| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2006563 | Peptides | 2011 | 5 Pages |
Gamma-Melanocyte Stimulating Hormone (Gamma-MSH) regulates sodium (Na+) balance and blood pressure through activation of the melanocortin receptor 3 (MC3-R). The mechanism of the natriuretic effect is proposed to involve binding of MC3-R either in the kidney to directly inhibit tubular Na+ transport or in the brain to inhibit central neural pathways that control renal tubular Na+ absorption. This study aimed to clarify the mechanism involved in the natriuretic effect of Gamma-MSH on MC3-R in kidney cells. In Ussing chamber studies, we observed no effects of Gamma-MSH on NaCl transport in the mouse inner medullary collecting duct cell line (mIMCD-K2). We also found that neither MC3-R protein nor mRNA was expressed in mouse kidney, suggesting that renal Gamma-MSH action may not be mediated through direct effects on tubular Na+ transport but rather through effects on central neural pathways that innervate the kidney.
Research highlights► Gamma-MSH induces urinary sodium (Na+) excretion and regulates blood pressure by unknown mechanisms. ► Gamma-MSH had no effect on ion transport or MC3-R signaling in the IMCD-K2 cell line. ► Mouse kidney does not express MC3-R protein or mRNA. ► Natriuretic mechanism of Gamma-MSH is likely mediated through central neural pathways. ► Available anti-MC3-R antibodies do not specifically detect MC3-R protein in mouse kidney or brain.
