Maximal cardiac output and oxygen uptake $(VO_{2max})$ were measured during treadmill exercise for seven top-class marathoners and nine non-athletes using impedance cardiograph developed by one of the authors (DW Kim). Results of this study are summarized as belows. 1) New shoes with sponge and silicon rubber attached to the soles were developed to reduce motion artifact during treadmill exercise. Ensemble everaging techneque with the developed shoes was also used to improve the measurement of stroke volume using impedance cardiography. 2) Maximal cardiac output of the athletes, 14.98 L/min, was significantly higher than that of the non-athletes, 13.46 L/min. As maximal heart rate of the marathoners is lower than that of non-athletes, stroke volume of the former is significantly larger than that of the latter. 3) $VO_{2max}$ of the marathoners, 59.38 ml/kg/min, was higher than that of the non-athletes, 40.22 ml/kg/min. At the anaerobic threshold. $VO_{2max}$ of the former was 62.3% of $VO_{2max}$ and this was significantly higher than that of the non-athletes, 57.2%, This results indicates that the marathoners have higher aerobic capacity than the non-athletes. 4) The marathoners showed larger $VO_2$ than the non-athletes at the same cardiac output, indicating that a-v $O_2$ of the former is higher than that of the latter. 5) Maximal systolic pressure of the marathoners was higher than that of the non-athletes, and so was maximal rate-pressure products. These results indicate that heart oxygen consumption rate $(hVO_2)$ of the marathoner is higher than that of the non-athletes is mainly due to higher stroke volume. And higher oxygen consumption of the marathoners is due to higher stroke volume. And higher oxygen consumption of the marathoners is due to their larger a-v $O_2$. The marathoners show both higher threshold and $VO_{2max}$. Especially, measurement of cardiac output during treadmill exercise by improved impedance cardiography is expected to contribute in study of cardiac function of athletes.

It has long been suggested that the cardiac atrium is a low pressure volume receptor controlling body fluid volume and blood pressure. Recently, the cardiac atrium has been found to contain a family of powerful peptides. To clarify the relationship between high blood pressure and the biologically active atrial peptides, experiments were done to define the characteristics of atrial natriuretic peptide secretion in the isolated perfused atria of renal hypertensive rats. Higher concentrations of plasma atrial natriuretic peptide and renin activity were observed in the two-kidney, one clip hypertensive rat compared to the normotensive rat. Atrial volume changes in response to pressure elevations were attenuated in hypertensive rats compared to normotensive rats. Incremental response to atrial volume changes in ANP secretion was accentuated in hypertensive rats. These date suggest that the accentuated atrial natriuretic peptide response to volume changes of hypertensive rats may be a physiological or pathphysiological adaptation to the high blood pressure and may be, at least in part, responsible for the elevated levels of plasma atrial natriuretic peptide observed in hypertensive rats.

The purpose of the present experiment was to determine the functional subclassification of renal adenosine receptor fer the hemdynamic, excretory and secretory functions in unanesthetized rabbits. Adenosine antagonist, 8-phenyltheophylline (8-PT) or theophylline, was infused into the left renal artery followed by an infusion of adenosine agonist, cyclohexyladenosine (CHA) or 5'-N-ethylcarboxamidoadenosine (NECA). Intrarenal arterial infusion of CHA or NECA caused decreases in urine volume, glomerular filtration rate, renal plasma flow and excreted amount of electrolytes and renin release in a dose-dependent manner. Dose-response curves in renal function by CHA or NECA was similar and shifted to the right with pretreatment of 8-PT or theophylline. No significant differences in renal response to CHA and NECA in antagonist-treated rabbits were observed. However, the decrease in renin secretion rate was not affected by the adminstration of adenosine antagonists. These results suggest that the renal effect of adenosine receptor agonists appears by way of specific adenosine receptor, but which is not functionally subclassified in the rabbit.

