• Title/Summary/Keyword: L-NAME

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Role of Endogenous Nitric Oxide in the Control of Salivary Secretion and Blood Flow (타액분비 및 선혈류 조절에 대한 내인성 산화질소의 역할)

  • Nam, Sang-Chae;Kim, Mi-Won;Kim, Won-Jae
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.6
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    • pp.809-816
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    • 1997
  • The present study was designed to investigate whether endogenous nitric oxide(EDNO) is involved in submandibular vasodilation and salivation induced by parasympathetic nerve stimulation. Effects of $N^w$-nitro-L-arginine-methyl ester (L-NAME) which blocks the synthesis of EDNO from L-arginine on the submandibular vasodilation and salivation induced by chords stimulation or administration of various vasodilators were examined in anesthetized cats. Effect of L-NAME on $K^+$ efflux induced by carbachol was also examined using the excised submandibular slice in vitro. In the submandibular slices, acetylcholine$(10^{-5}\;mol/L)$ or vasoactive intestinal polypeptide$(VIP,\;10^{-5}\;mol/L)$ increased $NO_2$ contents, which was Prevented by pretreatment with L-NAME. Salivary secretion in response to the chords stimulation$(3\;V,\;1\;msec,\;10{\sim}20\;Hz)$ was completely blocked by treatment with atropine(1 mg/kg). Increased blood flow response to the low frequency(1, 2, 5 Hz) stimulation was significantly reduced, whereas the blood flow induced by the higher frequency(10,20 Hz) stimulation was not affected. Lingual-arterial infusion of L-NAME(100 mg/kg) significantly diminished the vasodilatory and salivary responses to the chorda stimulation at all stimuli frequencies used. Intra-arterial infusion of L-NAME(100 mg/kg markedly diminished the vasodilatory responses to acetylcholine$(5\;{\mu}g/kg)$, VIP$(5\;{\mu}g/kg)$ or bradykinin$(5\;{\mu}g/kg)$. In the excised submandibular slice, $K^+$ efflux in response to carbachol$(10^{-5}\;mol/L)$ was significantly decrease by pretreatment with L-NAME$(10^{-5}\;mol/L)$. In the isolated submandibular artery precontracted with phenylephrine$(10^{-5}\;mol/L)$, the vasorelaxation induced by ACh$(10^{-7}\;mol/L)$ was reversed into a contraction by methylene blue$(10^{-4}\;mol/L)$. These results suggest that EDNO may play an important role in vasodilation and secretion of the submandibular gland.

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Effects of Yanggyuksanhwa-Tang(凉膈散火湯) on Cerebral Blood Flow and Ischemic Brain Damage in Rats (양격산화탕(凉膈散火湯)이 뇌혈류(腦血流) 및 뇌허혈(腦虛血) 손상(損傷)에 미치는 영향)

  • Shin, Min-Gyu;Song, Il-Byung;Son, Sang-Kon
    • Journal of Sasang Constitutional Medicine
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    • v.13 no.2
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    • pp.165-176
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    • 2001
  • This study demonstrates the effects of Yanggyuksanhwa-Tang, Sasang constitutional herb prescription reported its clinical effect on the stroke of the So-yang In(少陽人), on the cerebral blood flow changes induced by nitro L-arginine methyl ester (L-NAME) treatment and ischemic brain damage induced by the middle cerebral artery occlusion (MCAO) in the rats. The changes of the arterial blood pressure, cerebral blood flow, and the diameter of the pial artery were measured in rats treated with L-NAME. And the changes of the infarct size, volume, and plasma tumor necrosis factor alpha ($TNF-{\alpha}$) levels were measured in the rats that the middle cerebral artery has been occluded by the intraluminal suture thread method. Yanggyuksanhwa-Tang was administered by the i.v. injection on the L-NAME treated rats, by the i.o. administration on the MCAO rats. The results is 1. The changes of the arterial blood pressure was not different statistically between in the L-NAME treated control group and in the Yanggyuksanhwa-Tang administered group. 2. Increase in the cerebral blood flow induced by L-NAME treatment was attenuated in the Yanggyuksanhwa-Tang administered group significantly (P<0.05) as compared with the L-NAME treated control group. 3. Decrease in the diameter of the pial artery induced by L-NAME treatment was attenuated about 18% in the Yanggyuksanhwa-Tang administered group as compared with the L-NAME treated control group. 4. Ischemic damaged infarct areas were decreased significantly (P<0.05) in the interaural 12mm, 10mm, and 6mm brain sections of the Yanggyuksanhwa-Tang administered group as compared the MCA occluded control group. 5. Total ischemic infarct volume was decreased significantly (P<0.05) in the Yanggyuksanhwa-Tang administered group as compared the MCA occluded control group. 6. Plasma $TNF-{\alpha}$ levels were decreased significantly (P<0.01) in the Yanggyuksanhwa-Tang administered group as compared the MCA occluded control group.

