺, we studied effects on the temporal profile of ventilatory response to CO₂ of carbonic anhydrase (CA) inhibition with acetazolamide in the halothane anesthetized spontaneously breathing rat. Since hydration reaction of CO₂ yielding H⁺ is delayed by CA inhibition, the time courses of changes in tidal volume (VT), respiratory frequency (f), and minute ventilation (VE) in response to a stepwise increase in end-tidal P_CO2 (ΔPET_CO2 15mmHg) were compared before (control state) and after i.v. injection of acetazolamide (50mg/kg) in the hyperoxic condition. In the control state, an increase in VT was significantly slower than that in f, and the mean response half-times (T_1/2) for the increase in VT, f, and VE were 50.6, 18.1, and 31.0s, respectively. After acetazolamide administration, responses to CO₂, especially f -response and consequently VE-response became much slower, and the T_1/2 for VT, f, and VE were 67.9, 55.0, and 63.0s, respectively. The delay in VT-response was not statistically significant. The magnitude of increase in VE in the steady state hypercapnic stimulation was almost the same before and after acetazolamide administration. The results suggest that a rapid increase in f during CO₂ inhalation occurs predominantly through an increase in H⁺ produced by hydration of CO₂ with CA, whereas VT-response may occur without involvement of this process. The different time courses of VT- and f-responses and possible effects of molecular CO₂ and /or H⁺ on the regulatory mechanism for ventilatory pattern were discussed.

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We compared the responses of finger blood flow to local and/or whole body warming, as measured by laser Doppler flowmetry (PERIFLUX PF-ld) (LDF), and by venous occlusion plethysmography (BF). The subject's hands were immersed in a bath of water whose temperature (T_W) was initially set at 25°C. The tested hand was kept at about 10cm above heart level to facilitate the drainage of finger veins during measurement. The ambient temperature (T_a) was initially 20°C. Then, measurements were made under the following conditions on separate days: 1) local hand warming ony (LHW), Tw was raised from 25 to 40°C; 2) whole body warming only (WBW), Ta was raised from 20 to 35°C; and 3) LHW and WBW combined (CW), LHW (T_W was raised to 35°C and maintained) was followed by WBW. Results showed that both LHW and WBW increased LDF and BF. LDF signals correlated significantly with BF values in each condition (r=0.932-0.955). However, the slope of the line showing the relationship of LDF and BF, determined by least squares linear regression analysis, was steeper in LHW than in WBW. In CW, the slope showed a bend, creating two different sections in the relationship. Below the bend the relation was steeper and showed a similar slope as that in LHW; above the bend, the relation was more gradual and a similar slope as that in WBW. No such bend was observed in measurements of the forearm skin in CW. The present results suggest that partitional measurements of circulation between AVA's and superficial vessels can be made in the finger by the simultaneous use of laser Doppler flowmetry and venous occlusion plethysmography. Local warming of the hand increases finger blood flow mainly through capillaries and subpapillary vessels and indirect whole body warming increases finger blood flow predominantly through deeply located vessels, presumably including AVA's.

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Currents through the inwardly, rectifying K channel were studied under whole-cell clamp of collagenase-treated single ventricular cells of guinea-pigs. The inwardly rectifying K channel was fully activated by hyperpolarizing the membrane from the equilibrium potential for K⁺ (E_K) by 30-40mV. Following depolarization above E_K, a decaying outward current was elicited. Prolongation of the hyperpolarizing prepulse increased the amplitude of the decaying outward current, with a time course similar to the increase of the inward current during the prepulse. Time-dependent changes in both outward and inward currents could be fitted with a single exponential function and were attributed to deactivation and activation of the inwardly rectifying K channel. The instantaneous current-voltage relation was almost linear, indicating that the conductance of the channel is ohmic and that the rectification of the steady-state current was due to the kinetic properties of the inwardly rectifying K channel. The activation kinetics of the channel was measured at different concentrations of K⁺ in both the external and internal solutions. The time constant and the steady-state activation were not a function of the absolute membrane potential value, but were dependent on the driving force.

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The conduction profile of an action potential elicited by weak voluntary contraction of the m. biceps brachii was graphically displayed by unidimensional latency-topography, UDLT. The end-plate location and conduction velocity (CV) were determined by UDLT. The end-plate location of the m. biceps brachii was measured as 12-15cm proximal to the epicondylus medialis and remained at the same region independently of the elbow angle. The CV of the action potential of various muscles was also measured in five subjects to reveal inter-muscular variation. The variation in the CV among various muscles in the same subject and that among subjects was not statistically significant. The CV measured ranged from 3.4 to 3.8m/s.

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Changes in circulating blood volume, plasma Na concentration, and central venous pressure (CVP) after fluid intake were monitored continuously in water-deprived dogs. When dogs were allowed free access to fluid (tap water or 0.9% saline), rapid satiation appeared before any systemic changes in blood composition took place, and CVP increased remarkably (about 6mmHg) in association with drinking behavior. The possible roles of CVP as a controlling factor of drinking were hypothesized.

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Effects of temperature change on different dopamine-induced responses were studied in Aplysia ganglion cells. When the temperature was raised from 11 to 35°C, the K⁺-dependent inhibitory response to dopamine increased to reach a maximum at about 23°C, then decreased at higher temperature. The Na⁺-dependent slow excitatory one kept increasing without showing the maximum. On the contrary, the Na⁺-dependent fast excitatory one rather decreased to reach the minimum near 30°C.

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