Hypothalamic paraventricular nucleus mediates sodium-induced changes in cardiovascular and renal function in conscious sheep
Hypothalamic paraventricular nucleus mediates sodium-induced changes in cardiovascular and renal function in conscious sheep
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DOI：
10.1152/ajpregu.00058.2008
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发表时间：
2009-07-01
影响因子：
2.8
通讯作者：
Rundgren, Mats
中科院分区：
文献类型：
--
作者：
Frithiof, Robert;Ramchandra, Rohit;Rundgren, Mats
胡德江，胡德江，胡德江，胡德江，等。下丘脑室旁核在钠诱导的绵羊心血管和肾功能变化中的作用。[J] .中国生物医学工程学报，2009,31(2):559 - 563。2009年5月13日首次出版；doi: 10.1152 / ajpregu.00058.2008。-在有意识的绵羊中研究了下丘脑室旁核（PVN）在介导心血管、肾脏、激素和交感神经对脑脊液（CSF） [Na(+)]增加的反应中的作用。脑室内高渗NaCl （0.5 mol/l, 20 μ l/min，持续60 min）使动脉血压升高[AP；+13.4 (SD 2.0) mmHg, P < 0.001]和中心静脉压[CVP；+2.8 (SD 1.3) mmHg, P < 0.001]，但没有显著改变心率或心输出量（n = 6）。升高的CSF [Na(+)]也降低了血浆ANG II水平[-3.3 (SD 1.6) pmol/l, P = 0.004]，增加了肌酐清除率[+31.5 (SD 32.7) ml/min, P = 0.03]和肾钠排泄[+9.2 (SD 9.2) mmol/h, P = 0.003]。在ICV输注前向PVN注射利多卡因（1 μ l, 2%）本身无明显作用，但可以消除AP、CVP、肌酐清除率和ANG II对高渗NaCl的反应，并减少肾脏钠排泄的增加（n = 6）。随后的研究在有意识的绵羊中进行，长期植入电极来测量肾交感神经活动（RSNA）。在人工脑脊液500 nl中注射甘氨酸250 nmol pvn后，测定ICV高渗NaCl对AP和RSNA的影响。ICV NaCl升高AP，降低RSNA （P < 0.001）。甘氨酸显著降低了这些影响（P = 0.02-0.001, n = 5）。PVN内注射生理盐水（n = 5）或PVN外注射利多卡因（n = 6）对ICV高渗NaCl反应无影响。这些结果表明，PVN是脑诱导的钠浓度升高/高渗透压的稳态反应的重要介质。
Frithiof R, Ramchandra R, Hood S, May C, Rundgren M. Hypothalamic paraventricular nucleus mediates sodium-induced changes in cardiovascular and renal function in conscious sheep. Am J Physiol Regul Integr Comp Physiol 297: R185-R193, 2009. First published May 13, 2009; doi:10.1152/ajpregu.00058.2008.-The contribution of the paraventricular nucleus of the hypothalamus (PVN) in mediating cardiovascular, renal, hormonal, and sympathetic nerve responses to increased cerebrospinal fluid (CSF) [Na(+)] was investigated in conscious sheep. Intracerebroventricular hypertonic NaCl (0.5 mol/l, 20 mu l/min for 60 min) increased arterial blood pressure [AP; +13.4 (SD 2.0) mmHg, P < 0.001] and central venous pressure [CVP; +2.8 (SD 1.3) mmHg, P < 0.001], but did not significantly change heart rate or cardiac output (n = 6). Elevated CSF [Na(+)] also lowered plasma ANG II levels [-3.3 (SD 1.6) pmol/l, P = 0.004] and increased creatinine clearance [+31.5 (SD 32.7) ml/min, P = 0.03] and renal sodium excretion [+9.2 (SD 9.2) mmol/h, P = 0.003]. Lidocaine injection (1 mu l, 2%) into the PVN prior to the ICV infusion had no apparent effect per se, but it abolished the AP, CVP, creatinine clearance, and ANG II responses to hypertonic NaCl, as well as reducing the increase in renal sodium excretion (n = 6). Subsequent studies were performed in conscious sheep with chronically implanted electrodes for measurement of renal sympathetic nerve activity (RSNA). The effects of ICV hypertonic NaCl on AP and RSNA were measured before and after PVN-injection of glycine (250 nmol in 500 nl artificial CSF). ICV NaCl increased AP and decreased RSNA (P < 0.001). These effects were significantly reduced by glycine (P = 0.02-0.001, n = 5). Saline injected into the PVN (n = 5) or lidocaine injected outside the PVN (n = 6) had no effect on the response to ICV hypertonic NaCl. These results indicate that the PVN is an important mediator of cerebrally induced homeostatic responses to elevated sodium concentration/hyperosmolality.