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Immunohistochemical Changes of Apoptotic Control Genes by Chronic Inhibition of Nitric Oxide in Rats

  • Bae, Hyung-Joon
    • Biomedical Science Letters
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    • v.18 no.4
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    • pp.420-427
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    • 2012
  • Sprague-Dawley (SD) rats were orally administered with NG-nitro-L-arginine methyl ester (L-NAME), which inhibits or blocks the production of nitric oxide from L-arginine in vascular endothelial cells and vessel tissue. We examined the effects of nitric oxide on some physiological changes such as blood pressure and heart rate, and confirms the apoptosis induced by the suppressed nitric oxide activity in the kidney. This study was performed to investigate correlation between the activities of nitric oxide and apoptosis by immunohistochemical changes of apoptotic control proteins with regulated chronic inhibition of nitric oxide. In the kidney from L-NAME-treated group, immunohistochemical reaction to the antigens of apoptosis inhibiting proteins such as bcl-2 and bcl-xL, exhibited a time-dependent reduction. The expression of apoptosis-inhibiting proteins such as bax and p53 increased expression in proportion to the duration of treatment. The most sensitive apoptosis regulating proteins to L-NAME were p53 in stimulation and bcl-2 in inhibition, respectively.

Analgesic Effects of Triptolide and N-nitro-L-arginine Methyl Ester in Rat's Temporomandibular Joint Pain Model (흰 쥐의 측두하악관절 통증모델에서 Triptolide와 N-nitro-L-arginine Methyl Ester의 통증조절효과)

  • Kim, Yun-Kyung;Lee, Min-Kyung
    • Journal of dental hygiene science
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    • v.15 no.6
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    • pp.800-806
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    • 2015
  • The aim of this study was to investigate whether intracisternal administrations of triptolide and N-nitro-L-arginine Methyl Ester (L-NAME) are involved in the regulation of temporomandibular joint (TMJ) pain. The TMJ pain was induced by the injection of 5% formalin ($30{\mu}l$) into TMJ capsule of rats. The pain behavioral responses was recorded the number of grooming or scratching on the left TMJ area for 9 successive 5 minutes intervals. Triptolide and L-NAME were administrated intracisternally 10 minutes before formalin injection. The intra-articular injection of formalin produced a biphasic pattern of pain response (first phase: 0~10 minutes and second phase: 11~45 minutes). The intracisternal administration of triptolide ($1{\mu}g/10{\mu}l$) and L-NAME ($0.1{\mu}g/10{\mu}l$) suppressed the TMJ pain behavior in each experiment. Co-administration of two drugs was shown the enhanced effect than the analgesic effect by single-administration of triptolide ($1{\mu}g/10{\mu}l$). The triptolide could be a useful analgesic agent for the treatment of TMJ pain, and it is expected to reduce the substantial amount of it via co-administration of synthetic chemical compound and natural products.

Regulatory Role of Nitric Oxide on Atrial Natriuretic Peptide System in Normotensive and Hypertensive Rats

