1958 Volume 8 Pages 378-390
Experiments were performed on rabbits, dogs and cats and the followingresults were obtained.
1.γ-Aminobutyric acid caused fall of blood pressure accompanied with a slight bradycardia.
2. This acid had no direct action on the heart and the vessel following the administration of the dose effectual sufficiently on blood pressure.
3. The blood vessel of the spleen actively dilated.
But, this dilatation of the vessel in the spleen did not take place after the denervation.
4. The severance of the cervical vagi, the cervical sympathetics, the depressor nerves and the denervation of the carotid sini on both sides had no effect on the action of this acid on blood pressure. Bradycardia was more or less lessened, but the compelte disappearance hardly occurred by the section of the vagi.
5.γ-Aminobutyric acid showed no inhibiting effect on the superior cervical sympathetic ganglion of the cat. But, after the almost complete blockage of ganglia caused by tetraethyl-ammonium bromide or hexamethonium bromide, this acid affected no longer blood pressure.
6. In decerebrate animals, this acid showed the same effect as in the intact animal.
7. The latency of the fall of blood pressure was the shortest, when γ-aminobutyric acid was injected in the vertebral artery. The latency in the internal carotid injection was much longer than in the intravenous injection. The latency in the internal carotid injection was of the same order as in the injection into the subaxillary artery.
8. The intracisternal injection of γ-aminobutyric acid caused more marked and sustained fall of pressure than the intravenous injection. The inhibition of respiration became more evident. Bradycardia also took place.
9. The region of the central nervous system responsible for the effect of this acid was determined by means of transection of the brain stem and partial elimination of the medulla. The results revealed that the caudal part of the medulla was the concerned region.
10. The distribution of the points that responded with a fall in arterial pressure to topical application of this acid accorded with that of the depressor points stimulated electrically in the medulla.
11. The microinjection of γ-aminobutyric acid in the medial reticular formation of the medulla caused fall of pressure. The microinjection in the area postrema caused also fall of pressure. The minimal effective dose in microinjection was 0.5 μg in 10-3 ml.
12. It is inferred that γ-aminobutyric acid acts on the depressor points in the medulla and causes fall of blood pressure.