Abstract | PURPOSE OF REVIEW: RECENT FINDINGS: Both alpha- and gamma-MSH acutely elevate blood pressure and heart rate through central stimulation of sympathetic nervous outflow. This action of alpha-MSH is mediated by the melanocortin 4 receptor (MC4R), whereas sympathetic nervous stimulation by gamma-MSH does not involve its receptor MC3R but rather is likely due to activation of a sodium channel in the central nervous system. In contrast, gamma-MSH deficiency in rodents, or disruption of MC3R, leads to marked salt-sensitive hypertension, again through a central mechanism: a small dose of exogenous peptide delivered into the cerebroventricular system of mice with gamma-MSH deficiency restores blood pressure to normal. This salt-sensitive hypertension is accompanied by the development of insulin resistance; the mechanism linking these two consequences of a high- salt diet is not yet known but may involve activation of the sympathetic nervous system. SUMMARY:
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Authors | Michael H Humphreys |
Journal | Current opinion in nephrology and hypertension
(Curr Opin Nephrol Hypertens)
Vol. 16
Issue 1
Pg. 32-8
(Jan 2007)
ISSN: 1062-4821 [Print] England |
PMID | 17143069
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
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Chemical References |
- Receptors, Melanocortin
- Melanocyte-Stimulating Hormones
- Sodium
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Topics |
- Animals
- Cardiovascular System
(metabolism)
- Humans
- Insulin Resistance
- Kidney
(metabolism)
- Melanocyte-Stimulating Hormones
(physiology)
- Receptors, Melanocortin
(physiology)
- Rodentia
(metabolism)
- Sodium
(metabolism)
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