There is evidence that the effect of extracellular $Ca^{2+}$ on heart rate is temperature-dependent: at $38^{\circ}C$ excess $Ca^{2+}$ induces positive chronotropic response, whereas at $30^{\circ}C$ there is no significant chronotropic effect of $Ca^{2+}$. The cause of this temperature-dependency, however, remains still unclear. Therefore, this study was undertaken to investigate the chronotropic effect of external $Ca^{2+}$ at different temperature in the isolated rabbit atria and in the small strips of SA node cut perpendicularly to crista terminalis. In the isolated atria, the $Ca^{2+}$ effect was temperature-dependent: at $35^{\circ}C$ excess $Ca^{2+}$ evoked positive chronotropic response, while at $30^{\circ}C$ there was no significant changes in sinus rate. On the contrary, in the small SA strips external $Ca^{2+}$ induced negative chronotropic effect. At $35^{\circ}C$ changes in $Ca^{2+}$ concentration from 2 to 4, 6, and 10 mM decreased the sinus rate by $2.7{\pm}1.6%$, $11.2{\pm}3.7%$ and $23.2{\pm}8.1%$ respectively. Lowering the temperature to $30^{\circ}C$, the negative chronotropic effect of $Ca^{2+}$ became greater. With intracellular microelectrodes transmembrane potential was recorded in the small SA strips at $30^{\circ}C$, $35^{\circ}C$ and $38^{\circ}C$. As temperature increased from 30 to $38^{\circ}C$, sinus rate was accelerated by $13/min/^{\circ}C$, $APD_{50}$(action ptential duration from peak to 50% repolarization) decreased by $5\;msec/^{\circ}C$, and amplitude of action potential was slightly decreased. With an increase in $Ca^{2+}$ concentrations from 0.5 to 6 mM, overshoot increased and MDP decreased. These $Ca^{2+}$ effects on the overshoot and MDP of action potentials were not altered by temperature. But the $Ca^{2+}$ effects on the rates of diastolic depolarization, systolic depolarization and repolarization were modified by temperature. Discrpancy of the chronotropic effects of $Ca^{2+}$ between isolated atria and small SA strips was discussed.

Effects of synthetic atrial natriuretic peptide and furosemide on the cardiovascular and renal functions were examined in the freshwater turtle, Amyda japonica. Both atria and ventricle of turtle contained an immunoreactive atrial natriuretic peptide. Synthetic rat atrial natriuretic peptide (atriopeptin III) and turtle atrial extract caused a decrease in mean arterial blood pressure and the vasodepressor effect was dose-dependent. In hydrated turtles received either atriopeptin III or turtle atrial extract, no significant change in renal function was observed until 100 min except a slight natriuresis at 60 or 100 min after injection of 30 ug/kg atriopeptin III or atrial extract, respectively. However, furosemide, 2 mg/kg, caused marked diuresis, natriuresis and kaliuresis. In non-hydrated turtles, no significant change in renal function was observed until 6 hrs following injection of 30 ug/kg atriopeptin III. Plasma aldosterone decreased at 2 hr and increased at 24 hr after injection of atriopeptin III although plasma renin concentration did not change. But, furosemide caused persistent diuresis, natriuresis and kaliuresis. Additionally, plasma aldosterone and renin concentrations were significantly increased at 24 hrs after injection of furosemide. In conclusion, we suggest that the freshwater turtle may have an atrial natriuretic peptide in heart and vascular receptors for atrial natriuretic peptide, and that atrial natriuretic peptide is more important in the regulation of blood pressure rather than that of renal function in freshwater turtles. We also suggest that an increased plasma renin concentration caused by furosemide may not be due to the sodium concentration delivered to macula densa, but due to the dehydration caused by persistent diuresis and natriuresis.

