• The Korean Journal of Physiology and Pharmacology
• /
• v.20 no.1
• /
• pp.69-74
• /
• 2016

The present study was undertaken to investigate the influence of cardamonin on vascular smooth muscle contractility and to determine the mechanism(s) involved. Denuded aortic rings from male rats were used and isometric contractions were recorded and combined with molecular experiments. Cardamonin significantly relaxed fluoride-, phenylephrine-, and phorbol ester-induced vascular contractions, suggesting that it has an anti-hypertensive effect on agonist-induced vascular contraction regardless of endothelial nitric oxide synthesis. Furthermore, cardamonin significantly inhibited the fluoride-induced increase in pMYPT1 level and phenylephrine-induced increase in pERK1/2 level, suggesting inhibition of Rho-kinase and MEK activity and subsequent phosphorylation of MYPT1 and ERK1/2. This study provides evidence that the relaxing effect of cardamonin on agonist-induced vascular contraction regardless of endothelial function involves inhibition of Rho-kinase and MEK activity.

• Proceedings of the KIEE Conference
• /
• 1988.07a
• /
• pp.727-730
• /
• 1988

In this paper, cardiac parameters and relationship between stroke volume and impedance change were explained, and an impedance cardiograph was designed and constructed, and its accuracy was verified by experiment. Useful cardiac parameters such as stroke volume and contractility of cardiac muscle were measured noninvasively. The reproducibility of the instrument was measured to be better(less than 10%) than that of clinical standard method such as thermodilution. Hence impedance cardiography was found to be better technique for monitoring stroke volume and contractility of patients for pre and post operation, and pharmacological studies.

• Journal of Ginseng Research
• /
• v.21 no.1
• /
• pp.35-38
• /
• 1997

We investigated the effects of ginseng protopanaxadiol (PD) and protopanaxatriol (PT) saponins on the spontaneous contractility of intestine. Treatment with PD saponins showed a slight inhibition of spontaneous contraction of rabbit jejunum. In contrast, PT saponins showed much larger inhibition with dose-dependent manner in a range of 25~250 $\mu\textrm{g}$/ml. The inhibitory effect by PT saponins was not desensitized with continuous presence of PT saponins for several minutes. In addition, leu-enkephalin (1 PM) also inhibited the spontaneous contraction of rabbit jejunum but the in- hibition by leu-enkephalin was desensitized rapidly. The presence of PT saponins prevented the desenstization induced by leu-enkephalin. In conclusion, we found that PT saponins exert inhibition of spontaneous contractility of rabbit jejunum and the pattern of inhibition is different from that of opioid.

• YAKHAK HOEJI
• /
• v.58 no.5
• /
• pp.337-342
• /
• 2014

The present study was undertaken to investigate the influence of diosgenin on vascular smooth muscle contractility and to determine the mechanism involved. We hypothesized that diosgenin, the primary ingredient of Dioscorea villosa, plays a role in vascular relaxation through inhibition of Rho-kinase in rat aortae. Denuded arterial rings from male Sprague-Dawley rats were used and isometric tensions were recorded using a computerized data acquisition system. Interestingly, diosgenin inhibited fluoride-induced contraction but didn't inhibit phorbol ester-induced contraction suggesting that additional pathways different from endothelial nitric oxide synthesis such as inhibition of Rho-kinase might be involved in the vasorelaxation. Furthermore, diosgenin didn't inhibit thromboxane $A_2$-induced increases in pERK1/2 levels suggesting the mechanism excluding inhibition of thromboxane $A_2$-induced increases in ERK1/2 phosphorylation. This study provides evidence that diosgenin induces vascular relaxation through inhibition of Rho-kinase in rat aortae.

