• Development and Reproduction
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• v.6 no.2
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• pp.105-110
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• 2002

Numerous hormones are involved in the regulation of reproduction. Among them, estrogen and progesterone are the most important ovarian steroid hormones regulating female fertility. On the other hand, diverse stressors impede female receptivity and fertility. Since norepinephrine(NE) and epinephrine(E) are released from the adrenal during stress, it might play a role in stress-induced disruptions of fEmale reproductive parameters. The present study was performed to analyze the changes in adrenal catecholaminergic activities in cycling rats. The tissue content and secretion level of catecholamines were determined by high performance liquid chromatography coupled with electrochemical detector(HPLC-ECD). Adrenomedullary content of norepinephrine(NE) was increased on proestrus stage (59.47 $\pm$ 6.86 ug/gland), peaked on diestrus I stage(65.22 $\pm$ 5.99 ug/gland), and was nadir on diestrus II stage(41.63 $\pm$ 1.33 ug/gland). The highest E content was observed on proestrus stage(361.86 $\pm$ 15.58 ug/gland) while the lowest level was on diestrus II stage(285.58 $\pm$ 12.25 ug/gland). In addition to these observations, a significant reduction of the NE : E ratio was observed (1 : 4.81 on diestrus I vs 1 : 6.13～7.02 on other stages). In vitro secretion of adrenal NE and E was increased on proestrus stage, peaked on estrus stage, and decreased on diestrus II stage. Interestingly, the NE : E ratio in conditioned media was significantly increased on estrus stage (1 : 3.32 vs 1 : 2.34～2.65 on other stages. The biosynthesis of NE and E is mediated by tyrosine hydroxylase(TH) and phenylethanolamine-N-methyltransferase(PNMT) which acts conversion of tyrosine into DOPA and NE into E, respectively. These finding demonstrated that sex steroids, during setrous cycle, seem to be able to modify the adrenal catecholamines biosynthesis and secretion with stage-specific manner by modulation of the enzyme activities.

• Journal of Nutrition and Health
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• v.31 no.7
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• pp.1130-1138
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• 1998

The objective of this study was to investigate the relationship between changes in body temperature, adiposity and sympathoadrenal activity in normal weight female college students, eating an instant-noodle lunch in a laboratory setting at ambient temperatures of 22-24.8$^{\circ}C$. Preprandial epinephrine(EPI) concentration, as an indicator of adrenal activity, was inversely and significantly correlated with body weight, body mass index(BMI), and waist girth. Changes in pre- and postprandial EPI concentrations showed positive correlations with % body fat, fat mass, waist girth, hip girth, and waist/hip girth ratio(WHR). The preprandial norepinephrine (NE) concentration was negatively correlated with recovery time from the peak postprandial core temperature to the meal-start core temperature(RTST). However, the NE concentration, an indicator of sympathetic neural activity, was not related to anthropometric measurements in normal weight young women. In conclusion, adrenal activity was negatively associated with adiposity and central body fat distribution. Sympathetic activity was related to body temperature regulation capacity after a meal, but was not related to adiposity in normal weight young women. (Korean J Nutrition 31(7) 1130-1138, 1998)

• The Korean Journal of Pharmacology
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• v.19 no.1
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• pp.107-113
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• 1983

The influences of reserpine and cocaine on the changes of brain ana cardiac norepinephrine (NE) contents and plasma corticosterone level induced by ketamine in mice were studied. The results obtained were summarized as follow: 1) Various doses(5 mg, 10 mg, 20 mg and 40 mg/kg) of ketamine gradually increased the plasma corticosterone levels in 30 minutes, especially 20 mg/kg and 40 mg/kg dose treatments markedly increased the levels. 2) Brain and cardiac NE contents were decreased in 30 minutes and 60 minutes after ketamine treatment. 3) The plasma corticosterone level induced by ketamine was decreased by reserpine pretrement(36 hr.) but not affected by cocaine pretreatment(15 min.). 4) Brain and cardiac NE contents induced by ketamine were decreased by reserpine pretreatment, but increased by cocaine pretreatment.

