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心房利钠因子生理学的最新进展。

An update on the physiology of atrial natriuretic factor.

作者信息

Trippodo N C

机构信息

Division of Research, Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121.

出版信息

Hypertension. 1987 Nov;10(5 Pt 2):I122-7. doi: 10.1161/01.hyp.10.5_pt_2.i122.

Abstract

The atrial natriuretic factor (ANF) has pharmacological actions resulting in lower atrial and arterial pressures. Atrial distention stimulates ANF release, suggesting that ANF is an effector limb of a feedback loop for controlling cardiac filling pressure. To test this hypothesis it will be necessary to determine whether physiological atrial distention releases ANF in sufficient amounts to exert biological actions. Immunoblockade of endogenous ANF and attenuation of ANF release by atrial ablation inhibited volume-induced natriuresis in rats. Infusion of ANF in rats at doses mimicking those observed during experimental volume expansion produced a natriuresis sufficient to partly account for the volume-induced response. Infusion of ANF at doses expected to change plasma ANF levels minimally decreased arterial pressure in hypertensive rats over 7 days. In dogs, some studies suggest that increased plasma ANF levels following experimental changes in atrial pressure were not sufficient to exert acute cardiovascular or renal actions, whereas others support such a notion and indicate that ANF inhibited barostimulated renal renin release. This last action could alter arterial pressure in the long term by allowing sodium equilibrium at lower renal arterial pressure. Infusion of ANF in humans that produced plasma levels in the upper physiological range caused increased sodium excretion and decreased plasma renin activity. Although data are exiguous, justifying neither acceptance nor rejection of the hypothesis that ANF functions physiologically to regulate body fluid volume and arterial pressure, the current evidence slightly favors acceptance.

摘要

心房利钠因子(ANF)具有药理作用,可降低心房压和动脉压。心房扩张刺激ANF释放,这表明ANF是控制心脏充盈压的反馈回路的效应环节。为了验证这一假设,有必要确定生理性心房扩张是否能释放足够量的ANF以发挥生物学作用。内源性ANF的免疫阻断和心房切除对ANF释放的减弱抑制了大鼠容量诱导的利钠作用。以模拟实验性容量扩张期间观察到的剂量向大鼠输注ANF可产生足以部分解释容量诱导反应的利钠作用。以预期对血浆ANF水平影响最小的剂量向高血压大鼠输注ANF,在7天内可降低动脉压。在犬类中,一些研究表明,心房压力实验性改变后血浆ANF水平的升高不足以发挥急性心血管或肾脏作用,而其他研究则支持这一观点,并表明ANF抑制压力感受器刺激的肾脏肾素释放。这一最后的作用可通过在较低的肾动脉压下实现钠平衡而长期改变动脉压。向人体输注能使血浆水平处于生理范围上限的ANF可导致钠排泄增加和血浆肾素活性降低。尽管数据稀少,既不能证实也不能否定ANF在生理上发挥作用以调节体液容量和动脉压这一假设,但目前的证据略倾向于接受该假设。

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