• The Korean Journal of Physiology
• /
• v.30 no.2
• /
• pp.237-247
• /
• 1996

This study was carried out to determine the effect of $-6^{\circ}$ head-down bedrest on the cardiovascular and hormonal responses to orthostasis and to evaluate the mechanism of orthostatic intolerance. Ten healthy young men were changed the body position from $-6^{\circ}$ head-down or supine bedrest for 2 hr to $70^{\circ}$ head-up tilt for 20 min. During the bedrest, there were no differences in hemodynamic and hormonal changes between the head-down and the supine positions. However, the tendency of decreased end-diastolic volume and increased cardiac contractility during the later period of 2 hr showed that the cardiovascular adaptation could be accelerated within a relatively short period in the head-down bedrest. During the head-up tilt, presyncopal signs were developed in five subjects of the supine bedrest, and one of the same subjects of the head-down bedrest. In the tolerant subjects, the increase in cardiac contractility and plasma epinephrine level during the bend-up tilt was greater following the head-down bedrest than that following the supine bedrest to compensate for reduced venous return. The intolerant subjects showed the greater decrease in end-diastolic and stroke volume, and the greater increase in heart rate during the head-up tilt than the tolerant subjects. Cardiac contractility and plasma epinephrine level were remarkably increased. However, arterial pressure was not maintained at the level for the appropriate compensation of the reduced venous return. It seems that the tolerance to orthostasis is more effective after the short-term head-down bedrest than after the supine bedrest, and the secretion of epinephrine induces the higher cardiac performance as a compensatory mechanism fur the reduced venous return during the orthostasis following the head-down bedrest than the supine bedrest.

• Journal of Environmental Science International
• /
• v.12 no.6
• /
• pp.651-657
• /
• 2003

In order to examine if arsenic, one of environmental stresses, contributes to hypertension as one of cardiovas cular pathological factors, this study was perfarmed in vivo and in vitro, using intacted or pithed rats and aorta ring preparation, respectively. And also the relationship between expression of heat shock protein (HSP) 90 and vasoactives-induced contractile response was elucidated. To measure blood pressure, the carotid arterial pressure was recorded on physiograph(Grass Co. 79E) connected to strain gauge. On the other hand, contractile response of vascular ring preparation isolated from rat was determined in organ bath and was recorded on physiograph connected to isometric transducer. And HSP was detacted by Western blotting whole cell Iysis. Preganglionic nerve stimulation was increased by 26.0% in arterial pressure of rat treated with arsenic. Vascular contractile response was monitored and HSP were measured by Western blotting of whole Iysis prepared from samples exposed with 0, 0.5, 1, 2 and 4 mM of arsenic for 8 hours. The dose-vascular responses of potassium chloride were augmented by increasing dose of arsenic in the strips exposed to arsenic for 8 hours, and were not augmented for 1, 3, 5 hours. And the response of relaxation of rat aorta induced by histamine was not influenced by arsenic stress. The increase of HSP 90 expression in rat aorta was pronounced at 8 hours after 4 mM of arsenic treatment, but HSP 60 expression was not. Arsenic stress not only increased the expression of HSP 90 in the rat aorta, but also augmented contractions to potassium chloride. These results indicated that arsenic stress was sufficient to induce heat shock protein 90, resulting in increased vascular contractility in rat aorta.

• Biomolecules & Therapeutics
• /
• v.13 no.1
• /
• pp.26-31
• /
• 2005

The present study examined effects of a water-soluble fraction from mulberry leaves (ML water fraction) on the circulatory and autonomic nervous systems, which were compared with those of acetylcholine (ACh) used as a reference drug in order to elucidate its mechanism of action. Intravenous administration of ACh or a ML water fraction produced temporary depressor and tachycardiac responses in a dose-dependent manner in unrestrained, conscious Sprague-Dawley rats. The systemic hemodynamic effects of ACh and a ML water fraction were almost completely blocked by pretreatment with atropine, a muscarinic antagonist. The depressor responses to ACh and a ML water fraction were slightly enhanced and prolonged by pretreatment with neostigmine, an anticholinesterase, whereas the tachycardiac responses were remarkably blocked by pretreatment with pentolinium, a ganglionic blocking agent. In vitro experiments using the ileum isolated from rats showed that ACh and a ML water fraction increased ileal contractility in a dose-dependent manner. The increases in ileal contractility were also completely abolished in the presence of atropine. Finally, the specific binding of [$^3H$]quinuclidinyl benzilate, a muscarinic antagonist, to rat cortical synaptic membranes was inhibited by a ML water fraction in a concentration-dependent manner with an IC$_{50}$ value of 9.5 mg/ml. The results suggest that the effects of a ML water fraction are mediated through direct stimulation of muscarinic cholinergic receptors by unknown cholinomimetic substance(s) contained in that fraction.