The $Ca^{2+}-substitutional$ roles of strontium for the contractile processes were investigated in the rabbit renal artery. The contractions induced by either norepinephrine or high $K^+$ in the condition which intra- and extracellular $Ca^{2+}$ were replaced by $Sr^{2+}$, i.e. $Sr^{2+}-mediated$ contractions, were dose-dependent. And then the maximal amplitude of contraction, as compared with $Ca^{2+}-mediated$ contraction, was about 50% in norepinephrine and about 70% in high $K^+$. The $Sr^{2+}-mediated$ contractions were independent in the contraction by norepinephrine $(10^{-5}M)$ but dependent in those by high $K^+(100\;mM)$ on the extracellular $Sr^{2+}$ concentration. Also $Sr^{2+}-mediated$ contractions induced by norepinephrine were observed in the $Sr^{2+}-free$ Tyrode's solution. The $Sr^{2+}-mediated$ contractions induced by either norepinephrine or high $K^+$ were suppressed by verapamil, a $Ca^{2+}-channel$ blocker. By extracellular addition of $Sr^{2+}$, the $Ca^{2+}-mediated$ contractions induced by norepinephrine $(10^{-5}M)$ or 40 mM $K^+$ were inhibited but those by high $K^+(100\;mM)$ were increased. And the $Sr^{2+}-mediated$ contractions were increased by extracellular addition of $Ca^{2+}$ but did not reach the level of $Ca^{2+}-mediated$ contraction. Therfore it is suggested that in the vascular smooth muscle of rabbit renal artery $Sr^{2+}$ could enter the smooth muscle cells easily through the potential-operated calcium channel (POC) but not easily through the receptor-operated calcium channel (ROG), and $Sr^{2+}$ might be stored in the intracellular $Ca^{2+}-binding$ site and released by NE and induced the contraction by a way of activating directly the contractile apparatus.

The contractile action of barium $(Ba^{2+})$ was investigated in the arterial strip of rabbit renal artery. The helical strip of isolated renal artery was immersed in the Tris-buffered Tyrode's solution equilibrated with 100% $O_2$ at $37^{\circ}C$ and its isometric tension was measured. $Ba^{2+}-induced$ contraction of arterial strip was dose-dependent and its maximal tension corresponded to $92.1{\pm}4.5%$ of tension by $K^+(100\;mM)$. $Ba^{2+}-induced$ contraction did not show the tachyphylactic phenomenon in the normal Tyrode's solution. $Ba^{2+}$ induced the tonic contraction in the $Ca^{2+}-free$ tyrode's solution and that was increased by the extracellula addition of $Ca^{2+}$. During the repeated exposure of the same dose of $Ba^{2+}\;(10\;mM)$ in the $Ca^{2+}-free$ Tyrode's solution, $Ba^{2+}-induced$ contraction was progressively decreased. Even though the intracellular NE-and caffeine-sensitive $Ca^{2+}$ was depleted, $Ba^{2+}$ induced the tonic contraction. After the pretreatment of lanthnum or verapamil, $Ba^{2+}$ did not induce contraction. $Ba^{2+}-induced$contraction was suppressed by extracellular $K^+$ in the normal Tyrode's solution and that was dependent on $K^+$ concentration. Suppressive effect of $K^+\;(14\;mM)$ on the $Ba^{2+}-induced$ contraction was also dependent on the intracellular $Ca^{2+}$ concentration. From the above resuts, it is suggested that $Ba^{2+}$ activate indirectly the contractile process by promoting the mobilization of intracellular $Ca^{2+}$ and the influx of extracellular $Ca^{2+}$. It is also suggested that action of $Ba^{2+}$ on the $Ca^{2+}-activated$ $K^+$ channel can result in the depolarization of cell membrane in the rabbit renal artery.

