| First Author | Swoap SJ | Year | 2001 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 281 |
| Issue | 6 | Pages | H2473-9 |
| PubMed ID | 11709414 | Mgi Jnum | J:108672 |
| Mgi Id | MGI:3624494 | Doi | 10.1152/ajpheart.2001.281.6.H2473 |
| Citation | Swoap SJ (2001) Altered leptin signaling is sufficient, but not required, for hypotension associated with caloric restriction. Am J Physiol Heart Circ Physiol 281(6):H2473-9 |
| abstractText | 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. |
