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肾素-血管紧张素系统与钠食欲。

The renin-angiotensin system and sodium appetite.

作者信息

Fitzsimons J T, Wirth J B

出版信息

J Physiol. 1978 Jan;274:63-80. doi: 10.1113/jphysiol.1978.sp012134.

Abstract
  1. Bilateral nephrectomy or bilateral ureteric ligation greatly reduced the intake and retention of sodium in sodium-depleted adrenalectomized rats which were experienced at drinking aversive concentrations of saline and which otherwise would have drunk and retained substantial quantities of sodium.2. Pharmacological activation of the renin-angiotensin system with isoprenaline or phentolamine caused increased intake of water but did not stimulate sodium appetite in sodium-replete adrenalectomized rats, and decreased sodium appetite in sodium-depleted adrenalectomized animals.3. Neither I.P. injections of renin nor intravenous infusions of angiotensin II stimulated sodium appetite in normal rats or sodium-replete adrenalectomized rats.4. No differences were found in the saline preference-aversion curves of normal rats not maintained on saline given intracranial injections of angiotensin II or carbachol.5. Preoptic injections of renin, renin substrate or angiotensin II into sodium-replete adrenalectomized rats which were maintained on water and 2.7% saline induced immediate thirst followed by some saline intake. The saline intake was markedly less than the spontaneous saline intake of the same rats when sodium depleted.6. Similar preoptic injections in sodium-depleted adrenalectomized rats caused increased water intake but did not increase the saline intake any further.7. Intracranial injections of carbachol had little effect on saline intake in either sodium-replete or sodium-depleted adrenalectomized rats but caused increased water intake.8. In conclusion, peripheral activation of the renin-angiotensin system stimulates water intake but has no direct effect on sodium appetite. Secondly, central administration of components of the renin-angiotensin system causes thirst and does not inhibit sodium appetite whereas centrally administered carbachol causes thirst and inhibits sodium appetite. Therefore the renin-angiotensin system has only a minor role in sodium appetite.
摘要
  1. 双侧肾切除术或双侧输尿管结扎术极大地降低了钠缺乏的肾上腺切除大鼠对钠的摄取和潴留,这些大鼠对饮用具有厌恶浓度的盐水有经验,否则它们会饮用并潴留大量的钠。

  2. 用异丙肾上腺素或酚妥拉明对肾素 - 血管紧张素系统进行药理激活,可使钠充足的肾上腺切除大鼠的水摄入量增加,但不刺激其钠食欲,而使钠缺乏的肾上腺切除动物的钠食欲降低。

  3. 腹腔注射肾素或静脉输注血管紧张素II均未刺激正常大鼠或钠充足的肾上腺切除大鼠的钠食欲。

  4. 对未持续饮用盐水的正常大鼠进行颅内注射血管紧张素II或卡巴胆碱后,其盐水偏好 - 厌恶曲线未发现差异。

  5. 对维持饮水和2.7%盐水的钠充足的肾上腺切除大鼠进行视前区注射肾素、肾素底物或血管紧张素II,会立即引起口渴,随后有一些盐水摄入。当钠缺乏时,这些大鼠的盐水摄入量明显低于其自发的盐水摄入量。

  6. 对钠缺乏的肾上腺切除大鼠进行类似的视前区注射,会导致水摄入量增加,但不会进一步增加盐水摄入量。

  7. 颅内注射卡巴胆碱对钠充足或钠缺乏的肾上腺切除大鼠的盐水摄入量影响很小,但会导致水摄入量增加。

  8. 总之,肾素 - 血管紧张素系统的外周激活刺激水摄入,但对钠食欲无直接影响。其次,肾素 - 血管紧张素系统成分的中枢给药会引起口渴且不抑制钠食欲,而中枢给药的卡巴胆碱会引起口渴并抑制钠食欲。因此,肾素 - 血管紧张素系统在钠食欲中仅起次要作用。

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The renin-angiotensin system and sodium appetite.肾素-血管紧张素系统与钠食欲。
J Physiol. 1978 Jan;274:63-80. doi: 10.1113/jphysiol.1978.sp012134.
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Angiotensin, thirst, and sodium appetite.血管紧张素、口渴与钠食欲。
Physiol Rev. 1998 Jul;78(3):583-686. doi: 10.1152/physrev.1998.78.3.583.

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3
Aldosterone-elicited sodium appetite.
Endocrinology. 1971 Aug;89(2):538-44. doi: 10.1210/endo-89-2-538.
5
A flexible technique for long term infusions in unrestrained rats.
Pharmacol Biochem Behav. 1974 Jan-Feb;2(1):131-6. doi: 10.1016/0091-3057(74)90147-6.
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Thirst.口渴
Physiol Rev. 1972 Apr;52(2):468-561. doi: 10.1152/physrev.1972.52.2.468.

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