The present study was performed to investigate modification in the electrophysiological characteristics of cat dorsal horn cells during neurogenic inflammation induced by mustard oil. The results obtained were summarized as follows: 1) Following subcutaneous injection of mustard oil the majority of wide dynamic range (WDR) cells (10/15 units) showed enhanced responses (80%) to brush, while the responses to all types of mechanical stiumli were enhanced in 3/15 units. One cell was further activated by pinch and the another was not affected at all after induction of inflammation. 2) The sensitization of WDR cell was resulted from subcutaneous injection of mustard oil either inside or outside of the receptive field (RF), whereas the spontaneous activity increased only after mustard oil was injected inside of the RF. 3) In the animal with inflammation the responses of high threshold (HT) cell to noxious stimulus were not altered, while HT cell responded to such mechanical stimulus as pressure which was usually ineffective in normal animals. 4) After induction of inflammation, low threshold (LT) cell appeared to be converted to WDR cell, showing responses not only to brush but also to pressure and pinch. 5) The mustard oil-induced inflammation enhanced responses of WDR and HT cells to the thermal stimuli and also resulted in a pronounced after-discharge in WDR cells. 6) After subcutaneous injection of lidocaine, the increased background activity of WDR cells due to inflammation was almost completely abolished. 7) A subcutaneous injection of mustard oil inside of the RF invariably desensitized the dorsal horn cells which receive sensory inputs from the inflamed RF. From the results of Present study it was revealed that a neurogenic inflammation induced by mustard oil resulted in an enhancement of responses of cat dorsal horn cells to mechanical and thermal stimuli.

장기적으로 소금 섭취량을 달리 한 정상 및 고혈압쥐에서 atrial natriurectic peptide (ANP) 가 혈압, renin-aldosterone 및 신배설에 미치는 효과를 비교하였다. 생후 6주된 spontaneously hyper-tensive rate (SHR)와 Wistar 숫쥐를 각각 저염, 정상염 및 고염 (2, 10, 25 mmol NaCl/100g diet) 군으로 나누어 실험 식이를 6주동안 먹었다. 실험 당일 아침에 쥐를 ether로 마취시킨 상태에서 대퇴 동맥과 정맥 및 방광에 catheter를 삽입한 다음에 쥐를 restraining cage에 넣어 고정시켰다. 마취가 깨고 혈압이 안정된 후에 정맥관으로 0.9% saline을 0.02ml/min의 속도로 80분간 주입하고 안정시 뇨와 혈액을 채취하였다. 그후 ANP를 380 ng/kg/min의 속도로 20분간 주입하였으며 그동안 10분 간격으로 요를 채취한 다음 채혈하였다. 혈장 aldosterone 농도와 renin 활성도 (PRA)를 방사면역법으로 측정하였다. ANP를 주입하기 전에 SHR 고염군의 평균동맥압은 정사염이나 저염군보다 유의하게 높았으나, Wistar의 혈압은 소금군 사이에서 차이가 없었다. ANP 주입전의 혈장 aldosterone 농도는 소금 섭취량이 많을수록 유의하게 낮았으며, Wistal 군이 SHR 보다 높은 값을 보였다. 혈장 renin 활성도는 소금군 간에 차이가 없었으며, Wistar와 SHR 간에도 차이가 없었다. 요량이나 Na, K 배설률은 소금군 간에 유의한 차이가 없었으나, SHR이 Wistar 보다 높은 경향을 보였다. Hematocrit 값도 소금군 간에 차이가 없었으나, SHR의 값이 Wistar 보다 유의하게 높았다. ANP를 주입하는 동안 혈압이 점진적으로 감소하여 20분후에는 $20{\sim}30\;mmHg$ 정도 감소하였으나, 각 소금군사이에 차이가 없었다. 그러나, ANP에 의한 혈압 강하 정도는 SHR이 Wistar 보다 유의하게 높았다. ANP 주입 후에는 모든 군에서 aldosterone과 혈장 renin 활성도가 유의하게 감소하였는데, aldosterone의 감소 정도는 저염군에서 가장 크게 나타났다. ANP의 이뇨 및 Na 배설 항진효과는 Wistar에서는 소금군 간에 차이가 없었으나, SHR 에서는 고염군의 Na 배설률이 저염군보다 유의하게 높았다. ANP의 혈압강하 효과나 Na 배설 항진효과가 SHR에서 Wistar 보다 유의하게 높게 나타났으나, 이뇨반응, renin 및 hematocrit의 변화에는 차이가 없었다. 이상의 결과에서, 장기적으로 소금 섭취량이 다름에 따라 ANP의 효과 중에서 특히 aldosterone 분비나 SHR의 Na 배설에 차이가 나타났는데 그 작용 기전은 확실치 않다.

