Hjemdahl P, Fredholm B B
Acta Physiol Scand. 1976 Jul;97(3):319-24. doi: 10.1111/j.1748-1716.1976.tb10269.x.
Vasoconstriction due to parallel i.a. injections of NA were studied in subcutaneous adipose tissue and gracilis muscle preparations in dogs. The vasoconstrictor response to NA was significantly lower in adipose tissue than in muscle. Only in muscle did acidosis inhibit NA-induced vasoconstriction. The beta-receptor antagonist propranolol increased the vasoconstrictor response in adipose tissue to the level of skeletal muscle. The lack of significant inhibition of NA-induced vasoconstriction in adipose tissue may be due to the simultaneous inhibition of two opposing mechanisms-alpha-adrenergic vasoconstriction and beta-adrenergic vasodilatation. After propranolol acidosis inhibited NA-induced vasoconstriction equally in adipose tissue and muscle. The difference between adipose tissue and muscle may thus be due to a greater importance of a beta-adrenergic vasodilator mechanism in the former tissue. The metabolic response to isoprenaline was inhibited by acidosis, while the direct vasodilatation was unaffected. It is suggested that the beta-adrenergic vasodilator mechanism that is inhibited by acidosis is related to the metabolism of the tissue.
在犬的皮下脂肪组织和股薄肌制备物中,研究了通过股动脉平行注射去甲肾上腺素(NA)所引起的血管收缩。脂肪组织对NA的血管收缩反应明显低于肌肉。仅在肌肉中,酸中毒会抑制NA诱导的血管收缩。β受体拮抗剂普萘洛尔使脂肪组织中的血管收缩反应增加至骨骼肌的水平。脂肪组织中对NA诱导的血管收缩缺乏明显抑制作用,可能是由于两种相反机制同时受到抑制——α肾上腺素能血管收缩和β肾上腺素能血管舒张。普萘洛尔给药后,酸中毒在脂肪组织和肌肉中对NA诱导的血管收缩的抑制作用相同。因此,脂肪组织和肌肉之间的差异可能是由于β肾上腺素能血管舒张机制在前者组织中更为重要。酸中毒抑制了对异丙肾上腺素的代谢反应,而直接血管舒张不受影响。提示被酸中毒抑制的β肾上腺素能血管舒张机制与组织代谢有关。