Ohnishi A, Li P, Branch R A, Holycross B, Jackson E K
J Clin Invest. 1987 Jul;80(1):13-6. doi: 10.1172/JCI113038.
The purpose of this study was to determine if caffeine augments the slow-pressor response to chronic low-dose infusions of angiotensin II (AII) or the rapid-pressor response to acute infusions of AII. AII was infused (125 ng/min i.p.) for 12 d via mini-osmotic pumps in four groups of rats: group I, intact rats not treated with caffeine (n = 9); group II, intact rats treated with caffeine (0.1% in drinking water, n = 9); group III, rats previously sympathectomized with 6-hydroxydopamine, but not treated with caffeine (n = 10); and group IV, rats previously sympathectomized with 6-hydroxydopamine and treated with caffeine (n = 10). Chronic low-dose AII infusions slowly elevated systolic blood pressure in all groups. Caffeine greatly augmented this slow-pressor response to AII in intact animals; however, caffeine failed to enhance AII-induced hypertension in sympathectomized rats. Caffeine pretreatment did not enhance the rapid-pressor response to acute intravenous infusions of AII. We conclude that caffeine augmented the slow-pressor effect of chronic low-dose infusions of AII via a mechanism that involved the sympathetic nervous system.
本研究的目的是确定咖啡因是否会增强对慢性低剂量输注血管紧张素II(AII)的缓慢升压反应或对急性输注AII的快速升压反应。通过微型渗透泵对四组大鼠腹腔内输注AII(125 ng/分钟),持续12天:第一组,未用咖啡因处理的完整大鼠(n = 9);第二组,用咖啡因处理的完整大鼠(饮用水中含0.1%,n = 9);第三组,先前用6-羟基多巴胺进行交感神经切除术但未用咖啡因处理的大鼠(n = 10);第四组,先前用6-羟基多巴胺进行交感神经切除术并经咖啡因处理的大鼠(n = 10)。慢性低剂量AII输注使所有组的收缩压缓慢升高。咖啡因极大地增强了完整动物对AII的这种缓慢升压反应;然而,咖啡因未能增强交感神经切除大鼠中AII诱导的高血压。咖啡因预处理并未增强对急性静脉输注AII的快速升压反应。我们得出结论,咖啡因通过一种涉及交感神经系统的机制增强了慢性低剂量输注AII的缓慢升压作用。