Contribution of afferent renal nerve signals to acute and chronic blood pressure regulation in stroke-prone spontaneously hypertensive rats
Contribution of afferent renal nerve signals to acute and chronic blood pressure regulation in stroke-prone spontaneously hypertensive rats
复制标题
DOI：
10.1038/s41440-022-01091-z
复制
发表时间：
2022-11
影响因子：
5.4
通讯作者：
S. Ikeda;Keisuke Shinohara;Soichiro Kashihara;Sho Matsumoto;D. Yoshida;Ryosuke Nakashima;Y. Ono;Masaaki Nishihara;Kenichi Katsurada;H. Tsutsui
中科院分区：
文献类型：
--
作者：
S. Ikeda;Keisuke Shinohara;Soichiro Kashihara;Sho Matsumoto;D. Yoshida;Ryosuke Nakashima;Y. Ono;Masaaki Nishihara;Kenichi Katsurada;H. Tsutsui
交感神经系统的激活在高血压的发生发展中起着至关重要的作用。肾传入神经的传入可能影响中枢性交感神经流出，但其在高血压发病中的作用尚不清楚。我们用血压正常的Wistar-京都大鼠(WKY)和易卒中的自发性高血压大鼠(SHRSP)研究了肾传入神经在急、慢性血压调节中的作用。与WKY相比，急性化学刺激肾传入神经可引起9周龄SHRSP幼鼠血压和肾交感神经活动的较大幅度增加。选择性去传入肾神经(ARDN)和常规全肾去神经(TRDN)均能抑制慢性血压升高，但对SHRSP的慢性血压升高无明显影响。ARDN不影响血浆肾素活性或血浆血管紧张素II水平，而TRDN则两者均降低。TRDN和ARDN均不影响中枢交感神经流出和全身交感神经活动，分别由下丘脑室旁核和延髓头端腹外侧区的神经元活动和血、尿去甲肾上腺素水平决定。与WKY相比，青年SHRSP的肾脏损伤不明显，提示青年SHRSP的肾传入输入可能未被激活。结论：尽管SHRSP患者对肾传入神经的急性刺激可引起血压升高，但肾传入神经的慢性传入并不促进SHRSP高血压的发生。肾传出神经可能通过激活SHRSP的肾素-血管紧张素系统参与高血压的发生发展。
The activation of sympathetic nervous system plays a critical role in the development of hypertension. The input from afferent renal nerves may affect central sympathetic outflow; however, its contribution to the development of hypertension remains unclear. We investigated the role of afferent renal nerves in acute and chronic blood pressure regulation using normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). Acute chemical stimulation of afferent renal nerves elicited larger increases in blood pressure and renal sympathetic nerve activity in young 9-week-old SHRSP compared to WKY. Selective afferent renal denervation (ARDN) and conventional total renal denervation (TRDN) ablating both afferent and efferent nerves in young SHRSP revealed that only TRDN, but not ARDN, chronically attenuated blood pressure elevation. ARDN did not affect plasma renin activity or plasma angiotensin II levels, whereas TRDN decreased both. Neither TRDN nor ARDN affected central sympathetic outflow and systemic sympathetic activity determined by neuronal activity in the parvocellular region of hypothalamic paraventricular nucleus and rostral ventrolateral medulla and by plasma and urinary norepinephrine levels, respectively. Renal injury was not apparent in young SHRSP compared with WKY, suggesting that renal afferent input might not be activated in young SHRSP. In conclusion, the chronic input from afferent renal nerves does not contribute to the development of hypertension in SHRSP despite the increased blood pressure response to the acute stimulation of afferent renal nerves. Efferent renal nerves may be involved in the development of hypertension via activation of the renin-angiotensin system in SHRSP.