• 대한한방내과학회지
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• 제19권1호
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• pp.409-427
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• 1998

Insamjungchuntang has been used in Korea for many centuries as a treatment for respiratory disease. The effect of Insamjungchuntang on tracheal smooth muscle is not known. The purpose of the present study is to determine the effect of Insamjungchuntang on histamine and acetylcholine induced tracheal smooth muscle contraction in rats and guinea pigs. Guinea pig (500 g, male) and Sprague Dawley rats (200 g, male) were killed by $CO_2$ exposure and a segment (8-10 mm) of the thoracic trachea from each rat and guinea pig was cut into equal segments and mounted 'in pairs' in a tissue bath. Contractile force was measured with force displacement transducers under 0.5 g loading tension. The dose of histamine (His) and acetylcholine (Ach) which evoked 50% of maximal response $(ED_{50})$ was obtained from cumulative dose response curves for histamine and acetylcholine$(10^{-7}{\sim}10^{-4}\;M)$. Contractions evoked by His ($ED_{50}$) and Ach $(ED_{50})$ were inhibited significantly by Insamjungchuntang. In guinea pig tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $38.58\(p<0.05)\;after\;10{\mu}l/ml$ Insamjungchuntang, $90.75\(p<0.01)\;after\;30{\mu}l/ml$. Insamjungchuntang and $133.17\(p<0.01)\;after\;100{\mu}l/ml$ Insamjungchuntang. In rat tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $10.0\(p<0.05)\;after\;10{\mu}l/ml$ Insamjungchuntang, $80.71\(p<0.01)\;after\;30{\mu}/ml$ Insamjungchuntang and $118.29\(p<0.01)\;after\;100{\mu}l/ml$ Insamjungchuntang. Also, in guinea pig tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $45.5\(p<0.01)\;after\;10{\mu}l/ml$ lnsamjungchuntang, and $93.17\(p<0.01)\;after\;30{\mu}l/ml$. lnsamjungchuntang $134.50\(p<0.01)\;after\;100{\mu}l/ml$ Insamjungchuntang. In rat tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $37.83\(p<0.01)\;after\;10{\mu}l/ml$ lnsamjungchuntang, $90.5\(p<0.01)\;after\;30{\mu}l/ml$ Insamjungchuntang and $135.17\(p<0.01)\;after\;100{\mu}l/ml$ Insamjungchuntang. Propranolol $(10^{-7}\;M)$ slightly but significantly attenuated the inhibitory effects of Insamjungchuntang. Following treatment with propranolol, the mean percent inhibition caused by $100{\mu}l/ml$. Insamjungchuntang fell to 46.42% in guinea pig induced by acetylcholine contraction and by $100{\mu}l/ml$ Insamjungchuntang fell to 5.43% (p<0.05) in rat induced by acetylcholine contraction and the mean percent inhibition caused by $100{\mu}l/ml$ Insamjungchuntang fell to 49.0% in guinea pig induced by histamine contraction and by $100{\mu}l/ml$ Insamjungchuntang fell to 48.6% (p<0.05) in rat induced by histamine contraction. Indomethacin and methylene blue $(10^{-7}\;M)$ did not significantly alter the inhibitory effect of lnsamjungchuntang. Also, I could find the effects of lnsamjungchuntang and Insamjungchuntanggamorphine on the tracheal smooth muscle in guinea pig and rat did not change significantly. These results indicate that Insamjungchuntang can relax histamine and acetylcholine-induced contraction of guinea pig and rat tracheal smooth muscle, and that this inhibition involves sympathetic effects.

