Shen Y T, Young M A, Ohanian J, Graham R M, Vatner S F
Department of Medicine, Harvard Medical School, Brigham and Women's and Massachusetts General Hospital, Boston.
Circ Res. 1990 Mar;66(3):647-61. doi: 10.1161/01.res.66.3.647.
This study addresses the hypothesis that atrial natriuretic factor (ANF) is a primary vasodilator, which reduces arterial pressure directly and increases total peripheral resistance secondarily by reflex mechanisms. The effects of 30-minute infusions of ANF (0.3 micrograms/kg/min i.v.) were examined in conscious dogs, rats, and monkeys before and after ganglionic blockade with hexamethonium. In seven intact, conscious dogs, ANF reduced mean arterial pressure by 7 +/- 1% and cardiac output by 19 +/- 3% and increased total peripheral resistance by 15 +/- 3%. After ganglionic blockade, ANF reduced mean arterial pressure by 7 +/- 2% but still increased total peripheral resistance by 15 +/- 3%. Similar results were observed in four dogs with total cardiac denervation and in six dogs with arterial baroreceptor denervation. Furthermore, in two dogs, combined ganglionic and alpha 1-adrenoceptor blockades failed to alter the rise in total peripheral resistance observed with ANF. In six intact, conscious rats, ANF reduced mean arterial pressure by 8 +/- 2% and cardiac output by 27 +/- 2% and increased total peripheral resistance by 27 +/- 5%. After ganglionic blockade, ANF still increased total peripheral resistance by 13 +/- 3%. In six intact, conscious monkeys, ANF reduced mean arterial pressure by 14 +/- 2% and cardiac output by 26 +/- 3% and increased total peripheral resistance by 17 +/- 3%. However, after ganglionic blockade. ANF decreased total peripheral resistance by 11 +/- 2%. These data provide evidence for a fundamental species difference in the vascular actions of ANF. In conscious dogs, ANF elicits "direct" vasoconstriction, which increases total peripheral resistance, even in the presence of denervation of reflexes or autonomic blockade. In conscious rats, ANF elicits both direct and reflexly mediated vasoconstriction. In conscious monkeys, although a component of direct vasoconstriction may also be present, the most prominent component appears to be reflexly mediated, since it was abolished by ganglionic blockade.
心房利钠因子(ANF)是一种主要的血管扩张剂,它直接降低动脉血压,并通过反射机制继而增加总外周阻力。在用六甲铵进行神经节阻断前后,对清醒的犬、大鼠和猴进行了30分钟静脉输注ANF(0.3微克/千克/分钟)的效应研究。在7只完整的清醒犬中,ANF使平均动脉压降低7±1%,心输出量降低19±3%,总外周阻力增加15±3%。神经节阻断后,ANF使平均动脉压降低7±2%,但仍使总外周阻力增加15±3%。在4只完全心脏去神经的犬和6只动脉压力感受器去神经的犬中观察到了类似结果。此外,在2只犬中,联合神经节和α1-肾上腺素能受体阻断未能改变ANF引起的总外周阻力升高。在6只完整的清醒大鼠中,ANF使平均动脉压降低8±2%,心输出量降低27±2%,总外周阻力增加27±5%。神经节阻断后,ANF仍使总外周阻力增加13±3%。在6只完整的清醒猴中,ANF使平均动脉压降低14±2%,心输出量降低26±3%,总外周阻力增加17±3%。然而,神经节阻断后,ANF使总外周阻力降低11±2%。这些数据为ANF血管作用中存在基本的物种差异提供了证据。在清醒犬中,ANF引起“直接”血管收缩,即使在反射去神经或自主神经阻断的情况下,也会增加总外周阻力。在清醒大鼠中,ANF引起直接和反射介导的血管收缩。在清醒猴中,虽然可能也存在直接血管收缩成分,但最突出的成分似乎是反射介导的,因为它被神经节阻断所消除。