  • Choi, Eun-Hah;Kim, Mi-Won;Lee, Jong-Un
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.1
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    • pp.79-82
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    • 1997
  • The present study was aimed to explore an interaction between endothelium-derived nitric oxide (NO) and atrial natriuretic peptide (ANP) systems in normotensive and hypertensive states. Rats were made two-kidney, one clip (2K1C) hypertensive and supplemented with either $N^G-nitro-L-arginine$ methyl ester (L-NAME, 5 mg/100 ml drinking water) or L-arginine hydrochloride (400 mg/100 ml drinking water). One group supplied with normal tap water served as control. Sham-clipped rats were also divided into the L-NAME, L-arginine, and control groups. The plasma levels and atrial contents of ANP were determined at day 28 following clipping the renal artery. In 2K1C rats, the plasma level of ANP was higher and the atrial content was lower than in the sham-clipped control. L-Arginine increased the atrial content of ANP in association with a decreased plasma ANP, whereas L-NAME significantly affected neither parameter. The increase of blood pressure in 2K1C rats was not affected by L-arginine or L-NAME. In sham-clipped rats, the plasma level of ANP was significantly increased by L-NAME along with an increase in blood pressure. On the contrary, L-arginine did not affect the blood pressure or plasma ANP. The atrial content of ANP was significantly altered neither by L-arginine nor by L-NAME. These results suggest that NO plays a tonic inhibitory role on the ANP release with concomitant increases of the atrial tissue content. In addition, hypertension is suggested to modify the release and tissue storage of ANP.

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Kainic Acid-induced Neuronal Death is Attenuated by Aminoguanidine but Aggravated by L-NAME in Mouse Hippocampus

  • Byun, Jong-Seon;Lee, Sang-Hyun;Jeon, Seong-Ho;Kwon, Yong-Soo;Lee, Hee-Jae;Kim, Sung-Soo;Kim, Young-Myeong;Kim, Myong-Jo;Chun, Wan-Joo
    • The Korean Journal of Physiology and Pharmacology
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    • v.13 no.4
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    • pp.265-271
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    • 2009
  • Nitric oxide (NO) has both neuroprotective and neurotoxic effects depending on its concentration and the experimental model. We tested the effects of NG-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and aminoguanidine, a selective inducible NOS (iNOS) inhibitor, on kainic acid (KA)-induced seizures and hippocampal CA3 neuronal death. L-NAME (50 mg/kg, i.p.) and/or aminoguanidine (200 mg/kg, i.p.) were administered 1 h prior to the intracerebroventricular (i.c.v.) injection of KA. Pretreatment with L-NAME significantly increased KA-induced CA3 neuronal death, iNOS expression, and activation of microglia. However, pretreatment with aminoguanidine significantly suppressed both the KA-induced and L-NAME-aggravated hippocampal CA3 neuronal death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice ($iNOS^{-1-}$) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity.

Beneficial effects of Paeo-tang on cardiovascular and renal function in L-NAME-induced hypertensive rats (파어탕의 L-NAME 유도 고혈압 동물군에서의 혈압강하효과 및 심신기능 개선 효과)

  • Na, Se Won;Hong, Mi Hyeon;Kim, Hye Yoom;Jang, Youn Jae;Yoon, Jung Joo;Lee, Yun Jung;Kang, Dae Gill;Lee, Ho Sub
    • Herbal Formula Science
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    • v.28 no.3
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    • pp.271-280
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    • 2020
  • Hypertension has been approved to cause disharmony between the heart and kidney such as cardiac hypertrophy and kidney dysfunction. In traditional oriental medicine Paeo-tang (PET) has been shown to have effects on blood circulation improvement. However, the beneficial effect of PET on hypertension remains unknown. In this study, we investigated that PET attenuates blood pressure and improves cardiovascular and renal function in NG-nitro-L-arginine methylester (L-NAME) rat model. Hypertensive rat models were induced by the administration of L-NAME (40 mg/kg/day) and then PET (50 or 100 mg/kg/day) or Olmetec was treated for 2 weeks. PET treatment significantly suppressed the systolic blood pressure and decreased intima-media thickness in the thoracic aorta. PET ameliorated endothelium-dependent and independent vascular relaxation in the L-NAME-induced vascular dysfunction. PET ameliorated the functional decline in the kidney such as albumin and blood urea nitrogen in plasma. These results demonstrated that PET possesses protective effects against L-NAME-induced hypertension.

