The changes in membrane potential and intracellular $Ca^{2+}$ activities along with adenosine triphosphate (ATP) and creatine phosphate (CP) contents of guinea pig hearts were studied during the cardioplegia and recovery phase. The results obtained were summarized as follows: 1) A low concentration of $Ca^{2+}$ in the cardioplegic solution caused significant changes in membrane potential during the cardioplegia and action potential configurations of the first beat after cardioplegia. 2) Intracellular $Ca^{2+}$ activities were decreased significantly during cardioplegia and increased when the cardiac tissue was reperfused with the normal Tyrode solution. The magnitude of increase in intracellular $Ca^{2+}$ activities was larger in the 0.1 mM $Ca^{2+}-cardioplegic$ solution than the 1.8 mM $Ca^{2+}-solution$. 3) ATP and CP contents of cardiac ventricular tissue were decreased during the cardioplegia, regardless of $Ca^{2+}$ concentration in the cardioplegic solutions, and CP contents were recovered with the reperfusion of normal Tyrode solution faster than those of ATP. And, there were no significant differences in the recovery of CP contents with different concentrations of $Ca^{2+}$ in the cardioplegic solutions tested, while the recovery of ATP contents was faster with $15mM\;K^{+},\;0.1mM\;Ca^{2+}$ cardioplegic solution. These results suggest that the $Ca^{2+}$ concentration in the cardioplegic solution is one of major factors influencing the recovery of cardiac tissue from the cardioplegia.

In order to elucidate the regulatory mechanism of intracellular calcium ion concentrations, contractions or contractures induced by $Na^{+}-removal$, calcium-application or ouabain-treatment as an index of $Na^+/Ca^{2+}$ exchange activity were studied in atrial muscle or vascular smooth muscle (aorta and renal artery) of the rabbit. The magnitude of low sodium contractures in atrial trabeculae increased with sigmoid shape when external sodium concentrations were reduced to sodium-free condition, whereas that of calcium contracture intensified in a parabolic pattern when external calcium concentrations were elevated to 8 mM. $Na^{+}-removal$ contractures were induced in a duration-dependent manner to $K^{+}-free$ exposure and same findings were observed with ouabain treatment. $Na^{+}-free$ contractures were not affected by verapamil treatment, but stimulated by $100{\mu}M\;Mn^{2+}$ and inhibited by high concentrations of $Mn^{2+}\;(2{\sim}8mM)$ in a dose-dependent manner. Ryanodine which is known to suppress the release of calcium from internal store abolished spontaneous twitch contractions induced by $K^{+}-free$ solution, but had no effect on the development $Na^{+}-free$ contractures. Na-free contractures were not always induced in vascular smooth muscle preparations. Contractures by $O\;mM\;Na^+$ were usually seen in aorta, but not often in renal artery.$50\;mM\;K^+$, noradrenaline (NA) and angiotensin II (AII) always evoked very large contraction in all preparations of vascular smooth muscle. Contractures developed by $O\;mM\;Na^+$ were not sensitive to verapamil treatment as in atrial trabeculae, but were abolished by $100{\mu}M\;Mn^{2+}$. In contrast to $Na^{+}-free$ contractures, $Mn^{2+}(100{\mu}M)$ had no effect on the contractures induced by NA or 50 mM$K^+$. Caffeine in the concentration of 10 mM evoked transient contracture in the distal renal artery. The rate of spontaneous relaxation in caffeine contracture was dependent upon the concentrations of external sodium, and had double component of relaxation when the rate of relaxation was plotted in the semilogarithmic scale of relative tension versus time. Especially late components of relaxation had more direct relation to $Na^+$ concentrations. It could be concluded that $Na^+/Ca^{2+}$ exchange mechanism in the heart has a large capacity, inhibited by $Mn^{2+}$ but not by verapamil and ryanodine, while $Na^+/Ca^{2+}$ exchange system in vascular smooth muscle has a very low capacity especially in small artery, inhibited by low concentration of $Mn^{2+}\;(100{\mu}M)$ but not affected by verapamil and ryanodine.

This study was carried out to investigate the action of adenosine triphosphate (ATP) on the motility of immature pig uterine smooth muscle. ATP appeared contractile responses in a dose-dependent manner, showing the maximal contraction at the concentration of $10^{-3}M$ in the uterine smooth muscle strip. The contractile responses by $ATP(10^{-4}M)$ were not affected by atropine $(10^{-6}M)$, phentolamine $(10^{-6}M)$, propranolol $(10^{-6}M)$, pyrilamine $(10^{-6}M)$, cimetidine $(10^{-6}M)$, and theophyulline $(5{\times}10^{-5}M)$, but were inhibited uncompetitively by quinidine. The effects of these drugs on the contractile responses by prostaglandin $F_{2{\alpha}}(PGF_{2{\alpha}})$ were also comparable to those observed with ATP. When muscle strips were pretreated with indomethacin $(5{\times}10^{-5}M)$ for 20 min., the contractile responses by $ATP(10^{-4}M)$ were completely inhibited. But the contractile responses by $PGF_{2{\alpha}}$ were not affected by indomethacin. These results suggest that ATP elicited the contraction through noncholinergic- and nonadrenergic-receptor mediated by prostaglandin $F_{2{\alpha}}$ in pig uterine smooth muscle.

