Role of endogenous nitric oxide in the nucleus tratus solitarii on baroreflex control of heart rate in spontaneously hypertensive rats

Role of endogenous nitric oxide in the nucleus tratus solitarii on baroreflex control of heart rate in spontaneously hypertensive rats
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DOI:
10.1097/00004872-199816121-00021
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发表时间:
1998-12-01
影响因子:
4.9
通讯作者:
Michelini, LC
Michelini, LC
中科院分区:
医学2区
文献类型:
--
作者:
Pontieri, V;Venezuela, MK;Michelini, LC

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目的观察清醒自发性高血压(SHR)和正常血压(WKY)大鼠孤束核(NTS)内内源性一氧化氮(NO)对压力感受性反射控制心率的调节作用。在将载体(3 nl/min)N-G-单甲基-L-精氨酸(L-NMMA)和L-精氨酸(L-Arg)输注到NTS中期间记录压力感受器(苯丙氨酸/硝普钠,iv)加载/卸载期间的鼻压(AP)、心率(HR)和反射HR反应。通过其他SHR组和WKY组的背侧脑干中H-3-瓜氨酸的形成来推断组成型NO合酶(NOS)活性。(30 ng/kg/min)仅限于NTS,未改变AP和HR(分别为185 +/- 4 mmHg,373 +/- 12次/分),但HR范围缩小(57 +/- 7次/分,减少34%,P< 0.05)而不进一步改变HR的压力感受器反射控制的受损增益,在WKY组中,仅在高10倍剂量(L-NMMA(NTS)= 300 ng/kg/min)下获得相似结果(HR范围显著降低32%,增益不变),在小剂量下未观察到影响(HR范围= 163 +/- 12次/min)。在SHR中,L-Arg(NTS)(900 ng/kg/min)不能改善HR的压力反射控制,但在L-NMMA(NTS)后给予L-Arg(NTS)时,恢复了HR范围的抑制。结论在NTS水平,NO对SHR和WKY大鼠的压力感受性反射控制的调节作用不是通过改变增益,而是通过增加传入刺激时的HR幅度。J Hypertens 1998,16:1993-1999(C)1998 Lippincott威廉姆斯& Wilkins.
Objective Toinvestigate the modulatory effect of endogenous nitric oxide (NO) in the nucleus tractus solitarii (NTS) on the baroreceptor reflex control of heart rate in conscious spontaneously hypertensive (SHR) and normotensive (WKY) rats.Design and methods Male age- and weight-matched SHR and WKY chronically instrumented with cannulas in the NTS, artery and vein were used. nasal pressure (AP), heart rate (HR) and reflex HR responses during loading/unloading of baroreceptors (phenylephrine/ sodium nitroprusside, iv) were recorded during vehicle (3 nl/min) N-G-monomethyl-L-arginine (L-NMMA) and L-arginine (L-Arg) infusions into the NTS. Constitutive NO synthase (NOS) activity was inferred by H-3-citrulline formation in the dorsal brain stem of other SHR and WKY groups.Results In SHR a small dose of L-NMMA (30 ng/kg/min) restricted to the NTS did not change AP and HR (185 +/- 4 mmHg, 373 +/- 12 beats/min, respectively), but decreased the HR range (57 +/- 7 beats/min, a 34% reduction, P< 0.05) without changing further the impaired gain of baroreceptor reflex control of HR, In the WKY group similar results (significant 32% reduction in HR range, gain unchanged) were only attained with a dose 10 times higher (L-NMMA(NTS) = 300 ng/kg/min), no effect being observed with the small dose (HR range = 163 +/- 12 beats/min). In SHR, L-Arg(NTS) (900 ng/kg/min) did not improve baroreflex control of HR, but restored the depression of HR range when given after L-NMMA(NTS). Basal NOS activity in the dorsal brain stem was reduced in SHR (P< 0.05) when compared to WKY group.Conclusions NO modulates, at the NTS level, the baroreceptor reflex control of HR in both SHR and WKY not by altering the gain, but by increasing HR range during afferent stimulation In SHR the depressed NO modulation is in accordance with the smaller NOS activity in the dorsal brain stem. J Hypertens 1998, 16:1993-1999 (C) 1998 Lippincott Williams & Wilkins.