| Japanese |
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| Title | 体液と循環調節に対するVasopressinの作用とその中枢性調節機序 |
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| Subtitle | 特集 誌上シンポジウム ＝循環制御機構における神経・体液性因子の相互作用＝ |
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| Authors | 木村時久 |
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| Authors(kana) | |
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| Organization | 東北大学医学部第2内科 |
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| Journal | 循環制御 |
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| Volume | 14 |
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| Number | 3 |
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| Page | 261-266 |
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| Year/Month | 1993/ |
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| Article | 報告 |
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| Publisher | 日本循環制御医学会 |
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| Abstract | 「1. はじめに」体液や循環系の恒常性は主として交感神経系による心血管系の調節と腎におけるレニン−アンギオテンシン−アルドステロン(RAA)系およびバゾプレッシン(AVP)による水電解質代謝の調節と食塩や水分の摂取により維持されている. また, 体液の内部環境の変化は頸動脈や大動脈弓の高圧系にある圧受容体と心房等の低圧系にある容量受容体で感知し, 求心路(舌咽, 迷走神経)を介して延髄の血管運動中枢にいたる. この情報はさらに視床下部の高位の中枢で制御され液性または神経性因子を介して再び末梢にフィードバックされる. また, 体液の浸透圧の変化は視床下部の浸透圧受容体で感知され, 直接中枢に伝達されて, AVP分泌や飲水行動を制御する. これらの調整系の内, AVPは視床下部で産生され, その分泌が圧, 容量および浸透圧受容体により調節を受け, 心血管系(V1受容体)や腎水電解質代謝(V2受容体)に関与する多彩な生理作用を持つホルモンである(図1). |
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| Practice | 基礎医学・関連科学 |
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| English |
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| Title | Effects of vasopressin (AVP) on cardiovascular function and of central regulatory mechanisms on AVP release and blood pressure. |
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| Subtitle | |
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| Authors | Tokihisa Kimura |
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| Authors(kana) | |
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| Organization | The Second Department of Internal Medicine Tohoku University School of Medicine |
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| Journal | Circulation Control |
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| Volume | 14 |
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| Number | 3 |
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| Page | 261-266 |
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| Year/Month | 1993/ |
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| Article | Report |
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| Publisher | Japan Society of Circulation Control |
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| Abstract | The present study was undertaken not only to investigate effects of vasopressin (AVP) release in response to iv infusion of hypertonic NaCl on cardiovascular function and artial natriuretic peptide (ANP) release via V1 or V2 receptor in anesthetized anephric dogs, but also effects of hormones and neurotransmitters in the brain on AVP release and blood pressure in dogs or rats. V1 receptors decreased cardiac output (CO) and heart rate (HR) with increased total peripheral resistance (TPR), thereby resulting in decreased mean arterial blood pressure (MAP). V2 receptors increased MAP and HR with decreased TPR, but did not affect CO. AVP release in response to hypertonic NaCl was attenuated in anephric state, but bilateral vagotomy restored the AVP response to osmotic stimulation. ANP release was influenced by changes in plasma AVP, blood volume and cardiovascular function. Norepinephrine given intracerebroventricularly (icv) increased AVP release and MAP via α1 adrenoceptors, but decreased them via α2 adrenoceptors. Isopreterenole decreased MAP, without any changes in AVP release, and dopamine depressed AVP release and MAP. Icv acetlylcholine elevated AVP release and MAP via its nicotinic receptors, but depressed them via its muscarinic receptors. Icv anagiotensin II increased AVP release and MAP under iv infusion of hypertonic saline. Icv endothelin and interleukin also increased AVP release and MAP, but ANP decreased AVP release without changes in MAP. |
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| Practice | Basic medicine |
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