• 수면정신생리
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• 제18권1호
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• pp.40-44
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• 2011

기면병은 과도한 주간 졸림, 탈력발작, 수면 분절화, 입면환각의 특징을 가진 수면 질환이다. 기면병의 증상은 내과적, 신경과적 질환으로부터 생길 수도 있다. 17세의 고등학생 남자 환자가 3개월 전부터 발생한 참을 수 없는 과도한 주간 졸림으로 본원 수면클리닉을 통해 입원하였다. 내원 이후 측정된 체질량지수는 30.4 kg/$m^2$였고 맥박은 분당 70~90회, 혈압은 150/100~120/70 mmHg로 관찰되었다. 갑상선기능 검사에서 T3 391.2 ng/dL(60~181), free T4 4.38 ng/dL(0.89~1.76), TSH(thyroid stimulating hormone) <0.01 ${\mu}IU$/mL(0.35~5.5)로 갑상선 중독증이 시사되었다. 수면다원검사가 실시되었고, 수면 자세의 변환은 시간당 81 회로 매우 많은 편이었다. 입면 잠복기는 33.5분, 수면 효율은 47.9%, 입면에서 렘수면 입면시간은 153.6분으로 지연되었고 렘수면은 27.1%로 증가하였다. 주기성 사지 운동지수는 13.4/h로 나타났다. 수면잠복기반복검사에서 평균 입면잠복시간은 24초, SOREMP(sleep onset REM period)은 3회에서 관찰되었다. actogram상 수면-각성의 경계가 불분명하였고, HLA typing에서 DQB1 $^*0602$는 음성이었다. 환자의 갑상선중독증은 대해 3개월간 methimazole 30 mg, propranolol 40 mg이 투약되며 갑상선 기능이 호전되었다. 탈력발작은 venlafaxine 75 mg으로 조절되었고, 야간 수면 유지와 주기적 사지운동증을 치료 하기 위해 clonaze-pam 0.5 mg이 사용되었고 주관적인 야간 수면의 질은 향상되었다. 과도한 주간 졸림에 대해서는 3개월간 modafinil 200~400 mg이 투여되었고 부분적이긴 하지만 다소의 호전을 보이고 있다. 본 증례는 기면병으로 최종 진단된 환자에 있어 병력과 검사상 발견된 갑상선 중독증, 그리고 수면 효율 감소 등이 과도한 주간 졸림을 평가하는데 혼란 변수로 작용한 경우라 하겠다. 다만, 주간 과다 졸림이 modafinil에 부분적인 효과를 보이는 것, HLA DQB1 $^*0602$ 음성의 결과를 보인 환자에게 나타났던 탈력발작에 대해서도 더 설명이 필요할 것으로 보인다. 향후 CSF hypocretin level을 추가로 측정하고 수면 문제의 추이를 관찰하면서 추가적인 PSG와 MSLT가 필요할 것으로 사료된다.

• 대한약리학회지
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• 제11권2호
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• pp.29-40
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• 1975

1. 척수가토(脊髓家兎)에서 nicotine, DMPP, McN-A-343, AHR-602, tyramine, angiotensin및 neostigmine에 의한 심박증가(心搏增加)의 작용점(作用點)을 조사(調査)하였다. 2. 상기약물(上記藥物)에 의한 심박증가(心搏增加)는 reserpine 처리가토(處理家兎)에서는 대단히 약(弱)하였고, Propranolol 투여후(投與後)에는 거의 나타나지 않았다. 3. Tetrodotoxin, guanethidine은 isoproterenol, nicotine, DMPP, tyramine에 의한 심박증가(心搏增加)에는 영향(影響)을 미치지 않았으나 McN-A-343, AHR-602, angiotensin, neostigmine에 의한 심박증가(心搏增加)는 이를 현저(顯著)히 약화(弱化)시켰다. 4. Nicotine, DMPP의 심박증가(心搏增加)는 chlorisondamine으로 McN-A-343, AHR-602의 심박증가(心搏增加)는 atropine으로 각각(各各) 억제(抑制)되었다. 5. Isoproterenol, nicotine, DMPP, McN-A-343, tyramine, angiotensin, neostigmine은 적당량(適當量)을 우심방내(右心房內)에 주입(注入)하였을때 이들을 이정맥내(耳靜脈內)에 주사(注射)하였을 때와 비슷한 반응(反應)을 일으킬 수 있었다. 그러나 AHR-602 우심방내(右心房內) 주입(注入)은 유의(有意)한 심박증가(心搏增加)를 일으키지 않았다. 6. Nicotine, DMPP, neostigmine은 우심방내(右心房內) 주입시(注入時)는 현저(顯著)한 심박증가(心搏增加)를 일으켰으나, 동량(同量)을 우심실내(左心室內)에 주입(注入)하였을때는 증가(增加)를 일으키기 않았다. Isoprotereool 및 tyramine에 대한 반응(反應)은 우심실내(右心室內) 주입(注入)보다도 우심방내(右心房內) 주입시(注入時) 훨씬 컸다. 7. McN-A-343, angiotensin의 우심실내(右心室內) 주입시(注入時)는 우심방내(右心房內) 주입시(注入時)보다도 훨씬 현저(顯著)한 심박증가(心搏增加)를 일으켰고, AHR-602의 우심실내(左心室內) 주입(注入)도 현저(顯著)한 반응(反應)을 일으켰다. 8. Nicotine, DMPP, tyramine은 심장(心臟)의 aenergic nerve의 말단(末端) 또는 extraneuronal norepinephrine-store에 작용(作用)하여, Mcn-A-343, AHR-602, angiotensin은 심장(心臟)의 adrenergic nerve에 작용(作用)하여 심박증가(心搏增加)를 일으키며, nicotine, DMPP, tyramine, neostigmine의 작용점(作用點)은 주(主)로 우심방(右心房)에 McN-A-343, AHR-602, angiotenisin의 작용점(作用點)은 주(主)로 우심실(右心室)에 존재(存在)하는것으로 추론(推論)하였다.