What makes glucose transport function sensitive to insulin in one cell type such as adipocyte, and insensitive in another such as liver cells is unresolved question at this time. Recently it is known that insulin stimulates glucose transport in adipocytes largely by redistributing transporter from the storage pool that is included in a low density microsomal fraction to plasma membrane. Therefore, insulin sensitivity may depend upon the relative distribution of gluscose transporters between the plasma membrane and in an intracellular storage compartment. In hepatocytes, the subcellular distribution of glucose transporter is less well documented. It is thus possible that the apparent insensitivity of the hepatocyte system could be either due to lack of the constitutively maintained, intracellular storage pool of glucose transporter or lack of insulin-mediated transporter translocation mechanism in this cell. In this study, I examined if any intracellular glucose transporter pool exists in hepatocytes and this pool is affected by insulin. The results obtained summarized as followings: 1) Distribution of subcellular fractions of hepatocyte showed that there are $24.9{\pm}1.3%$ of plasma membrane, $36.9{\pm}1.7%$ of nucleus-mitochondria enriched fraction, $23.5{\pm}1.2%$ of lysosomal fraction, $9.6{\pm}1.0%$ of high density microsomal fraction and $4.9{\pm}0.5%$ of low density microsomal fraction. 2) In adipocyte, there were $29.9{\pm}2.6%$ of plasma membrane, $19.4{\pm}1.9%$ of nucleus-mitochondria enriched fraction, $26.7{\pm}1.8%$ of high density microsomal fraction and $23.9{\pm}2.1%$ of low density microsomal fraction. 3) Surface labelling of sodium borohydride revealed that plasma membrane contaminated to lysosomal fraction by $26.8{\pm}2.8%$, high density microsomal fraction by $8.3{\pm}1.3%$ and low density microsomal fraction by $1.7{\pm}0.4%$ respectively. 4) Cytochalasin B bound to all of subcellular fractions with a Kd of $1.0{\times}10^{-6}M$. 5) Photolabelling of cytochalasin B to subcellular fractions occurred on 45 K dalton protein band, a putative glucose transporter and D-glucose inhibited the photolabelling. 6) Insulin didn't affect on the distribution of subcellular fractions and translocation of intracellular glucose transporters of hepatocytes. 7) HEGT reconstituted into hepatocytes was largely associated with plasma membrane and very little was found in low density microsomal fraction which equals to the native glucose transporter distribution. Insulin didn't affect on the distribution of exogeneous glucose transporter in hepatocytes. From the above results it is concluded that insulin insensitivity of hepatocyte may due to lack of intracellular storage pool of glucose transporter and thus intracellular storage pool of glucose transporter is an essential feature of the insulin action.

To determine the role of sulfhydryl group in transport of organic ions across the basolateral membrane of renal proximal tubules, effect of p-chloromercuribenzoic acid (PCMB) on the transport of tetraethylammonium (TEA) and p-aminohippurate (PAH) was studied in rabbit renal cortical slices. PCMB caused irreversible inhibition of TEA and PAH uptake in a dose-dependent manner, with $I_{50}$ value (concentration for 50% inhibition) of $30\;{\mu}M$ for TEA and $75\;{\mu}M$ for PAH. Kinetic analysis of TEA and PAH uptakes showed that PCMB decreased Vmax $(62.35\;vs.\;28.32\;n\;mole/g{\cdot}min\;fur\;TEA:\;385.24\;vs.\;170.36\;n\;mole/g{\cdot}min\;for\;PAH)$ without changing Km. The inhibitory action of PCMB on TEA and PAH uptakes was independent of pH of the pretreatment medium. The inhibitory effect of PCMB on the uptake of TEA or PAH was prevented by dithiothreitol, but not by the substrate. PCMB inhibited Na-K-ATPase activity in a dose-dependent manner with $I_{50}$ value of $50\;{\mu}M$, which is similar to those for TEA and PAH uptake. These results suggest that PCMB inhibits the transport of organic cations and anions in the renal basolateral membrane by directly affecting the SH-group in the transporter molecules or secondly by altering the Na-K-ATPase activity.

