Krstić M K
Arch Int Pharmacodyn Ther. 1984 May;269(1):52-62.
The effect of SKF 525A (20 mg/kg i.v.) on pressor responses of various origin was studied. SKF 525A abolished or markedly reduced the pressor responses to ganglionic stimulants (DMPP and McN-A-343), but potentiated those to noradrenaline (in normal and pithed animals), adrenaline, tyramine, oxytocin and carotid occlusion. After recovery of the pressor effect of McN-A-343 from the SKF 525A-induced suppression, the pressor effect of noradrenaline was still further enhanced. The abolition of the pressor responses to ganglionic stimulants is due to the ganglion and adrenal-medullary blocking action of SKF 525A. This action of SKF 525A is of secondary importance for its potentiating effect. It is tentatively suggested that for the SKF 525A-induced potentiation a partial depolarization of arterial smooth muscle membrane resulting from a prolonged release of subthreshold concentrations of catecholamines from tissue stores, may be of primary importance.
研究了SKF 525A（静脉注射20毫克/千克）对各种来源的升压反应的影响。SKF 525A消除或显著降低了对神经节兴奋剂（DMPP和McN-A-343）的升压反应，但增强了对去甲肾上腺素（在正常和去脑动物中）、肾上腺素、酪胺、催产素和颈动脉闭塞的升压反应。在McN-A-343的升压作用从SKF 525A诱导的抑制中恢复后，去甲肾上腺素的升压作用仍进一步增强。对神经节兴奋剂升压反应的消除是由于SKF 525A的神经节和肾上腺髓质阻断作用。SKF 525A的这一作用对其增强作用而言是次要的。初步认为，对于SKF 525A诱导的增强作用，组织储存中阈下浓度的儿茶酚胺长时间释放导致动脉平滑肌膜部分去极化可能是主要的。