• 대한한방내과학회지
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• 제18권2호
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• pp.1-26
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• 1997

Chunggeumtang has been used in Korea for many centuries as a treatment for respiratory disease. The effect of Chunggeumtang on tracheal smooth muscle is not konwn. The purpose of the present study is to determine the effect of Chunggeumtang on histamine and acetylcholine induced tracheal smooth muscle contraction in rats and guinea pigs. Guinea pig(500g, male) and Sprague Dawley rats (250g, male) were killed by $CO_2$ exposure and a segment (8-10mm) of the thoracic trachea from each rat and guinea pig was cut into equal swegments and mounted 'in pairs' in a tissue bath. Contractile force was measured with force diplacement transducers under 0.5g loading tension. The dose of histamine (His) and acetylcholine (Ach) which evoked 50% of maximal response ($ED_{50}$) was obtained from cumulative dose response curves for histamine and acetylcholine($10^{-7}{\sim}10^{-4}M$). Contractions evoked by His ($ED_{50}$) and Ach ($ED_{50}$) were inhibited significantly by Chunggeumtang. In guinea pig tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $6.1%after\;30{\mu}l/ml$ Chunggeumtang, and 49.4% (p<0.01) after $100{\mu}l/ml$ Chunggeumtang. In rat tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $6.7%\;after\;30{\mu}l/ml$ Chunggeumtang, and $54.2%\;(p<0.01)\;after\;100{\mu}l/ml$ Chunggeumtang. Also, in guinea pig tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $30.6%\;(p<0.05)\;after\;30{\mu}l/ml$ Chunggeumtang, and $53.0%\;(p<0.01)\;after\;100{\mu}l/ml$ Chunggeumtang. In rat tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $24.1%\;(p<0.05)\;after\;30{\mu}l/ml$ Chunggeumtang, and $55.3%\;(p<0.01)\;after\;100{\mu}l/ml$ Chunggeumtang. Propranolol and indomethacin($10^{-7}M$) slightly but significantly attenuated the inhibitory effects of Chunggeumtang. Following treatment with propranolol, the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 27.6% in guinea pig induced by acetylcholine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 28.7% (p<0.05) in rat induced by acetylcholine contraction and the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 16.2% in guinea pig induced by histamine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 28.7% (p<0.05) in rat induced by histamine contraction. Indomethacin, the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 20.0% in guinea pig induced by acetylcholine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 16.9% (p<0.05) in rat induced by acetylcholine contraction and the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 16.4% in guinea pig induced by histamine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 23.1% (p<0.05) in rat induced by histamine contraction. Methylene blue($10^{-7}M$) did not significantly alter the inhibitory effect of Chunggeumtang. Also, I could find the effects of Chunggeumtang and Chunggeumtanggamorphine on the tracheal smooth muscle in guinea pig and rat did not change significantly. These results indicate that Chunggeumtang can relax histamine and acetylcholine-induced contraction of guinea pig and rat tracheal smooth muscle, and that this inhibition involves sympathetic effects and the release of cyclooxygenase products.

