Dorward P K, Bell L B, Rudd C D
Baker Medical Research Institute, Melbourne, Australia.
Hypertension. 1990 Aug;16(2):131-9. doi: 10.1161/01.hyp.16.2.131.
We have studied the effect of acute hypertensive episodes on the renal sympathetic baroreceptor reflex in conscious rabbits and the role played by cardiac afferents and endogenous opiate mechanisms. Renal sympathetic nerve activity was recorded during brief perivascular balloon-induced ramp changes in mean arterial pressure before and during 40-minute elevations in resting pressure. Methoxamine infusion was adjusted to increase pressure by +30 and +45 mm Hg in the presence of autonomic blockade of the heart with atenolol and methscopolamine. Experiments were repeated in other rabbits after blocking cardiac afferents with 5% intrapericardial procaine or during intravenous naloxone (4-6 mg/kg, then 0.12 mg/kg/min). We found a progressively severe attenuation of the renal sympathetic baroreceptor reflex during increasing elevations in resting pressure. The upper plateau and range of the reflex curve were both reduced by one third and two thirds during moderate and severe hypertension, respectively. The average gain fell by 64% and 87%, and the range-independent gain and hypotensive reversal response were also reduced. There was no resetting of the reflex to higher pressures as would be expected. One third of the reflex inhibition was prevented by blocking cardiac afferents; none of it was affected by intravenous naloxone, which had previously been shown to reverse the renal baroreceptor reflex depression elicited by hemorrhagic hypotension. Factors possibly responsible for the remaining two thirds of the hypertension-induced sympathoinhibition are suggested to be either central depression of sympathetic tone after elevation of arterial baroreceptor discharge during the hypertensive episode or additional inhibitory afferent input arising from the pulmonary circulation.
我们研究了急性高血压发作对清醒家兔肾交感压力感受器反射的影响，以及心脏传入神经和内源性阿片机制所起的作用。在静息压力升高40分钟之前和期间，通过短暂的血管周围气囊诱导平均动脉压呈斜坡式变化，记录肾交感神经活动。在使用阿替洛尔和甲基东莨菪碱对心脏进行自主神经阻滞的情况下，调整甲氧明输注量，使压力分别升高30和45 mmHg。在用5%的心包内普鲁卡因阻断心脏传入神经后，或在静脉注射纳洛酮（4 - 6 mg/kg，然后0.12 mg/kg/min）期间，在其他家兔身上重复进行实验。我们发现，随着静息压力升高幅度的增加，肾交感压力感受器反射逐渐严重减弱。在中度和重度高血压期间，反射曲线的上平台和范围分别降低了三分之一和三分之二。平均增益下降了64%和87%，与范围无关的增益和降压逆转反应也降低了。并未出现预期的反射向更高压力的重调定。阻断心脏传入神经可防止三分之一的反射抑制；静脉注射纳洛酮对其无影响，而纳洛酮此前已被证明可逆转出血性低血压引起的肾压力感受器反射抑制。导致高血压诱导的交感神经抑制中其余三分之二的可能因素被认为要么是高血压发作期间动脉压力感受器放电增加后交感神经张力的中枢性抑制，要么是来自肺循环的额外抑制性传入输入。