• Korean Journal of Veterinary Research
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• v.40 no.2
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• pp.291-299
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• 2000

Magnesium ($Mg^{2+}$) transport across the plasma membrane of cardiac myocytes appears to be under hormonal control. Repeated stimulations with adrenergic or histaminergic agonist produced a progressive decrease in $Mg^{2+}$ efflux from hearts. Thus we hypothesized that the $Mg^{2+}$ efflux may be resulted from a down-regulation of receptors or from a depletion of $Mg^{2+}$ from intracellular pool(s) in the hearts. In the present study, the regulation of $Mg^{2+}$ homeostasis by receptor stimulation was studied in perfused rat and guinea pig hearts. The successive short addition of norepinephrine (NE) to rat and guinea pig, and of histamine (HT) to perfused guinea pig hearts induced a progressive decrease in $Mg^{2+}$ efflux. These $Mg^{2+}$ effluxes were blocked by propranolol or ranitidine, respectively. These decrease in $Mg^{2+}$ efflux were inhibited by sodium cyanide (NaCN), which increases intracellular $Mg^{2+}$ ($[Mg^{2+}]_i$) levels. When NE (or HT) was added after HT (or NE), this efflux was also decreased in the guinea pig hearts. In the rat hearts and myocytes, HT did not stimulate $Mg^{2+}$ efflux. But NE produced a large $Mg^{2+}$ efflux after stimulation with HT. 8-(4-Chlorophenylthio)-adenosine cAMP (cAMP), like NE and HT, also induced a progressive decrease in $Mg^{2+}$ efflux in guinea pig hearts. This effect was inhibited by NaCN. These data provide evidence that the progressive decrease in receptor-stimulated $Mg^{2+}$ efflux is considered to be due to a decrease in $[Mg^{2+}]_i$ levels rather than receptor down-regulation.

• Korean Journal of Acupuncture
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• v.30 no.1
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• pp.37-46
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• 2013

Objectives : The Meridians and acupuncture points are the fundamental theories for acupuncture therapy. They have been associated with nervous system, but It is not well defined. We investigated that the effects of acupuncture at the river points(LU8, HT4, PC5, SP5, KI7, LR4) on the changes in the expression of nNOS, iNOS, eNOS, and NE in rats. Methods : The Male Sprague-Dawley rats were divided into 6 groups each non-acupuncture and acupuncture group. We inserted needle and retained for 5 minutes on both left and right sides of LU8, HT4, PC5, SP5, KI7, LR4 which were the river points of five transport points for 6 yin meridian vessels. After that, blood was drawn via cardiac puncture, and tissues for each point near meridian vessels were extracted to examine the changes in the changes of nNOS, eNOS, iNOS and NE. Results : The LU8 and HT4 group showed a significant decrease on nNOS. In terms of eNOS and iNOS, the LU8 group decreased significantly while the KI7 group increased significantly. However, the experimental groups didn't show any significant changes on the plasma and tissue norepinephrine without plama NE in SP5 group. Conclusions : The effect on the nNOS, iNOS, eNOS of acupuncture at LU8 and KI7 could be observed, and it is considered that the effect of acupuncture related with on nervous system could be studied by additional researches based on this one.

• The Journal of Pediatrics of Korean Medicine
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• v.12 no.1
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• pp.163-181
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• 1998

The purpose of this study was to analyze the Rhizoma on the blood pressure, heart rate and to define the mechanism of Notopterygii Rhizoma-induced relaxation in rabbit common carotid arterial contracted by agonists. Method : In order to explore the effect of Notopterygii Rhizoma on the blood pressure and heart rate, Notopterygii Rhizoma extract was injected in vein of rabbit ear. In order to investigate the effect of Notopterygii Rhizoma on norepinephrine(NE)-induced contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of Notopterygii Rhizoma-induced relaxation, Notopterygii Rhizoma extract infused into NE-induced contracted strips induced by agonists after treatment of methylene blue, propranolol, ouabain and it infused into serotonin, potassium chloride-induced contracted strips. Result : The blood pressure was significantly decreased by Notopterygii Rhizoma, but heart rate was insignificantly. In addition, Notopterygii Rhizoma significantly relaxed the norepinephrine, serotonin, potassium-induced contracted strips with intact endothelium or damaged endothelium. The relaxing effect of Notopterygii Rhizoma In NE-induced contracted strips with damaged endothelium by pretreatment of methylene blue, propranolol was not changed, but Ouabain was significantly decreased. Conclusion : These results were shown that Notopterygii Rhizoma affected the NE -induced contracted smooth muscle without the participation of endothelium, and demonstrated that the mechanism of NotoDtervgii Rhizoma-induced relaxation was the obstruction of receptor-operated Ca2+ channel.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.2
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• pp.71-80
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• 2002