The present study was undertaken to clarify the involvement of atrial natriuretic peptide in the development of hypertension in spontaneously hypertensive rats. Plasma concentration of immunoreactive atrial natriuretic peptide was higher in spontaneously hypertensive rats than in normotensive Sprague-Dawley and Wistar rats. Plasma renin concentration was lower in SHR than in normotensive rats, as observed in earlier experiments. Hydration-induced increase in urine flow and urinary excretions of sodium and potassium were smaller in SHR than in normotensive control rats. Intraarterial infusion of atrial natriuretic peptide resulted in increases in urine flow, urinary excretions of sodium and potassium in both hypertensive and normotensive rats. Renal response to atrial natriuretic peptide was markedly suppressed in SHR. Plasma renin and aldosterone concentration were suppressed by atrial natriuretic peptide in both SHR and normotensive rats. The responses were not significantly different in both groups. These results suggest that the renal responsiveness to atrial natriuretic peptide may be suppressed in SHR by some mechanisms still remaining obscure.

가토 신피질 절편에서 p-aminohippurate (PAH) 이동에 대한 카드뮴 이온(Cd)의 영향을 조사하여 다음과 같은 결과를 얻었다. 조직절편과 용액내의 PAH 농도비(S/M PAH)는 용액내에 Cd이 0.1 mM이상 존재할 때에 현저히 감소되었다. PAH influx에 대한 동력학적 분석결과 Cd에 의하여 influx의 최대이동율(즉 $V_{max}$)은 심하게 감소되지만 운반체와 기질간의 친화력(즉 $K_{m}$)에는 변화가 없었으며, 수동적 influx 역시 변화되지 않았다. 신피질조직의 산소 소모율은 1 mM Cd에 의하여 35% 가량 억제되었으며, 신피질 microsome 분획의 Na-K-ATPase 활성도는 Cd 농도가 $10^{-7}M$ 이상일 때 의의있게 억제되었다. 이상의 결과로 미루어 볼 때 신장조직이 카드뮴이온에 직접 노출될 경우 유기음이온의 능동적 이동능이 심하게 저해된다고 사료된다.

This study was carried out to investigate relationships between maximal running time (MRT) and glycogen supercompensation in fast twitch white fibers (white vastus, WV), fast twitch red fibers (red vastus, RV) and slow twitch red fibers (soleus muscle, SM) of endurance-trained rats. Male rats of a Sprague-Dawley strain were divided into the trained groups and untrained groups. Untrained groups were acquired to run on the treadmill 10 minutes for 3 days and remained rest and maintained with mixed diet for 4 weeks. For last 10 days of resting period, the untrained rats were divided into 3 groups i.e. mixed diet (untrained control), high and low carbohydrate (CHO) diet groups. And each group was subdivided into 2 groups, one group was tested for the MRT and the other was sacrificed to measure the blood glucose, blood lactate, glycogen contents of liver and muscles. The experimental groups were trained on treadmill by a modified method of Constable et al. (1984) maintained with mixed diet for 4 weeks. After measurement of MRT of this group, they were also divided into high and low CHO groups and fed with these diet for 2 days and MRT of each group was measured again to see the effect of high or low CHO feeding on the MRT. Each group was maintained with the same diet for next 2 days during which some of the rats were sacrificed at given time intervals for the measurements of blood glucose and lactate, liver and the muscles glycogen. The results were summarized as follows; 1) In the untrained group, there were no significant differences between subgroups in MRT, glycogen conent of SM, RV and WV. But blood glucose concentration and glycogen content of liver of low CHO group were significantly lower than those of mixed diet group. 2) The MRT and glycogen content of SM, RV and WV of trained mixed diet group were significantly increased compared to those of untrained mixed diet group, but there was no significant difference in glycogen content of liver. 3) MRT of trained mixed, high CHO and low CHO groups were $137{\pm}9.8,\;176{\pm}9.8\;and\;129{\pm}7.3\;min$ respectively with the significant difference between them. 4) There were no differences in blood lactate concentrations between the trained high and low CHO groups immediately after maximal running and during recovery period. 5) Glycogen contents in RV and SM of trained high CHO group were significantly increased, and glycogen contents in RV, WV and liver of trained low CHO group were significantly decreased compared to those of trained mixed diet group. 6) Immediately after maximal running, the blood glucose concentrations of trained high CHO and low CHO groups were $73{\pm}4.0\;and\;67{\pm}6.9mg%$ respecitively. The blood glucose of the trained high CHO group was fully recovered within one hour by feeding. But blood glucose concentration of low CHO group was slowly recovered up to $114{\pm}4.1mg%$ after two hours of feeding and maintained. Those values were still significantly lower than that of trained mixed diet group. The synthetic rates of glycogen in liver and muscles during the recovery period followed the similar time course of the blood glucose recoveries in each group. These results suggest that an increase in MRT of trained high CHO group was attributed to the glycogen supercompensation in slow twitch muscle fibers. And a decrease in MRT of trained low CHO may be due to decreased glycogen contents of liver and muscles. The results also suggest that glycogen supercompensation was more evident in slow twitch red fibers of endurance-trained rats and blood glucose is one of the limiting factors of glycogen synthesis.

