Interleukin-1β and neurogenic control of blood pressure in normal rats and rats with chronic renal failure
Interleukin-1β and neurogenic control of blood pressure in normal rats and rats with chronic renal failure
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DOI：
10.1152/ajpheart.2000.279.6.h2786
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发表时间：
2000-12-01
影响因子：
4.8
通讯作者：
Campese, VM
中科院分区：
文献类型：
--
作者：
Ye, SH;Mozayeni, P;Campese, VM
交感神经系统（SNS）活动的增加在慢性肾衰竭（CRF）大鼠高血压的发生中起作用。神经元一氧化氮合酶（NOS） mRNA的局部表达和NO2/NO3的生成增加，减轻了中枢SNS活性的升高。由于白细胞介素(IL)-1 β可能激活大脑中的一氧化氮，我们已经验证了IL-1 β可能通过调节CRF和对照大鼠大脑中神经元NOS （nNOS）的局部表达来调节SNS活性的假设。为此，我们首先发现在对照组和CRF大鼠侧脑室给予IL-1 β降低血压和下丘脑后部（PH）的去甲肾上腺素（NE）分泌，并增加NOS mRNA表达。其次，我们观察到在侧脑室急性或慢性注射IL-1 β特异性抗体会升高对照组和CRF大鼠的血压和PH的NE分泌，并降低PH的NOS mRNA丰度。最后，我们通过RT-PCR检测了CRF大鼠和对照组大鼠PH、蓝斑核和室旁核中IL-1 β mRNA的丰度，发现CRF大鼠的IL-1 β mRNA丰度高于对照组大鼠。总之，这些研究表明，IL-1 β调节中枢神经系统SNS的活性，这种调节是通过局部nNOS mRNA表达增加介导的。
Increased sympathetic nervous system (SNS) activity plays a role in the genesis of hypertension in rats with chronic renal failure (CRF). The rise in central SNS activity is mitigated by increased local expression of neuronal nitric oxide synthase (NOS) mRNA and NO2/NO3 production. Because interleukin (IL)-1 beta may activate nitric oxide in the brain, we have tested the hypothesis that IL-1 beta may modulate the activity of the SNS via regulation of the local expression of neuronal NOS (nNOS) in the brain of CRF and control rats. To this end, we first found that administration of IL-1 beta in the lateral ventricle of control and CRF rats decreased blood pressure and norepinephrine (NE) secretion from the posterior hypothalamus (PH) and increased NOS mRNA expression. Second, we observed that an acute or chronic injection of an IL-1 beta -specific antibody in the lateral ventricle raised blood pressure and NE secretion from the PH and decreased NOS mRNA abundance in the PH of control and CRF rats. Finally, we measured the IL-1 beta mRNA abundance in the PH, locus coeruleus, and paraventricular nuclei of CRF and control rats by RT-PCR and found it to be greater in CRF rats than in control rats. In conclusion, these studies have shown that IL-1 beta modulates the activity of the SNS in the central nervous system and that this modulation is mediated by increased local expression of nNOS mRNA.