Neural and hormonal control of blood pressure in conscious monkeys.

Neural and hormonal control of blood pressure in conscious monkeys.
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清醒猴子血压的神经和激素控制。

DOI:
10.1152/ajpheart.1990.258.1.h107
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发表时间:
1990
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Iaffaldano,R
Iaffaldano,R
中科院分区:
--
文献类型:
--
作者:
Cornish,KG;Barazanji,MW;Iaffaldano,R

文献摘要

相似文献

研究了自主神经系统、血管紧张素II (ANG II)和精氨酸抗利尿素(AVP)对12只长期使用仪器的系留猴子血压(BP)的控制作用。将抗利尿激素拮抗剂[d(CH2)5AVP] (Manning Compound, MC)、ANG II拮抗剂saralasin (SAR)和神经节阻断药物六甲氧铵(Hx)按随机顺序注射到左心房(LA),同时监测血压和心率(HR)。当作为第一拮抗剂给予时,MC引起血压轻微下降;无论给药顺序如何,SAR都没有显著降低血压,而Hx则导致血压持续下降35-50 mmHg。另外7只动物(4只完整,3只肾去神经)参与出血实验。出血后血压降至50-60 mmHg,然后自行恢复。出血结束后10 ~ 15 min给予MC。当血压稳定后,给予SAR。出血后血压恢复到80 - 90mmhg。MC对血压恢复无影响;然而,萨拉拉西素将其降低到出血后的水平。我们可以得出结论,在有意识的灵长类动物中,交感神经系统是BP的主要控制机制,AVP只起了很小的作用。肾素的释放似乎主要受交感神经系统的控制。
The contribution of the autonomic nervous system, angiotensin II (ANG II), and arginine vasopressin (AVP) to the control of blood pressure (BP) was examined in 12 chronically instrumented tethered monkeys. The vasopressin antagonist, [d(CH2)5AVP] (Manning Compound, MC), the ANG II antagonist, saralasin (SAR), and the ganglionic blocking drug, hexamethonium (Hx), were injected in a random sequence into the left atrium (LA) while BP and heart rate (HR) were monitored. When given as the first antagonist, MC caused a slight decrease in BP; SAR did not significantly decrease BP regardless of the sequence of administration, whereas Hx caused a consistent decrease in blood pressure of 35–50 mmHg. Seven (4 intact and 3 with renal denervation) additional animals were involved in hemorrhage experiments. Blood pressure was reduced to 50–60 mmHg by hemorrhage and then allowed to return spontaneously. Ten to 15 min after the end of the hemorrhage, MC was given. When blood pressure had stabilized, SAR was given. Blood pressure returned to 80–90 mmHg after the hemorrhage. MC did not affect the blood pressure recovery; however, saralasin reduced it to the post-hemorrhage levels. We would conclude that the sympathetic nervous system is the primary controlling mechanism for BP in the conscious primate, with AVP making a minor contribution. The release of renin would appear to be primarily under the control of the sympathetic nervous system.