INCREASED SODIUM APPETITE IN THE RAT INDUCED BY INTRA-CRANICAL ADMINISTRATION OF COMPONENTS OF THE RENIN-ANGIOTENSIN SYSTEM
INCREASED SODIUM APPETITE IN THE RAT INDUCED BY INTRA-CRANICAL ADMINISTRATION OF COMPONENTS OF THE RENIN-ANGIOTENSIN SYSTEM
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DOI：
10.1113/jphysiol.1980.sp013210
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发表时间：
1980-01-01
影响因子：
5.5
通讯作者：
FITZSIMONS, JT
中科院分区：
文献类型：
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作者：
AVRITH, DB;FITZSIMONS, JT
大鼠在正常水和钠平衡条件下，脑内注射肾素-血管紧张素系统各组分，在持续18小时的试验过程中，立即引起口渴，随后钠的食欲逐渐增加，对水和钠摄入量的影响呈剂量依赖关系。长期(7天)将血管紧张素II以1或10pmol/h的速度注入第三脑室，可显著增加水和2.7%氯化钠的摄入量。每天的摄入量有时超过100毫升2.7%氯化钠，但在停止输液后很快就恢复正常。颅内注射或输注卡巴胆碱可引起一过性摄水量增加，但对2.7%氯化钠的摄入量无影响。由于大鼠可以选择水，等摩尔浓度的氯化钠和氯化钾只摄入水和氯化钠，所以血管紧张素诱导的钠的食欲是钠所特有的。这类似于钠缺乏大鼠的情况。钠的食欲增加并不是水摄入量增加的次要原因，因为它发生在只有2.7%的氯化钠可供饮用的时候。由于血管紧张素刺激的大鼠进入正钠平衡，钠摄取增加并不继发于钠排出增加，而颅内肾素不能引起钠负荷大鼠钠排泄增加，无尿大鼠对肾素的反应表现出明显的钠摄取。大脑中的血管紧张素可能在钠的食欲发育中起作用。
Intracranial injections of components of the renin-angiotensin system in rats in normal water and Na balance caused an immediate thirst followed by a progressive increase in Na appetite during a test session which lasted 18 h. The effect on water and Na intake was dose-dependent. Long-term (7 day) infusions of angiotensin II into the 3rd cerebral ventricle at rates of 1 or 10 pmol/h produced large and sustained increases in intake of water and 2.7% NaCl. Intakes sometimes exceeded 100 ml 2.7% NaCl per day but quickly fell to normal when the infusion was stopped. Intracranial injection or infusion of carbachol caused a transient increase in water intake but had no effect on the intake of 2.7% NaCl. The Na appetite induced by intracranial injection of angiotensin was specific for Na since rats offered a choice of water and equimolar concentrations of NaCl and KCl took only water and NaCl. This resembles the pattern seen in Na-depleted rats. Increased Na appetite was not secondary to increased water intake since it occurred when only 2.7% NaCl was available to drink. Increased Na appetite was not secondary to natriuresis since the angiotensin-stimulated rats went into positive Na balance and, intracranial renin did not cause increased Na excretion in Na-loaded rats and anuric rats showed a significant Na appetite in response to renin. Angiotensin in the brain may play a role in the development of Na appetite.