This study was carried out to investigate the characteristics of lithium concentration difference between maternal and fetal plasma and the effect of previous lithium loading on rapid transplacental transport of large amounts of lithium. Pregnant rabbits at $20{\sim}22\;days$ of gestation were divided into two groups: chronic $Li^+$ injection group and chronic plus acute $Li^+$ injection group. Small amounts of LiCl (1 mmol/kg per day) were given intraperitoneally to all rabbits of both group, for 5 days before sacrifice. The rabbits of chronic plus acute injection group, received additional intravenous injections of large amounts of LiCl (2 mmol/kg) one hour before sacrifice. Maternal arterial blood, placental sinus blood, fetal blood and amniotic fluid were drawn and analyzed for the plasma concentrations of $Li^+$, $Na^+$ and $K^+$ and for osmolartiy. Followings are the results obtained. 1) There was no difference in the $Li^+$ concentration between maternal plasma and placental sinus plasma in chronic lithium group, although the $Li^+$ concentration of placental sinus plasma was slightly lower than that of maternal arterial plasma in the chronic plus acute lithium group. 2) The $Li^+$ concentration of fetal plasma was much lower than that of placental sinus plasma in both groups, the ratio being $0.76{\pm}0.250$ ($mean{\pm}95%$ confidence interval) for the chronic $Li^+$ group and $0.78{\pm}0.366$ for the chronic plus acute $Li^+$ group. 3) The ratio of $Li^+$ concentration of fetal plasma to maternal arterial plasma was $0.71{\pm}0.196$ in the chronic group and $0.59{\pm}0.261$ in the chronic plus acute group. 4) $Li^+$ concentration of amniotic fluid was much higher than that of fetal plasma in the chronic $Li^+$ group but not significantly different in the chronic plus acute $Li^+$ group. 5) An acute loading of $Li^+$ did not produce any detectable changes in $Na^+$ and $K^+$ concentrations and osmolarity of the maternal plasma. The above results may suggest that: (a) The placental barrier maintains steady state lithium concentration gradient between placental sinus plasma and fetal plasma. (b) In rabbits chronically treated with $Li^+$ the steady state $Li^+$ gradient is established within one hour after an acute $Li^+$ loading, provided that the $Li^+$ concentration in the maternal plasma is less than 4 mmole/l.

It has been well known that estrogens stimulate the uterine contractility and progestins inhibit it. Then, one may expect that the uterine contractility and sensitivities to oxytocin (OT) and prostaglandin $F_{2{\alpha}}\;(PGF_{2{\alpha}})$ would be different among the estrus cycle. These hypotheses were tested using the mature female rat. Spontaneous isometric contractions of isolated uterine strips $(1{\times}0.3\;cm)$ from cyclic rats in various stages of the estrus cycle, bilateral ovarectomized rats and hypophysectomized rats were recorded in absence or presence with $estradiol-17{\beta}\;(E_2)$, progesterone $(P_4)$, OT and $PGF_{2{\alpha}}$. The results were summarized as follows: 1) The spontaneous uterine contractile force was the highest in the estrus rat and the lowest in the ovarectomized or the hypophysectomized rat. In the proestrus rat, the contractile frequency was the lowest (2.7 beats/10 min) and the contractile duration was the longest (70 sec). In the other groups, there were no any differencies in frequency (9 beats/10 min) and in duration (30 sec). 2) OT and $PGF_{2{\alpha}}$ stimulated the uterine contractility in all groups tested except in the hypophysectomized rat in which OT failed to stimulate the uterine contraction. $PGF_{2{\alpha}}$ was more effective in stimulating the uterine contraction than OT in all groups tested except in the estrus rat. OT-induced contraction was the highest in the estrus rat and $PGF_{2{\alpha}}-induced$ contraction was the lowest in the hypophysectomized rat. 3) Uterine contractilities were not changed by the in vitro treatments of $E_2$ or $P_4$ under the influence of endogenous steroids, however, $E_2$ and $P_4$ stimulated the uterine contraction in the ovarectomized rat in which endogenous steroids were almost abolished. 4) Increased uterine contraction by the treatment of OT was suppressed by in vitro $E_2$ or $P_4$ in the estrus rat, while it was potentiated by the $P_4$ in the proestrus rat. In other groups, exogenous $E_2$ or $P_4$ did not affect the OT-induced uterine contraction. 5) $PGF_{2{\alpha}}-induced$ uterine contraction was suppressed in the ovarectomized rat by $E_2$ and $P_4$, in the diestrus and proestrus rats by $P_4$ and in the hypophysectomized rat by $E_2$. In other groups, exogenous $E_2$ or $P_4$ was ineffective in altering the $PGF_{2{\alpha}}-induced$ uterine contraction. According to the above results, it may conclude that the mechanisms of the different uterine contractility and the different uterine sensitivity to OT or $PGF_{2{\alpha}}$ according to the estrus cycle are not explicable with only the serum concentrations of steroids, OT and $PGF_{2{\alpha}}$ but also other unknown factors.