• The Korean Journal of Physiology
• /
• v.26 no.2
• /
• pp.129-136
• /
• 1992

The effects of $Cd^{2+}$ on spontaneous contraction, and the contractures induced by $0mM\;Na^+,\;60mM\;K^+\;and\;10^{-6}\;M$ acetylcholine, 1mM caffeine were studied in order to elucidate diverse actions of $Cd^{2+}$ on the $Ca^{2+}$ mobilization related with contractility in the antral circular muscle of guinea pig stomach. $Cd^{2+}$ inhibited the spontaneous contraction in a does dependent manner $(10^{-6}\;M\;10^{-4}\;M).\;Cd^{2+}\;(3{\times}10^{-5}M)$ suppressed 60 mM $K^+$ induced contracture composed or a phasic and a tonic response and the increased tonic response by the increased external $Ca^{2+}$ concentration. $Cd^{2+}$ also suppressed acetylcholine induced contracture composed of repetitive phasic and a tonic component and the increased tonic response by the increased external $Ca^{2+}$ concentration. Caffeine in the concentration of 1mM evoked contracture but $Cd^{2+}$ suppressed the contracture. $Cd^{2+}$ suppressed the amplitude of the $Na^+$ tee contracture dose dependently and the amplitude of $Na^+$ free contracture almost decreased to 20% of control amplitude in the concentration of $10^{-4}\;M\;Cd^{2+}$. From the above results, it is suggested that $Cd^{2+}$ may inhibit not only $Ca^{2+}$ influx via voltage sensitive, receptor operated $Ca^{2+}$ channel and Na/ca exchange but also intracellular $Ca^{2+}$ release from the sarcoplasmic reticulum in the antral circular muscle of guinea pig stomach.

• The Korean Journal of Pharmacology
• /
• v.30 no.1
• /
• pp.59-65
• /
• 1994

The experiments were performed to determine whether lidocaine interferes with the utilization of lipid as source of energy fuel for the contractile process by the isolated rat atria. Rats were starved for two days in order to inerease the lipid content of the heart. Atria from starved rats were better able to maintain their contractility in the absence of exgenous substrate, and also were more resistant to depression by lidocaine than atria from fed rats. Starvation results in a marked loss of body weight in rats. In contrast to the starved rats, the body weight of fed rats inereased with time. The smaller reduction in contractile activity of atria from the starved rats may suggest that endogenous lipid accumulates during starvation period and is used as an energy source for the contractile process in the face of a lidocaine-induced blockade in glycolysis.

• The Korean Journal of Physiology and Pharmacology
• /
• v.18 no.1
• /
• pp.47-53
• /
• 2014

In this study, we propose that diprophylline exerts bidirectional modulation (BM) on the isolated rat jejunal segment depending on its contractile state. The results supported the hypothesis. Diprophylline ($20{\mu}M$) exerted stimulatory effects on the contractility of jejunal segment in six low contractile states while inhibitory effects in six high contractile states, showing the characteristics of BM. Diprophylline-induced stimulatory effect was significantly blocked by atropine, indicating the correlation with cholinergic activation. Diprophylline-induced inhibitory effect was partially blocked by phentolamine, propranolol, and L-N-Nitro-Arginine respectively, indicating their correlation with sympathetic activation and nitric oxide-mediated relaxing mechanisms. Diprophylline-induced BM was abolished by tetrodotoxin or in a $Ca^{2+}$ free condition or pretreated with tyrosine kinase inhibitor imatinib, suggesting that diprophylline-induced BM is $Ca^{2+}$ dependent, and that it requires the presence of enteric nervous system as well as pacemaker activity of interstitial cells of Cajal. Diprophylline significantly increased the reduced MLCK expression and myosin extent in constipation-prominent rats and significantly decreased the increased MLCK expression and myosin extent in diarrhea-prominent rats, suggesting that the change of MLCK expression may also be involved in diprophylline-induced BM on rat jejunal contractility. In summary, diprophylline-exerted BM depends on the contractile states of the jejunal segments, requires the presence of $Ca^{2+}$, enteric nervous system, pacemaker activity of interstitial cells of Cajal, and MLCK-correlated myosin phosphorylation. The results suggest the potential implication of diprophylline in relieving alternative hypo/hyper intestinal motility.