• 동의생리병리학회지
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• 제16권2호
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• pp.389-396
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• 2002

In the present work, we examined the mechanism of vasorelaxant effect of scopoletin, an active constituent of Artemisia capillaris on rat thoracic descending aortic rings. Scopoletin induced a concentration-dependent relaxation in rat thoracic descending aortic rings pre-contracted with phenylephrine (EC/sub 50/ = 238.94±37.4 μM), while it was less effective in rat thoracic descending aortic rings precontracted with high potassium solution (KCI 30 mM). Vasorelaxation by scopoletin was significantly inhibited after endothelial removal, but recovered at high concentration. Pretreatment of rat thoracic descending aortic rings with N/sup G/-nitro-L-arginine (100 μM), a nitric oxide synthase inhibitor, and atropine (1 μM), a muscarinic receptor antagonist, significantly inhibited scopoletin-induced relaxation of rat thoracic descending aortic rings. Neither indomethacin (3 μM), an inhibitor of cydooxygenase, nor propranolol (1 μM), a β -adrenoceptor antagonist, modified the effect of scopoletin. The combination of N/sup G/ -nitro-L-arginine (100 μ M) and miconazole (10 μ M), an inhibitor of cytochrome P 450, did not modify the effect of scopoletin, when compared with pretreatment with N/sup G/-nitro-L-arginine(100 μM) alone. Vasorelaxant effect of scopoletin was inverted by pretreatment with diltiazem (10 μM), a Ca/sup 2+/-channel blocker, at low concentration, while restored at high concentration. Apamin (K/sub ca/-channel blocker, 1 μM), 4-aminopyridine (4-AP, K/sub v/-channel blocker, 1 mM), and tetrodotoxin (TTX, Na/sup +/-channel blocker 1 μM) potentiated the vasorelaxant effect of scopoledn, but glibendamide (K/sub ATP/-channel blocker, 10 μM), tetraetylammonium(TEA, non-selective K-channel blocker, 10 mM) did not affect the relaxation of scopoletin. Free radical scavengers (TEMPO, catalase, mannitol) did not modify vascular tone. These results suggest that nitric oxide, Ca/sup 2+/ -channels play a role in endothelium-dependent relaxations to scopoletin in rat aortas, that apamin, 4-AP, TTX but not glibenclamide, TEA potentiated relaxation to scopoletin mediated by these channels, and that free radicals do not concern to the vasorelaxant effect of scopoletin.

• 대한수의학회지
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• 제34권3호
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• pp.493-500
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• 1994

The purpose of this study was to investigate the effects of neurotransmitters and the source of $Ca^{2+}$ in the effects of neurotransmitters on the motility of pig oviductal isthmic smooth muscle. The motility of the isolated smooth muscle was recorded by using physiological recording system. The results were summarized as follows; Acetylcholine, norepinephrine, histamine and prostaglandin $F_{2{\alpha}}(PGF_{2{\alpha}})$ caused the contraction and the contractile responses were increased in a dose-dependent manner from the concentration of $10^{-7}$ to $10^{-4}M$. The maximum contractility of acetylcholine, norepinephrine, histamine and $PGF_{2{\alpha}}$ was 65.99, 28.66, 83.99 and 47.33% of 100 mM K contraction, respectively. The contractile response induced by acetylcholine$(10^{-6}M)$ was completely blocked by the pretreatment with cholinergic receptor blocker, atropine$(10^{-6}M)$, the contractile response induced by norepinephrine$(10^{-5}M)$ was blocked by the pretreatment with ${\alpha}$-adrenergic receptor blocker, phentolamine$(10^{-6}M)$ but was not blocked and rather increased by the pretreatment with ${\beta}$-adrenergic receptor blocker. propranolol$(10^{-6}M)$, the contractile response induced by histamine$(10^{-6}M)$ was completely blocked by the pretreatment with $H_1$-histaminergic receptor blocker, pyrilamine$(10^{-6}M)$ but was increased by the pretreatment with $H_2$-histaminergic receptor blocker, cimetidine$(10^{-6}M)$. The contractile response induced by acetylcholine$(10^{-6}M)$, norepinephrine$(10^{-5}M)$ and histamine$(10^{-6}M)$ was weakly contracted response in $Ca^{2+}$-free medium, but the contractile response induced by $PGF_{2{\alpha}}(10^{-6}M)$ was disappeared. The contractile response induced by acetylcholine$(10^{-6}M)$, norepinephrine$(10^{-5}M)$ and histamine$(10^{-6}M)$ was powerfully depressed by the pretreatment with $Ca^{2+}$-channel blocker, verapamil$(10^{-5}M)$ but the contractile response induced by $PGF_{2{\alpha}}(10^{-6}M)$ was completely inhibited.