It has been reported that the luteal function may be regulated by the intracellular $Ca^{++}$ level which may be adjusted partially by the high affinity $Ca^{++}-ATPase$ in luteal cell membranes. Then, one may expect that luteotropic and/or luteolytic agents, such as gonadotropins, prostaglandin $F_{2{\alpha}}\;(PGF_{2{\alpha}})$ and ouabain, affect the intracellular $Ca^{++}$ level. In this present study, therefore, we examined the effects of luteinizing hormone (LH, or human chorionic gonadotropin, hCG), $PGF_{2{\alpha}}$ and ouabain on the kinetic properties of the high affinity $Ca^{++}-ATPase$ in light membrane, heavy membrane, and microsomal fractions from the highly luteinized ovary. LH (or hCG) increased the affinity and the Vmax for $Ca^{++}$ both in light membrane and heavy membrane. $PGF_{2{\alpha}}$ increased the Vmax in light membrane and decreased the Km in heavy membrane for $Ca^{++}$ at low concentration $(5\;{\mu}g/ml)$. At higher concentration, however, $PGF_{2{\alpha}}$ oppositly affected on kinetic properties, that shown at low concentration. Ouabain, a potent inhibitor of $Na^+-K^+-ATPase$, increased the Km at high concentration $(10^{-4}\;M)$, however, decreased the Vmax for $Ca^{++}$ in light membrane at low concentration $(10^{-6}\;M)$. Also, ouabain increased the Km for $Ca^{++}$ in heavy membrane without changes in the Vmax at both concentrations. It seems that LH and low dose of $PGF_{2{\alpha}}$ increase the intracellular $Ca^{++}$ level and cause in activation of $Ca^{++}-ATPase$, however, higher dose of $PGF_{2{\alpha}}$ and ouabain inhibit directly $Ca^{++}-ATPase$ activity and result in increase in intracellular $Ca^{++}$ level. According to the above results, we suggest that luteotropic and/or luteolytic agents regulate the luteal progesterone $(P_4)$ production through two different pathways; one is cyclic adenosine monophosphate (cAMP)-dependent and another is $Ca^{++}-dependent$. Intracellula. $Ca^{++}$ level regulated by the high affinity $Ca^{++}-ATPase$ may affect both pathways in a time-dependent fashion. LH (or hCG) acts on the luteal $P_4$ production via both pathways. The initial step is $Ca^{++}$ dependent, and the late step is cAMP dependent. $PGF_{2{\alpha}}$ and ouabain increase the intracellular $Ca^{++}$ concentration so that basal luteal $P_4$ production is increased and LH-stimulated $P_4$ production is inhibited by the inhibiting LH-dependent adenylate cyclase activity.

This study was aimed to investigate whether the conduction velocity of nerve impulses through the ventral afferent fibers is constant along their entire courses in dorsal as well as in ventral roots. Cats were anesthetized with ${\alpha}-chloralose$ (60 mg/kg, i.p.) and artificially ventilated. Laminectomies were done on L4-S1 spinal vertebrae to expose the lumbosacral spiral cord. Both ventral and dorsal roots of L7 or S1 spinal segments were isolated and cut near the spinal cord. Ventral roots were placed on 6-lead stimulating electrodes and stimulated with supra C-threshold intensity. Divided dorsal root fascicles were placed on bipolar recording electrodes and single fiber units activated by the stimulation of the ventral roots were identified. Followings are the results obtained: 1) A total of 27 VRA units were identified. 10 units of them conducted impulses slower than 2 m/sec. Conduction velocities of the remaining units were in the range of 3.11-20.91 m/sec. 2) In 12 Units conduction velocities Of the VRA units through dorsal$(CV_{DR})$ and venral root$(CV_{DR})$ were determined respectively. There was a tendency to conduct impulses faster through dorsal roots$(CV_{DR}=8.19{\pm}3.26\;m/sec)$ than ventral roots$(CV_{DR}=3.46{\pm}1.02\;m/sec)$. From the above results we confirmed that there exist nerve fibers in continuity between the spinal ventral and dorsal roots but we could not ascertain whether there is a change in conduction velocity through the entire course of ventral afferent unit.

