• The Korean Journal of Physiology
• /
• v.28 no.1
• /
• pp.27-35
• /
• 1994

We investigated the alterations in basal tone of aortic strips by changing the Ca concentration, basal $^{45}Ca$ uptake and $^3H-nitrendipine$ binding of the single cells of aortic smooth muscles in the spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. While the basal tone of the aortic strips in WKY rats was not affected by alteration of Ca concentration, that in SHR was decreased by the removal of Ca from the bath solution and was recovered by the restoration of Ca to normal levels. This contraction increased in a Ca concentration-dependent manner and reached a maximum at 2 mM Ca. The basal tone of aorta in SHR was suppressed by verapamil $(10^{-6}M)$. The basal tone of aorta in SHR increased about 50% in the strips of endothelial rubbing, compared with that of intact endothelium. Basal $^{45}Ca$ uptake in the aortic single smooth muscle cells of SHR was greater than that of WKY (p<0.01), Specific bindings of $[^3H]nitrendipine$ in the aortic single smooth muscles of SHR and WKY were saturable. The dissociation constant $(K_d)\;was\;0.71{\pm}0.15\;and\;1.18{\pm}0.08nM$ SHR, respectively, and the difference in $K_d$ between two strains was statistically significant (p<0.03). The maximal binding capacity $(B_{max})\;was\;34.6{\pm}3.2\;and\;47.4{\pm}4.3\;fmol/10^6$ SHR respectively, and the difference of $(B_{max})$ between two strains was statistically significant (p<0.05). from the above results, it is suggested that the increase of Ca influx via potential-operated Ca channels and the increase of the number of dihydropyridine-sensitive Ca channels contribute to high basal tone of the aortic strips in SHR.

• The Korean Journal of Physiology and Pharmacology
• /
• v.9 no.2
• /
• pp.77-86
• /
• 2005

In this study, we examined the morphine-induced modulation of the nociceptive spinal dorsal horn neuronal activities before and after formalin-induced inflammatory pain. Intradermal injection of formalin induced time-dependent changes in the spontaneous activity of nociceptive dorsal horn neurons. In naive cats before the injection of formalin, iontophoretically applied morphine attenuated the naturally and electrically evoked neuronal responses of dorsal horn neurons. However, neuronal responses after the formalin-induced inflammation were significantly increased by morphine. Bicuculline, $GABA_A$ antagonist, increased the naturally and electrically evoked neuronal responses of dorsal horn neurons. This increase in neuronal responses due to bicuculline after the formalin-induced inflammation was larger than that in the naive state, suggesting that basal $GABA_A$ tone increased after the formalin injection. Muscimol, $GABA_A$ agonist, reduced the neuronal responses before the treatment with formalin, but not after formalin treatment, again indicating an increase in the GABAergic basal tone after the formalin injection which saturated the neuronal responses to GABA agonist. Morphine-induced increase in the spinal nociceptive responses after formalin treatment was inhibited by co-application of muscimol. These data suggest that formalin-induced inflammation increases $GABA_A$ basal tone and the inhibition of this augmented $GABA_A$ basal tone by morphine results in a paradoxical morphineinduced increase in the spinal nociceptive neuronal responses after the formalin-induced inflammation.

• Korean Journal of Bronchoesophagology
• /
• v.4 no.1
• /
• pp.64-72
• /
• 1998

This study aimed at observing the effect of diazepam on the contractility of trachealis muscle isolated from canine trachea, possible involvement of central or peripheral type benzodiazepine receptor, and the calcium related mechanism of action of diazepam. Trachealis muscle strips of 15 mm long were suspended in an isolated organ bath containing 1 ml of physiologic salt solution maintained at $37^{\circ}C$, and aerated with 95% $O_2$ /5% $CO_2$. Isometric myography was performed. Diazepam reduced the basal tone concentration dependently, and this inhibitory action was not affected by neither flumazenil, a central benzodiazepine receptor antagonist, nor PK11195, a peripheral benzodiazepine receptor antagonist. Pretreatment with diazepam showed the inhibitory effect on the concentration-response curves to agonists such as bethanechol, 5-hydroxytryptamine and histamine. Diazepam also caused concentration-related inhibition of contraction with potassium chloride 30 mM. The effect of diazepam on the basal tone and potassium chloride-induced contraction with calcium channel blockers were compared. Similar results were obtained in canine trachealis with verapamil, nifedipine and diltiazem. These results suggest that diazepam relax an airway muscle not via specific receptors but by a similar action as calcium channel blockers in canine trachealis muscle.

