Takeshita A, Mark A L, Brody M J
Am J Physiol. 1979 Jan;236(1):H48-52. doi: 10.1152/ajpheart.1979.236.1.H48.
Salt-induced hypertension in Dahl's genetically hypertensive rat has been attributed to humoral or renal factors. However, a recent study from our laboratory suggested that neurogenic mechanisms contribute to salt-induced increased in hindquarters vascular resistance in Dahl salt-sensitive (S) rats. In the present study, we examined the hypothesis that "chemical sympathectomy" with 6-hydroxydopamine (6-OHDA) prevents salt-induced hypertension and increased vascular resistance in S rats. Hypertension did not develop during high-salt diet (8% NaCl) in S rats treated with 6-OHDA, (75--100 mg/kg ip), whereas in rats treated with vehicle, hypertension developed after 4 wk of high salt diet. Chow consumption, sodium excretion, and weight gain were not altered by 6-OHDA. Hindquarters vascular resistance and neurogenic vasoconstrictor tone were significantly lower in S rats treated with 6-OHDA than in S rats treated with vehicle. 6-OHDA also significantly reduced responses to direct sympathetic nerve stimulation and tyramine. These results suggest that an intact sympathetic nervous system plays an essential role in the development of salt-induced increase in blood pressure in Dahl S rats.
达尔遗传性高血压大鼠的盐诱导性高血压一直被归因于体液或肾脏因素。然而,我们实验室最近的一项研究表明,神经源性机制导致了达尔盐敏感(S)大鼠后肢血管阻力因盐诱导而增加。在本研究中,我们检验了以下假设:用6-羟基多巴胺(6-OHDA)进行“化学交感神经切除术”可预防S大鼠的盐诱导性高血压和血管阻力增加。在用6-OHDA(75 - 100 mg/kg腹腔注射)处理的S大鼠中,高盐饮食(8%氯化钠)期间未出现高血压,而在用赋形剂处理的大鼠中,高盐饮食4周后出现了高血压。6-OHDA未改变食物摄入量、钠排泄量和体重增加。用6-OHDA处理的S大鼠的后肢血管阻力和神经源性血管收缩张力显著低于用赋形剂处理的S大鼠。6-OHDA还显著降低了对直接交感神经刺激和酪胺的反应。这些结果表明,完整的交感神经系统在达尔S大鼠盐诱导性血压升高的发展中起重要作用。