外因性ノルエピネフリンに対する摘出イヌ内頸動脈標本の低反応性

The mode of low responsiveness of isolated canine internal carotid artery to exogenous norepinephrine

　一般に，頭蓋内血管のカテコラミン，セロトニン等の血管作動物質に対する反応性は，他の頭蓋外の血管群とは著しく異なる^3,9,16,19）。さらに，摘出したイヌの内頸動脈標本における血管作動物質に対する反応性にも，頭蓋内血管と同様の特徴が認められ，ノルエピネフリン（NE）による収縮は弱く，セロトニンに対して強い収縮反応を示す^5,19）。最近著者らは，内頸動脈と外頸動脈の反応性に差が存在することから，NE投与により両血管の分岐部において血流量の再分配が惹起されることを報告した^14）。しかしながら，内頸・外頸動脈の間に認められるこのNE反応性の差異がなぜ生じるかについては，いまだに不明の点が多い。

　本研究では，摘出したイヌの内頸・外頸動脈標本を用いて，1）血管壁平滑筋含量，2）交感神経ならびに神経外組織によるNE取り込み量，3） activator Caの起源の各観点から，両血管のNE反応性に差が生ずる原因について検討を加えた。

The response of isolated canine internal carotid artery to norepinephrine was compared with that of external carotid artery from the pharmacological and morpholo-gical points of view. Norepinephrine produced signifi-cantly greater contractions in the external carotid arteries than in the internal carotid arteries, although threshold doses of the contractile responses were not different. Cocaine (uptake 1 blocker) enhanced contra-ctile responses of the internal carotid arteries to low concentrations of norepinephrine, but did not in the external carotid arteries. The norepinephrine dose-response curves of the two carotid arteries, however, were not significantly affected by the pretreatment with hydrocortisone (uptake 2 blocker). Propranolol, beta adrenergic antagonist, had no effect on the responses of internal and external carotid arteries to norepinephrine. Verapamil dose-dependently suppressed the contractile response of the internal carotid artery to norepinephrine. The maximal contraction induced by 10_-4M norepine-phrine reduced to 39.0±7.0% and 8.0±1.7% of control in the presence of 10_-7M and 10_-6M of vera-pamil, respectively. On the other hand, in the external carotid arteries treated with 10_-7M and 10_-6M verapa-mil, the contractions induced by 10_-4M norepinephrine decreased to 67.2±5.7%and 37.8±1.9%, respectively. Thus, the reductions produced by two concentrations of verapamil in the external carotid artery were significa-ntly less than those in the internal carotid artery. In both arteries, norepinephrine (10_-7~10_-4M) caused no vasoconstriction in calcium-free Krebs solution containing 1mM EGTA. These results suggest that the differences in sources of activator calcium and in development of neuronal uptake mechanisms may account for the smaller contractile responses of internal carotid arteries to nor-epinephrine than those of external carotid arteries.