• Journal of Yeungnam Medical Science
• /
• v.11 no.2
• /
• pp.363-374
• /
• 1994

The purpose of this study was to investigate the characteristics or the potassium channels existing in the rat urinary bladders. Smooth muscle strips of rat detrusor urinae were examined by isometric myography. Relaxation responses of detrusor muscle strips to the three potassium channel openers pinacidil, a cyanoguanidine derivative, BRL 38227, a benzopyran derivative and RP 52891, a tertrahydrothiopyran derivative were examined. The potassium channel openers reduced the basal tone, and the rank order of potency was RP 52891>pincidil>BRL 38227. Procaine, an inhibitor of the voltage-sensitive potassium channel tended to increase the basal tone, but it did not affect the relaxant effects of the calcium-activated potassium channel opener did not antagonize the relaxant effects, but it reduced the Emax of RP 52891 and BRL 38227. Glibenclamide, an inhibitor of the ATP-sensitive potassium channel, antagonized the relaxant effects of pinacidil, RP 52891 and BRL 38227 reducing the Emax of RP 52891 and BRl 38227. Galanin which inhibits secretion of insulin through opening the ATP-sensitive potassium channels in pancreatic ${\beta}$-cells rather increased the basal tone of the isolated detrusor strips. These results suggest that the urinary bladder of the rat has mainly the ATP-sensitive, glibenclamide sensitive potassium channel, which is a different type from that in the pancreatic ${\beta}$-islet cells..

• The Korean Journal of Pharmacology
• /
• v.28 no.2
• /
• pp.147-162
• /
• 1992

The objectives of the present experiments were to characterize the effects of the peptides belonging to the pancreatic polypeptide family on the contractility of cerebral arteries and to observe the interactions of these peptides with the cyclic nucleotide activators and the potassium channel openers. Dogs of either sex, $20{\sim}30\;Kg$ in weight, were sacrificed. Basilar and middle cerebral arteries from brain were isolated and prepared for myography in the PSS equilibrated with 95% $O_2$ and 5% $CO_2$ at $37^{\circ}C$. The endothelial cells of the spiral strips were removed by CHAPS solution (0.3% w/v, 15 seconds). 1. PP, PYY and NPY contracted the arterial strips concentration-dependently with a rank order of potency of PYY>NPY>PP. These peptides were 20 to 200 times more potent than norepinephrine, and only PYY showed a greater potency than 5-HT. 2. Cyclic nucleotide activators, forskolin (for cAMP) and sodium nitroprusside (for cGMP) reduced the basal tone and inhibited the PP-, PYY- and NPY- induced contractions by concentration-dependent manners. Forskolin was more potent in reducing basal tone than sodium nitroprusside. 3. Potassium channel openers, RP 49356, P 1060 and BRL 38227 reduced the basal tone concentration-dependently and tended to inhibit the PP-, PYY- and NPY- induced contractions. Notably, BRL 38227 with low concentration $(0.1\;{\mu}M)$ enhanced the contractions induced by those peptides while P 1060 inhibited the contractions concentration-dependently. 4. The combinations of the cyclic nucleotide activators and the potassium channel openers were slightly additive in reducing the basal tone. P 1060 and BRL 38227 enhanced the relaxant effect of sodium nitroprusside significantly. On the PYY-induced contration $(0.1\;{\mu}M)$, $K^+$ channel openers tended to inhibit the inhibitory actions of forskolin and sodium nitroprusside. P 1060 and BRL 38227 antagonized the inhibitory action of sodium nitroprusside significantly. The results of the present study may be summarized that in canine cerebral arteries, not only NPY but also PYY may play a role in a cerebrovascular spasm, and intracellular concentration of either cAMP or cGMP may be involved in the mechanism of vasoconstrictive actions of these peptides, which may be affected either positively or negatively by a $K^+$ channel opener.

