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首页> 外文期刊>American Journal of Physiology >Hypotension and bradycardia during caloric restriction in mice are independent of salt balance and do not require ANP receptor.
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Hypotension and bradycardia during caloric restriction in mice are independent of salt balance and do not require ANP receptor.

机译：小鼠热量限制期间的低血压和心动过缓与盐平衡无关，不需要ANP受体。

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We hypothesized that caloric restriction (CR)-induced hypotension would correlate with increased sodium excretion through an atrial natriuretic peptide (ANP)-dependent mechanism. To test this hypothesis, the cardiovascular parameters of c57/Bl mice were measured with radiotelemetry while urine was collected. The 23-h mean blood pressure (BP) dropped from 108.6 +/- 1.8 to 92.7 +/- 2.4 mmHg, and 23-h heart rate dropped from 624 +/- 5 to 426 +/- 13 beats/min over 7 days of CR at 29 degrees C. Contrary to our hypothesis, urine sodium excretion decreased by 55% by day 7 of CR. Consistent with decreased sodium excretion was the drop in plasma ANP (from 82.4 +/- 4.3 to 68.0 +/- 5.8 pg/ml). To explore the possibility that CR lowers BP through an ANP receptor-dependent mechanism that is independent of its effect on sodium retention, we measured the cardiovascular parameters of mice deficient in the ANP receptor (NPR1(-/-)) or the ANP clearance receptor (NPR3(-/-)). Mean BP fell from 117.1 +/- 3.9 to 108.0 +/- 4.7 mmHg in the NPR1(-/-) mice and from 87.0 +/- 2.4 to 78.4 +/- 1.7 mmHg in the NPR3(-/-) mice during CR. These data indicate that the hypotension induced by CR does not depend on increased sodium excretion. Rather, it appears that the mouse responds to the low BP induced by CR with an increase in sodium reabsorption. Furthermore, circulating ANP levels and data from NPR1(-/-) and NPR3(-/-) mice suggest that the ANP pathway may not be involved in the cardiovascular response to CR.
机译：我们假设热量限制（CR）引起的低血压将通过心钠素（ANP）依赖性机制与钠排泄增加相关。为了检验该假设，在收集尿液的同时通过放射遥测法测量了c57 / B1小鼠的心血管参数。 23小时的平均血压（BP）在7天之内从108.6 +/- 1.8降至92.7 +/- 2.4 mmHg，23小时的心率从624 +/- 5降至426 +/- 13次/分钟与我们在29摄氏度时的CR相反。与我们的假设相反，到CR的第7天尿钠排泄减少了55％。与钠排泄减少相一致的是血浆ANP下降（从82.4 +/- 4.3降至68.0 +/- 5.8 pg / ml）。为了探索CR通过ANP受体依赖性机制（其对钠retention留的影响独立）来降低BP的可能性，我们测量了ANP受体（NPR1（-/-））或ANP清除受体不足的小鼠的心血管参数（NPR3（-/-））。在CR期间，NPR1（-/-）小鼠的平均BP从117.1 +/- 3.9降至108.0 +/- 4.7 mmHg，NPR3（-/-）小鼠从87.0 +/- 2.4降至78.4 +/- 1.7 mmHg 。这些数据表明CR引起的低血压不依赖于钠排泄的增加。而是，小鼠对钠引起的钠吸收增加的反应是由CR诱导的低血压。此外，循环的ANP水平和NPR1（-/-）和NPR3（-/-）小鼠的数据表明，ANP途径可能不参与对CR的心血管反应。

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