Previous studies have suggested that brain stem noradrenergic inputs differentially modulate neurons in the paraventricular nucleus (PVN). Here, we compared the effects of norepinephrine (NE) on spontaneous GABAergic inhibitory postsynaptic currents (sIPSCs) in identified PVN neurons using slice patch technique. In 17 of 18 type I neurons, NE $(30{\sim}100{\mu}M)$ reversibly decreased sIPSC frequency to $41{\pm}7%$ of the baseline value $(4.4{\pm}0.8\;Hz,\;p<0.001).$ This effect was blocked by yohimbine $(2{\sim}20{\mu}M),$ an ${\alpha}_2-adrenoceptor$ antagonist and mimicked by clonidine $(50{\mu}M),$ an ${\alpha}_2-adrenoceptor$ agonist. In contrast, NE increased sIPSC frequency to $248{\pm}32%$ of the control $(3.06{\pm}0.37\;Hz,\;p<0.001)$ in 31 of 54 type II neurons, but decreased the frequency to $41{\pm}7$ of the control $(5.5{\pm}1.3\;Hz)$ in the rest of type II neurons (p<0.001). In both types of PVN neurons, NE did not affect the mean amplitude and decay time constant of sIPSCs. In addition, membrane input resistance and amplitude of sIPSC of type I neurons were larger than those of type II neurons tested (1209 vs. 736 $M{\Omega},$ p<0.001; 110 vs. 81 pS, p<0.001). The results suggest that noradrenergic modulation of inhibitory synaptic transmission in the PVN decreases the neuronal excitability in most type I neurons via ${\alpha}_2-adrenoceptor,$ however, either increases in about 60% or decreases in 40% of type II neurons.

• The Korean Journal of Physiology
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• v.24 no.2
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• pp.281-291
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• 1990

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.

• Korean Journal of Psychosomatic Medicine
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• v.9 no.1
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• pp.81-92
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• 2001

Stress has been linked to the pathophysiology and pathogenesis of various psychiatric illnesses. Over the past few years, our understanding of the brain and neuroendocrine systems that are linked to stress responses has increased enormously. This article reviews a series of animal and human studies to understand what are the central pathways by which stress is perceived, processed, and transduced into a neuroendocrine response. We focus on the limbic-hypothalamic-pituitary-adrenal(LHPA) axis and several neurotransmitter systems such as norepinephrine, CRF, serotonin, acetylcholine, and dopamine. LHPA stress circuit is a complex system with multiple control mechanisms which are altered in pathological states. CRF and related peptides in the central nervous system appear to enhance behavioral responses to stressors. Norepinephrine systems are also activated by stressors and cause the release of catecholamines from the autonomic nervous system. CRF-norepinephrine interaction makes a feed-forward system which may be important for an organism to mobilize not only the pituitary system but also the central nervous system, in response to environmental challenges. The interactions among several neurotransmitters and endocrine systems appear to play key roles in mediating various behavioral and psychological stress responses involving abnormal responses to stressors such as anxiety and affective disorders.

• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.13-21
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• 1989

The circadian rhythm of spontaneous motor activity was not significantly altered by $T_4$(4mg/kg, i.p. inj. once a day for 5 days: $T_4$) and PTU (fed ad lib in 0.01% drinking water for 5 weeks: PTU). The plasma thyroxine level was markedly increased by $T_4$ but reduced by PTU, and the plasma thyrotropin level was markedly increased by PTU but moderately increased by $T_4$. Clonidine slightly increased the plasma CS level, but the clonidine effect was significantly enhanced by $T_4-pretreatment$. The brain NE and MHPG contents were little affected by $T_4$ but the NE content was significantly decreased by PTU. The SS-induced increase of plasma CS level was moderately decreased by PTU but increased by $T_4$. However, clonidine significantly inhibited the SS-induced increase, and the inhibitory effect of clonidine was not significantly affected by PTU and $T_4$, respectively. The brain MHPG content and MHPG/NE ratio were significantly decreased by clonidine but increased by SS. The clonidine- and SS-induced changes of brain MHPG content and MHPG/NE ratio were not altered by $T_4$. PTU did not affect the SS-induced increase of brain NE turnover but significantly attenuated the clonidine-induced decrease. The SS-induced increases of brain MHPG content and MHPG/NE rtatio were markedly inhibited by clonidine, and the inhibitory effect of clonidine was not affected by $T_4$ and PTU, respectively. These results suggest that the responses to swim-stress is not signigicantly affected by the alteration of thyroid function and that the hypothalamo-adenohypophysis-adrenocortical stimulation in response to swim-stress seems to be mediated via hypothalamic noradrenergic activation, and the stress response may be inhibited by the agonistic activity of clonidine on the presynaptic ${\alpha}_2-adrenoceptor$.