• The Korean Journal of Physiology
• /
• v.22 no.2
• /
• pp.189-206
• /
• 1988

The effects of ouabain on the contractile and electrical activities were investigated in the isolated preparations of guinea-pig taenia coli, and compared with those of vanadate. Spontaneous contractions were recorded with force transducer, and electrical activites were measured by use of suction electrode, or single sucrose-gap technique. The contractions were induced by the electrical stimulation for 5 seconds every 1 minute with alternating current (60 Hz, 3.0 V/cm) through the platinum electrodes located in parallel with the long axis of the preparation. All experiments were performed in tris-buffered Tyrode solution which was aerated with $100%{\;}O_2$ and kept at $35^{\circ}C$. The results obtained were as follows: 1) Responses of spontaneous contractions to ouabain were concentration-dependent; $10^{-7}M$ ouabain caused a rise of basal tone. Above the concentration of $10^{-6}M$ ouabain, an initial increase followed by a decrease in tension was observed. 2) A continuous spike discharge was induced by the administration of $10^{-7}M$ ouabain. Above $10^{-6}M$ ouabain, a transient initial increase followed by a decrease in spike frequency and amplitude was produced, and finally membrane potential was sustained at a certain level without a spike discharge. 3) The characteristic response to $10^{-7}M$ ouabain was not blocked by the pretreatment with $10^{-7}M$ atropine. 4) The electrically induced contractions were completely suppressed at the concentration of $2{\times}10^{-7}M$ ouabain. These contractions were blocked more rapidly in paralled with the increase in ouabain concentration. 5) Effects of vanadate on the spontaneous activities were quite different from those of ouabain; $10^{-6}M$ vanadate increased the amplitude of contractions and $10^{-5}M$ vanadate increased slightly both amplitude and frequency of spontaneous contractions. $10^{-4}M$ vanadate showed irregular phasic contractions superimposed on the increased basal tone. 6) $10^{-5}M$ vanadate depolarized the membrane potential and shortened the interval between the bursts of spike discharge, whereas $10^{-4}M$ vanadate induced continuous spike discharge with membrane depolarization. 7) Vanadate caused a characteristic inhibitory response to the contractions induced by electrical stimulation; An initial rapid inhibition of tension development and then gradual recovery to a certain level. From the above results, the following conclusions could be made: 1) The rise of basal tone at $10^{-7}M$ ouabain is due to continuous spike discharge without a silent period. The continuous spike discharge is likely to be associated with a slight membrane depolarization caused by the blockage of Na pump. 2) The biphasic response induced by above $10^{-6}M$ ouabain seems to occur by the different mechanisms. The initial increase in tension is associated with depolarization along with an increase in spike frquency, whereas the subsequent relaxation occurs through a non-electrical mechanism. 3) The characteristic response to $10^{-7}M$ ouabain is resulted not from the action on intrinsic nerve terminal, but from its direct action on the membrane of smooth muscle cells. 4) The phasic contractions superimposed on the increased basal tone at the concentration of $10^{-4}M$ vanadate is resulted from the continuous spike discharge with membrane depolarization, of which mechanism remains unknown. 5) The inhibitory action of ouabain on the electrically induced contractions suggests that the increasein intracellular Na in some way inhibits the electrically induced $Ca^{2+}$ influx. The mechanism of vanadate action on the induced contractions remains unknown.

