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首页> 外文期刊>American Journal of Physiology >Altered leptin signaling is sufficient, but not required, for hypotension associated with caloric restriction.
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Altered leptin signaling is sufficient, but not required, for hypotension associated with caloric restriction.

机译：瘦素信号改变对于与热量限制有关的低血压是足够的，但不是必需的。

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摘要

Caloric restriction of mammals leads to decreases in blood pressure and heart rate. Although relevant clinically, the mechanisms involved, in terms of hormones and signaling pathways invoked, are currently not known. Circumstantial evidence suggests that leptin signaling may be involved with the bradycardia and hypotension associated with caloric restriction. This hypothesis was specifically tested using leptin-deficient mice (ob/ob) or leptin-receptor rats (Koletsky). Ob/ob mice were hypertensive during the light cycle relative to littermate controls (108 +/- 2 vs. 100 +/- 2 mmHg, respectively). Both ob/ob mice and wild-type mice exhibited hypotension and bradycardia on initiation of a 50% caloric restriction regime, suggesting that the loss of leptin during caloric restriction is not required to explain the cardiovascular effects. Blood pressure in Koletsky rats did not drop in response to caloric restriction during the light cycle, whereas blood pressure in littermate control rats significantly dropped. These data suggest that at least two pathways are involved with cardiovascular effects of caloric restriction: one dependent on leptin signaling and the other independent of the leptin axis.
机译：哺乳动物的热量限制会导致血压和心率降低。尽管在临床上相关，但目前尚不了解所涉及的激素和信号传导途径的机制。间接证据表明，瘦素信号传导可能与心律不齐相关的心动过缓和低血压有关。使用瘦素缺陷型小鼠（ob / ob）或瘦素受体大鼠（Koletsky）专门测试了该假设。相对于同窝对照，Ob / ob小鼠在轻度周期内高血压（分别为108 +/- 2 vs. 100 +/- 2 mmHg）。 ob / ob小鼠和野生型小鼠在50％的热量限制机制启动时均表现出低血压和心动过缓，这表明热量限制期间瘦素的损失不需要解释心血管作用。轻度循环期间，Koletsky大鼠的血压并未因热量限制而下降，而同窝出生的对照组大鼠的血压却显着下降。这些数据表明，热量限制的心血管作用至少涉及两种途径：一种依赖于瘦素信号传导，另一种依赖于瘦素轴。

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