Chemistry:Gamma-Melanocyte-stimulating hormone

From HandWiki
Gamma-Melanocyte-stimulating hormone
Names
IUPAC name
L-Tyrosyl-L-valyl-L-methionylglycyl-L-histidyl-L-phenylalanyl-L-arginyl-L-tryptophyl-L-α-aspartyl-L-arginyl-L-phenylalaninamide
Other names
gamma-MSH, γ-melanotropin, γ-melanocortin, γ-intermedin
Identifiers
Properties
C72H97N21O14S
Molar mass 1570.77396 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Infobox references

γ-Melanocyte-stimulating hormone (γ-MSH) is an endogenous peptide hormone and neuropeptide.[1] It is a melanocortin, specifically, one of the three types of melanocyte-stimulating hormone (MSH), and is produced from proopiomelanocortin (POMC).[1] It is an agonist of the MC1, MC3, MC4, and MC5 receptors.[1] It exists in three forms, γ1-MSH, γ2-MSH, and γ3-MSH.[2]

Gamma-MSH regulated cardiovascular functions. Gama-MSH effects are measured through the effects it has on the central neural pathway dispersed throughout the kidney.[3] It is not moderated based on tubular sodium transport. Gamma-MSH activates MC3R in renal tubular cells by limiting sodium absorption by inhibiting the central neural pathway.[3]This regulates sodium balance and blood pressure. If MC3R is absent then there is resistance in γ-MSH which results in hypertension on HSD.[4]

See also

References

  1. 1.0 1.1 1.2 Handbook of Biologically Active Peptides. Academic Press. 26 January 2013. pp. 838–844. ISBN 978-0-12-385096-6. https://books.google.com/books?id=Xz4yFpdSRrwC&pg=PA838. 
  2. Peptides from A to Z: A Concise Encyclopedia. John Wiley & Sons. 8 September 2008. pp. 216–. ISBN 978-3-527-62117-0. https://books.google.com/books?id=doe9NwgJTAsC&pg=PA216. 
  3. 3.0 3.1 "The natriuretic mechanism of Gamma-Melanocyte-Stimulating Hormone". Peptides 32 (5): 1068–1072. May 2011. doi:10.1016/j.peptides.2011.02.006. PMID 21335042. 
  4. "Salt-sensitive hypertension: if only it were as simple as rocket science". The Journal of Clinical Investigation 111 (8): 1115–1116. April 2003. doi:10.1172/jci200316993. PMID 12697727.