• Restorative Dentistry and Endodontics
• /
• v.27 no.5
• /
• pp.543-551
• /
• 2002

Nitric oxide (NO) is a small molecule (mol. wt. 30 Da) and oxidative free radical. It is uncharged and can therefore diffuse freely within and between cells across membrane. Such characteristics make it a biologically important messenger in physiologic processes such as neurotransmission and the control of vascular tone. NO is also highly toxic and is known to acts as a mediator of cytotoxicity during host defense. NO is synthesized by nitric oxide synthase (NOS) through L-arginine/nitric oxide pathway which is a dioxygenation process. NO synthesis involves several participants, three co-substrates, five electrons, five co-factors and two prosthetic groups. Under normal condition, low levels of NO are synthesized by type I and III NOS for a short period of time and mediates many physiologic processes. Under condition of oxidant stress, high levels of NO are synthesized by type II NOS and inhibits a variety of metabolic processes and can also cause direct damage to DNA. Such interaction result in cytostasis, energy depletion and ultimately cell death. NO has the potential to interact with a variety of intercellular targets producing diverse array of metabolic effects. It is known that NO is involved in hemodynamic regulation, neurogenic inflammation, re-innervation, management of dentin hypersensitivity on teeth. Under basal condition of pulpal blood flow, NO provides constant vasodilator tone acting against sympathetic vasoconstriction. Substance P, a well known vasodilator, was reported to be mediated partly by NO, while calcitonin-gene related peptide has provided no evidence of its relation with NO. This review describes the roles of NO in dental pulp in addition to the known general roles of it.

• Journal of Acupuncture Research
• /
• v.20 no.1
• /
• pp.97-103
• /
• 2003

Objective : Auricular acupuncture is a method of treatment that involves needling the ear in order to produce relief of symptoms. This concept was first developed by P.Nogier, french doctor and referred to as somatotopic representation. Many authors have commented the fact that the vagus nerve supplies the external auditory and the concha. The aim of this randomised, single blind study was to investigate whether auricular acupuncture of the ear produced changes in the pulse rate, an indicator of vagal tone. Methods: 10 healthy man volunteers were divided into normal and epinephrine stimulation group. Then each group was divided into vagus area acupuncture and control area acupuncture group again. Epinephrine stimulation group was injected by epinephrine 0.3cc twice, first. All of them were needled in either the vagus area or control area of the ear, and pulse rate changes were measured by patient monitor over 1 hour. Results : In the epinephrine stimulation group, there was significant differences in the pulse rate change between vagus area acupuncture and control area acupuncture group. After injection of epinephrine, the basal pulse rate was increased 1.3~1.4 times in the control group. However, in the vagus area acupuncture group the basal pulse rate was increased only 1.1~1.2 times.

• Journal of Korean Neurosurgical Society
• /
• v.38 no.5
• /
• pp.380-383
• /
• 2005

Glutaric aciduria type 1 is an inborn error of lysine, hydroxylysine, and tryptophan metabolism caused by deficiency of glutaryl-coenzyme A dehydrogenase. The disease often appears in infancy with encephalopathy episode that results in acute basal ganglia and white matter degeneration. The majority of patients develop a dystonic-dyskinetic syndrome. This reports 6year-old boy who had been done previous gastrostomy due to swallowing difficulty underwent bilateral pallidotomy with intraoperative electromyography[EMG] monitoring for disabling dystonia. Intraoperative EMG was used to assess stimulation thresholds required for capsular responses and muscle tone. Surface EMG electrodes were placed on the face and cricopharyngeal muscles. Exact target were directly modified according to MRI-visualized anatomy. EMG response was consistently seen prior to visual observation of muscle activity. The surgery improved dystonic symptoms without swallowing difficulty.

• Journal of Korean Physical Therapy Science
• /
• v.2 no.2
• /
• pp.533-544
• /
• 1995

Multiple sclerosis is a chronic, pregressive, demyelinating, disease of the central nervous system. It is named for the formation of disseminated scarlike lesions primarily in the central white mattrer of the brain and spinal cord. These plaques are commonly found in the regions of the optic tracts, third and fourth ventricles, basal ganglia, midbrain, pons, and spinal cord. Multiple sclerosis is an unpredictable disease, typically presenting with an exacerbating-remitting course, although other clinical courses have been recognized. Common clinical findings include disturbances in sensation, muscle strength, tone, fatigue, coordination, vision, communication, bladder and bowel function, and cognitive and behavioral function. Physical therapy of the patient with multiple sclerosis is centered around decreasing symptoms, improving function, prevention secondary complications, and promoting successful psychological adjustment. It requires the comprehensive efforts of a health care team to provide coordinated and continuing care.