Fluoride (F-), a known stimulator of G-protein, induced strong contraction in rabbit trachealis muscle. $AlCl_3\;(5{\sim}20\;{\mu}M)$, which is required for G-protein stimulation by $F^-$, potentiated the contractile response to $F^-$. $Ca^{2+}-removal$ and verapamil, a calcium channel blocker, inhibited the fluoroaluminate-induced contraction. Fluoroaluminate increased $^{45}Ca$ influx in the absence and presence of verapamil. In heparin-loaded muscle high $K^+-induced$ contraction was not affected, but acetylcholine and fluoroaluminate-induced contractions were inhibited. The fluoroaluminate-induced contraction was partially relaxed by isoproterenol, a stimulator of adenylate cyclase. Pertussis toxin partially inhibited fluoroaluminate-induced contraction and potentiated isoproterenol-induced relaxation in the presence of fluoroaluminate, but had no effect on acetylcholine-induced contraction and the isoproterenol-induced relaxation in the presence of acetylcholine. These results suggest that fluoroaluminate has the ability to stimulate at least two putative G-proteins in rabbit trachealis muscle; One causes $Ca^{2+}$ influx through the potential-operated $Ca^{2+}$ channel and the other induces intracellular $Ca^{2+}$ release by the increase of inositol-1, 4, 5-triphosphate.

The present investigation was performed to purify bombesin-like immunoreactivity (BBS-LI) from the skin of frogs, B. orientalis inhabiting Korea. For extraction of BBS-LI, the fresh skin of 360 g from frogs was immersed in 1,800 ml of 100% methanol and then kept at $4^{\circ}C$ for 5 days. BBS-LI was partially purified by liquid chromatography using an alkaline alumina column followed by a Sephadex G-10 column. BBS-LI was further purified by using sequential HPLC of reversed phase C18 preparation, gel permeation, SP-ion exchange and reversed phase C18 analysis. BBS-LI in fractions of each step was monitored by radioimmunoassay for which bombesin antiserum with a titer of 1 : 188,800 was raised in a guinea pig. Eventually, two different BBS-LI were successfully purified and each BBS-LI showed the following character. 1) BBS-LI was well separated into two peaks in SP-ion exchange HPLC. One (BBS-LI-K1) bound to the column while the other (BBS-LI-K2) did not. 2) BBS-LI-K1, 73.8% of total BBS-LI, was not differentiated from synthetic bombesin in reversed phase C18 analytical and gel permeation HPLC. 3) BBS-LI-K2, 26.2% of total BBS-LI, eluted later than synthetic bombesin in reversed phase C18 analytical HPLC, but it eluted with a retention time identical to that of synthetic bombesin in gel permeation HPLC. 4) The two forms of BBS-LI and synthetic bombesin identically stimulated gastrin release and pancreatic exocrine secretion including volume, protein output and amylase output in anesthetized rats. It is concluded from the above results that the skin of B. orientalis contains two different forms of BBS-LI which are very identical to bombesin immunologically and biologically. In comparison with synthetic bombesin containing 14 amino acid residues, the major form shows quite similar pattern in all HPLC used in the present study, but the minor form exhibits quite different pattern in SP-ion exchange and reversed phase C18 analytical HPLG.