• Biomolecules & Therapeutics
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• 제10권2호
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• pp.71-77
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• 2002

Heme oxygenase-1 (HO-1) is the inducible from of the rate-limiting enzyme of heme degradation; it regulates the cellular contents of heme. HO-1 is up-regulated by various stimuli including oxidative stress so that it is thought to participate in general cellular defense mechanisms against oxidative stress in mammalian cells. To investigate the role of the cAMP-dependent protein kinase A (PKA) signaling pathway on nitrogen oxidative stress-induced HO-1 gene expression, RAW 264.7 cell cultures were treated with sodium nitroprusside (SNP). SNP increased the expression of HO-1 mRNA and protein, time- and concentration-dependently. Treatment with H89, PKA inhibitor, but not LY83583, guanylate cyclase inhibitor, significantly diminished the HO-1 expression by SNP, indicating that cAMP plays a crucial role in the induction of HO-1. Incubation with cAMP-elevating agents, such as forskolin or isoproterenol resulted in up-regulation of the expression of HO-1. Forskolin-induced expression of HO-1 was inhibited by H89. Furthermore, propranolol, $\beta$-adrenoceptor blocker, inhibited the isoproterenol-induced HO-1 expression, supporting the importance of cAMP in the induction of HO-1 expression. Higenamine-S, but not higenamineR, enhanced the HO-1 expression induced by SNP. Furthermore, cellular toxicity induced by hydrogen peroxide was attenuated by the presence of SNP, which was further increased by the presence of ZnPPIX, HO-1 inhibitor. Collectively, these results strongly suggest that up-regulation of HO-1 expression in RAW 264.7 cells involves PKA signal pathway.

• 사상체질의학회지
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• 제12권1호
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• pp.228-239
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• 2000

1. 연구목적 소음인(少陰人) 성향정기산(星香正氣散)은 "동의수세보원(東醫壽世保元)"의 곽향정기산(藿香正氣散)에 남성(南星)과 목향(木香)의 두 가지 약물이 가미되어 이루어진 처방이다. 이는 소음인이한병(少陰人裏寒病)을 치료하는 처방으로 근래에는 뇌졸중을 비롯한 중추신경계통 질환에 많이 사용되고 있다. 이러한 소음인(少陰人) 성향정기산(星香正氣散)의 용도를 과학기기를 이용하여 기전을 규명하고자 하였다. 2. 연구방법 백서를 urethane으로 마취시키고 소음인(少陰人) 성향정기산(星香正氣散)을 투여한 후 Pressure Transduer와 Laser-Doppler flowmetry를 이용하여 백서의 혈압과 국소뇌혈류량을 측정하였으며 이를 구성약물까지 진행하였다. 또한 소음인(少陰人) 성향정기산(星香正氣散)의 대뇌혈류에 관한 기전 규명을 위하여 propranolol과 methylene blue로 전처치한 후 소음인(少陰人) 성향정기산(星香正氣散)을 투여하여 이를 분석하였다. 3. 결과 및 결론 소음인(少陰人) 성향정기산(星香正氣散)의 투여로 혈압의 유의한 변화는 없었으며, 국소뇌혈류량은 유의하게 증가되었다. 구성약물 중 소엽(蘇葉), 창출(蒼朮), 대복피(大腹皮), 남성(南星)은 국소뇌혈류량을 유의하게 증가시켰으며 목향(木香)은 국소뇌혈류량을 유의하게 감소시켰다. 이 실험으로 소음인(少陰人) 성향정기산(星香正氣散)의 국소뇌혈류량 증가의 기전은 교감신경 ${\beta}$-수용체와 cyclic GMP의 생성효소인 guanylyl cyclase의 작용과 관련이 있는 것으로 생각된다.