Effect of intravenously injected clonidine on the flexion reflex was studied in 15 decerebrated and spinalized cats. The flexion reflex was elicited by electrical stimulation of the tibial nerve or the common peroneal nerve and it was recorded as single unit activity from filaments of the L6 or L7 ventral roots. In order to obtain the late flexion reflex discharges, $A{\delta}$ and C afferent fibers were stimulated with single or train electrical pulses respectively. The flexion reflex, especially the late component, was markedly inhibited after intravenous administration of clonidine. The clonidine-induced inhibition of the flexion reflex was compared before and after treatment of the animals respectively with yohimbine and naloxone. The inhibitory effect on the flexion reflex of clonidine was not altered by naloxone, a ${\mu}-opioid$ receptor blocker, whereas it was completely blocked by yohimbine, an ${\alpha}_2-adrenergic$ antagonist. These results indicate that clonidine inhibits the flexion reflex through excitation of ${\alpha}_2-adrenoceptors$ even at the spinal cord level.

The present experiment was performed in 35 normal male volunteers to evaluate the effect of electroacupuncture on the human nociception more clearly and to demonstrate the effect of different parameters of electrical stimulation through acupuncture needles. The threshold of the pain(Tp) and the nociceptive flexion reflex(Tr), the threshold for intolerable pain(Tip) and that for obtaining maximal reflex response(Tmr) were studied before and after electroacupuncture performed on the acupoints of tsusanli and hsuanchung. 1) For the pricking pain, electroacupuncture with intermittent stimulation induced a significant decrease in Tp which recovered after removal of the needles. There was no significant change in other thresholds. 2) For the dull pain, electroacupuncture with intermittent stimulation produced a significant increase in Tp which continued after removal of the needles. But there was no signifcant change in Tip. Electroacupuncture with continuous stimulation induced a slight increase in Tp. 3) After resting without electroacupuncture, Tp and Tip of the dull pain were slightly decreased. These results suggest that electroacupuncture had no significant analgesic effect on the pricking pain induced by electrical stimulation of the foot skin. However, electroacupuncture with intermittent stimulation had significant analgesic effect on the weak dull pain and it had slightly greater analgesic effect than electroacupuncture with continuous stimulation.

The present experiment was carried out, in the rabbit and cat, in order to explore functional interrelationship between the vestibular semicircular canals and extraocular muscles, which are involved in the vestibulooculomotor reflex as the receptor and effector organ respectively. Semicircular canals were subjected to electrical stimulation, lymphatic fluid flow or acute freezing, and responses of the extraocular muscles were recorded in terms of changes in electromyographic activity and isometric tension. Electrical stimulation of a unilateral canal elicited contraction of the superio-medial muscle group (superior oblique, superior rectus and medial rectus muscles) in the ipsilateral eye and the inferio-lateral muscle group (inferior oblique, inferior rectus and lateral rectus muscles) in the contralateral eye. Thus a simple and distinct axiom was found in the pattern of the reflex-response of the extraocular muscles. Inhibition of the unilateral canals elicited the extraocular muscle responses contrary to those observed by excitation of the canal. Based on the present experimental results, it was demonstrated that the functional interrelations between the semicircular canals and extraocular muscles are rather equivalent in the frontal eyed cats (with binocular vision) and lateral eyed rabbits (with monocular vision). Therefore the previous thesis that the vestibuloocular relations vary from species to species awaits experimental reevaluation.