Antihypertensive Effects of the Methanol Extract of Sorbus Cortex in the Nitric Oxide-deficient Hypertensive Rat

  • Kang Dae-Gill;Sohn Eun-Jin;Choi Deok-Ho;Lee Seung-Ju;Lee Ho-Sub
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.20 no.1
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    • pp.181-186
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    • 2006
  • A pharmacological inhibition of nitric oxide synthase (NOS) in rats produces vasoconstriction, renal dysfunction, and hypertension. The present study was aimed at investigating whether the methanol extract of Serous commixta cortex (MSC) ameliorates $N^G$-nitro-L-arginine methylester (L-NAME) induced hypertension in rats. Treatment of rats with L-NAME (10 mg/kg/day in drinking water, 5 weeks) caused a sustained increase in systolic blood pressure (SBP). Administration of MSC (100 or 200 mg/kg/day, p.o) significantly lowered the SBP in the L-NAME-treated rats and this effect was maintained throughout the whole experimental period. Moreover, ecNOS expression in aorta and kidney tissue from L-NAME treated rats was significantly restored dy administration of MSC. Furthermore, the impairment of acetylcholine (ACh)-induced relaxation of aortic rings in the L-NAME treated rats was reversed dy administering of MSC. The renal functional parameters including urinary volume, sodium excretion, and creatinine clearance (Ccr) were also restored by administering MSC. Taken together, the present study suggeststhat MSC prevents the increase in SBP in rats with L-NAME-induced hypertension, which may result from the up-regulation of the vascular and renal ecNOS/No system.

Nitric Oxide Impairs the Recovery from Hemorrhagic Hypotension in Conscious Rats

  • Park, Yoon-Yub;Lee, Young-Man
    • The Korean Journal of Physiology and Pharmacology
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    • v.2 no.3
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    • pp.345-351
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    • 1998
  • The role of nitric oxide (NO) in the hemorrhagic hypotension was examined using a NO synthase inhibitor, $N^{\omega}-nitro-L-arginine$ methyl ester (L-NAME), in conscious rats. The rats were bled at a constant rate (2 ml/kg/min) through a femoral arterial catheter until the mean arterial pressure (MAP) was reduced by 50 mmHg. We studied the responses to hemorrhage under normal condition (Control) and after the pretreatment with 3 doses of L-NAME (1.6, 8, 40 mg/kg i.v. of NOX1.6, NOX8, and NOX40, respectively). Intravenous bolus injection of L-NAME produced a sustained increase in MAP and decrease in heart rate (HR). During hemorrhage, the MAP fell faster in the NOX8 and NOX40-treated groups than in Control group, but the control group showed same response to NOX1.6. HR greatly increased in NOX groups. The recovery from hemorrhagic hypotension was slowed in the control group, which was not treated with L-NAME. In comparison with the control group, NOX8 and NOX1.6-treated groups registered a significant recovery in MAP during the 15 min recovery period, but NOX40 brought about only a slight increase in MAP. NO precursor, L-arginine (150 mg/kg i.v.), produced significant bradycardic responses before and after hemorrhage and significant depressor response only after hemorrhagic hypotension regardless of pretreatment with L-NAME. These data suggest that the role of NO in blood pressure regulation is greater after hemorrhagic hypotension than basal condition, but the effect of NO can be detrimental to the recovery from hemorrhagic hypotension. In addition, the bradycardic response of L-arginine provides indirect evidence that NO may inhibit sympathetic activity, especially after hemorrhagic hypotension.

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Effect of Bangpoongtongsungsan on the Hypertention induced by L-NAME injection and SHR in Rats (방풍통성산(防風通聖散)이 L-NAME 유발 및 SHR 흰쥐의 고혈압에 미치는 영향)

  • Lee, Young-Hwa;Kim, Kyung-Chul;Lee, Yong-Tae
    • Journal of Oriental Physiology
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    • v.14 no.2 s.20
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    • pp.43-54
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    • 1999
  • In order to get the effect of Bangpoongtongsungsan (BPS) water extract on the blood pressure of every 5 group of rats (in normal state of after 3 hours of unanesthetized) was measured and following results were obtained. 1. BPS intraperitoneal injection was not recognized as having the effect of decreasing blood pressure compared with Control on hypertension induced by L-NAME in young rats. 2. BPS oral administration was recognized as having the effect of decreasing blood pressure compared with Control on hypertension induced by L-NAME in young rats. 3. BPS oral administration was recognized as having the effect of decreasing blood pressure compared with Control on hypertension induced by L-NAME's continual injection and BPS continual oral administration in young rats. 4. BPS oral administration was recognized as having the effect of decreasing blood pressure compared with Control on hypertension induced by L-NAME's in adult rats. 5. BPS oral administration was not recognized as having the effect of decreasing blood pressure compared with Control on spontaneous hypertension rats. According to the above results. it is known that BPS extract oral administration decreased the blood pressure of hypertension induced by and more effective to the youth.

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