• 한국환경과학회지
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• 제18권3호
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• pp.245-254
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• 2009

In recent years, environmental pollution by phannaceuticals and personal care products (PPCPs) in the aquatic environment is of great concern worldwide. Recent studies have been reported to occur in a variety of environmental organisms such as surface, drinking and ground water, soils, sediments and hospitals. The purpose of this study was to evaluate the occurrence and environmental behavior of fourteen human PPCPs in surface waters of Mankyung River in South Korea. We were conducted to field survey for water quality and PPCPs analysis at November, 2006. PPCPs were analyzed by liquid chromatograph coupled with a tandem mass spectrometer (HPLC-MS/MS). The concentration of COD was measured to be 2.37$\sim$19.71 mg/L, which was belong to 4$\sim$5 grade in water quality criteria of lake. Station 2 that there is no pollution in upper stream, was appeared to lower concentration. The concentration of TN and TP, that is cause matter of eutrophication, were found to be 7.78$\sim$35.42 mg/L and 0.08$\sim$0.95 mg/L, respectively, which were exceeding 5 grade in Lake water quality criteria. The 11 kind of PPCPs compounds except levofloxacin and triclosan were detected to Mankyung river. PPCPs concentrations of STP(Sewer Treatment Plant) effluents and aquatic environment in Mankyung river have been detected in the range from dozens of ng/L to hundreds of ${\mu}g/L$ that by order of atenolol, carbamazepine, propranolol, Ibuprofen, erythromycin, ifenprodil, clarithromycin, mefenamic acid, fluconazole, indomethacin, disopyramide. PPCPs concentration of Station 1 and 5, which was influenced by Jeonju STP and Wanju STP, was detected high values. Station 2 that there is no pollution, showed lower values. Station 3 which joined Gosan stream and Jeonju stream and station 4 which influenced by stock wastewater was detected to low values.

• 한국어류학회지
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• 제12권1호
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• pp.38-45
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• 2000

어종에 따라 혈관의 긴장도 조절은 다양한 신경전달물질에 의하여 조절되고 있다. 그러나 아직 대부분의 어종에서 자율신경계 신경전달물질 및 혈관긴장도 조절인자들의 기능에 대하여 명확하게 규명되어 있지 않다. 본 연구는 아직 연구되지 않은 분야인 이스라엘잉어에서의 자율신경계 신경전달물질들의 혈관긴장도 조절에서의 역할을 규명하고자 적출복대동맥을 이용하여 시험하였다. 이 적출혈관에서 아세틸콜린 (ACh)은 정상혈관과 미리 일정수준 수축시킨 혈관 모두에서 수축을 유발하였으며 수축작용은 무스카린성 길항제인 아트로핀에 의해 거의 완벽하게 차단되었다. 여러 가지 아드레날린성 수용체를 동시에 흥분시키는 내인성 물질인 에피네프린 (Epi)은 혈관의 조건에 상관없이 이완반응을 유발하였다. 그러나 유사한 내인성물질인 노르에피네프린 (NE)은 정상혈관에서는 미약한 수축율, 미리수축된 혈관에서는 이완작용을 유발하였다. 한편 ${\alpha}_1$ 아드레날린성 수용체 흥분제인 페닐에프린은 수축을, $\beta$수용체 홍분제인 이소프로테레놀은 이완을 각각 유발하였으며 ${\alpha}_2$수용체 흥분제인 클로니딘은 아무런 반응을 유발하지 않았다. Epi, NE 및 이소프로테레놀에 의해 유발된 혈관이완 반응은 $\beta$ 아드레날린성 수용체 길항제인 프로프라놀롤에 의해 유의하게 억제되었다. 따라서 살아있는 상태의 이스라엘 잉어에서는 ACh는 주로 무스카린성 수용체 활성화에 의한 혈관을 수축하는 기능을, Epi과 NE는 $\beta$수용체 흥분에 의한 이완작용을 각각 발휘하는 것으로 판단된다.