Ca movements during the late plateau phase in rabbit atrium implicate Na-Ca exchange. In single atrial cells isolated from the rabbit the properties of the inward current of Na-Ca exchange were investigated using the whole cell voltage clamp technique. The inward currents were recorded during repolarization following brief 2 ms depolarizing pulse to +40 mV from a holding potential of -70 mV. Followings are the results obtained: 1) When stimulated every 30 sec, the inward currents were activated and reached peak values $6{\sim}12\;ms$ after the beginning of depolarizing pulse. The mean current amplitude was 342 pA/cell. 2) The current decayed spontaneously from the peak activation and the timecourse of the relaxation showed two different phases: fast and slow phase. 3) The recovery of the inward current was tested by paired pulse of various interval. The peak current recovered exponentialy with a time course similar to that of Ca current recovery. 4) Relaxation timecourse was also affected by pulse interval and time constant was reduced almost linearly according to the decrease of pulse interval between 30 sec and 1 sec. 5) The peak inward current was increased by long prepulse stimulation, Bay K, isoprenaline or c-AMP. 6) The relaxation time constant of the inward current was prolonged by Bay K or c-AMP, and shortened by isoprenaline. From the above results, it could be concluded that increase of the calcium current potentiates and prolongs intracellular calcium transients, while shortening of the timecourse by isoprenaline or short interval stimulations might be due to the facilitation of Ca uptake by SR.

The physiological characteristics of the neurons receiving the ventral root afferent inputs were investigated in the cat. A total of 70 cells were identified in the lumbosacral spinal cord. All these cells responded only to the C-strength stimulation of the distal stump of cut ventral root and the estimated conduction velocities of the VRA fibers were not faster than 4 m/sec. The majority of them were silent in resting state. For 49 cells, their peripheral receptive fields were characterized. Among them, 25 cells were exclusively excited by VRA inputs, 8 were inhibited and the remaining cells recevied both excitatory and inhibitory VRA inputs. According to the response pattern to the mechanical stimuli applied to their receptive fields, only a fourth of them were typical high threshold cell, a sixth, wide dynamic range cells, while remainings were a rather complex cells. Most of the cells receiving VRA inputs, received only the A ${\delta}-peripheral$ nerve inputs. Intravenous injection of morphine decreased the response of spinal cells to the VRA activation. The responses were abolished completely by counter irritation to the common peroneal nerve with C-strength-low frequency stimuli. These physiological properties of the spinal neurons receiving the VRA inputs are differ in some aspect from the spinal neurons receiving nociceptive inputs from the periphery, but still were consistent with the contention that VRA system might carry nociceptive informations arising from the spinal cord and/or neraby surrounding tissues.

The present investigation was performed to see a possible influence of the dorsal raphe nucleus (DRN) on pancreatic exocrine secretion in anesthetized rats since the DRN had been known to exert a regulatory mechanism on sympathetic activity which was known to be very important for pancreatic exocrine secretion, particularly in rats. Twenty-nine Sprague-Dawley rats fasted for 24 hours were anesthetized by i.p. injection of 1 g/kg of urethane. The pancreatic duct was cannulated to collect pancreatic juice while bile juice was diverted into the jejunum. The duodenopyloric junction was tightly ligated. After surgery for collection of pancreatic exocrine secretion and recording of carotid blood pressure, a coaxial electrode was stereotaxically inserted in the DRN with a guide of a brain atlas. And then, electrical stimulus of biphasic square wave with 2 v, 2 msec, 40 Hz was applied on the electrode for 10 minutes. Pancreatic volume flow and protein output secreted in 10 min were measured. Either bilateral cervical vagotomy or spinal cord transection at the level of $C4{\sim}C5$ was performed 20 min prior to stimulation of the DRN. 1) Electrical stimulation of the DRN resulted in significant (p<0.05) increase in pancreatic volume flow and protein output. These stimulatory effects were not affected by cervical vagotomy but completely abolished by cervical cord transection. 2) Electrical stimulation of the DRN also resulted in significant (p<0.05) rise of blood pressure of the carotid artery. The hypertensive effect was not affected by cervical vagotomy but completely abolished by cervical cord transection. The results strongly suggest that the DRN, a part of the central serotonergic system, could exert a stimulatory influence on pancreatic exocrine secretion by increasing the sympathetic activity in anesthetized rats.