The effect of cervical proprioceptors on the control of eye movement and body posture was examined in unanesthetized labyrinthine intact and bilateral labyrinthectomized cats. Cervico-ocular reflex(COR) was elicited by stimulation of the cervical proprioceptors by means of sinusoidal rotation of head or body in the darkness. The following results were obtained: 1) In labyrinthine intact cats, sinusoidal rotation of the whole body elicited compensatory eye movement(vestibulo-ocular reflex: VOR); the direction of eye movement was opposite to the direction of head rotation. 2) Anticompensatory eye movement was observed by sinusoidal rotation of the body with head fixed in labyrinthine intact cats; the direction of eye movement was the same as the direction of head rotation. 3) Compensatory eye movement was observed by sinusoidal rotation of the head with body fixed or sinusoidal rotation of the body with head fixed in both acute and chronic bilateral labyrinthectomized cats. These results suggest that the cervical proprioceptors are important in the control of ocular movement and posture in the bilateral labyrintectomized cats, although they are questionable in labyrinthine intact cats.

Effect of clonidine on the dorsal horn cell responses to mechanical stimulations were studies in 3 spinalized cats and 10 cats with intact spinal cord. The type of dorsal horn cells was determined according to their response patterns to four graded mechanical stimulations (brush, pressure, pinch and squeeze) applied to the respective receptive fields. In the present study the results obtained only from the wide dynamic range (WDR) cells were included. The responses of the WDR cells to noxious mechanical stimuli were selectively suppressed following intravenous administration of clonidine into the experimental animals. The clonidine-induced changes in responses of the WDR cells to mechanical stimulation were not affected by naloxone or propranolol whereas effect of clonidine on WDR cell responses was almost completely abolished after intravenous administration of yohimbine. Also in the spinalized cats results parallel to those observed in cats with intact spinal cord were obtained. The results of present study strongly implies that analgesic action of clonidine can be mediated through excitation of ${\alpha}_{2}-adrenoceptor$ even at the spinal cord level without supraspinal mechanism.

최근에 마취한 흰쥐에서 중뇌망상체를 전기적으로 자극하면 췌장의 외분비 기능이 증가하며 이러한 결과는 망상체의 자극으로 인하여 교감신경계의 활성도가 상승하기 때문이라는 보고가 있다. 한편 교감신경계의 활성도가 상승할 경우 교감신경계의 전달 물질인 catecholamine이 교감신경 종말 뿐만 아니라 부신수질에서도 유리된다고 알려져 있다. 그러므로 본 연구에서는 중뇌망상체의 자극으로 인하여 췌장의 외분비 기능이 증가함에 있어 교감신경계가 중요한 역할을 담당하는지를 확인하고, 이때 부신수질이 관여하는가를 알아보고자 하였다. 마취한 흰쥐에게 atropine (1mg/kg) 또는 reserpine (5mg/kg)을 투여하거나 또는 부신을 적출한 다음 중뇌망상체를 전기 자극하면서 췌장액을 채취하였다. 사용한 전기자극의 매개변수는 1.3V, 40Hz, 2msec이었다. atropine과 reserpine을 투여하면 마취한 흰쥐의 자발적 췌장액 분비량과 단백질 분비량은 모두 유의하게 감소하였으나 부신을 제거하면 췌장액 분비량에는 이렇다할 변동이 없는 반면에 단백질 분비량은 유의하게 감소하였다. 중뇌망상체를 전기자극하면 췌장액 분비량과 단백질 분비량 모두가 유의하게 증가하였다. 이러한 망상체의 자극효과는 atropine 전처치에 의하여 이렇다할 영향을 받지 않았으나 reserpine 전처치에 의하여 소실되었다. 그러나 부신을 적출하면 망상체 자극에 의한 췌장액 분비량의 증가는 유지되는 반면에 단백질 분비량의 증가는 소실되었다. 한편 미주신경을 절단한 흰쥐에서 중뇌망상체를 자극하는 동안에 경동맥의 수축기 및 이완기 혈압이 상승하였는데 이러한 망상체의 자극효과도 reserpine의 투여에 의하여 유의하게 감소되었다. 본 실험의 결과를 종합하여 보면 마취한 흰쥐에서 중뇌망상체의 자극은 교감신경계를 활성화시켜 췌장액 분비량과 단백질 분비량에 촉진적인 영향을 미치며, 이때 활성화된 교감신경계는 부분적으로 부신을 경유하게 췌장의 단백질 분비에 촉진적인 영향을 미치는 것으로 생각된다.