Suppression of γ-Melanocyte-Stimulating Hormone Secretion Is Accompanied by Salt-Sensitive Hypertension in the Rat

Haim Mayan, Xi Ping Ni, Shlomo Almog, Michael H. Humphreys*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


γ-Melanocyte-stimulating hormone (γ-MSH) is a natriuretic peptide derived from proopiomelanocortin (POMC) in the pituitary neurointermediate lobe (NIL); its plasma concentration in rats doubles after ingestion of a high (HSD; 8% NACl) compared with a low sodium diet (LSD; 0.07%). Because NIL function is regulated through dopaminergic pathways, we asked whether dopaminergic stimulation with bromocriptine (5 mg/kg IP daily for 1 week) or inhibition with haloperidol (5 mg/kg IP for 1 week) alters the γ-MSH response to a HSD. In vehicle-treated rats, plasma γ-MSH and NIL γ-MSH content on the HSD were both markedly elevated over values in rats on the LSD (P<0.001); no difference in mean arterial pressure (MAP) occurred. In haloperidol-treated rats on the LSD, both plasma γ-MSH and NIL γ-MSH content were greater than in vehicle-treated rats (P<0.05) and did not increase further on the HSD; MAP was also no different. In bromocriptine-treated rats, neither plasma γ-MSH nor NIL γ-MSH content increased on the HSD versus LSD, and MAP was markedly elevated on the HSD (132±3 versus 106±3 mm Hg, P<0.001). Intravenous infusion of γ-MSH (0.4 pmol/min) to bromocriptine-treated rats on the HSD restored plasma γ-MSH concentration to a level appropriate for the HSD and lowered MAP from 131±6 to 108±5 mm Hg (P<0.01). These results demonstrate that the increases in NIL content and plasma concentration of γ-MSH normally occurring during ingestion of the HSD are prevented by dopaminergic suppression of NIL function. This results in deficiency of γ-MSH on the HSD and is accompanied by elevated blood pressure, which is corrected by infusion of the peptide. γ-MSH may be an important component in the normal response to a HSD; interruption of this response leads to salt-sensitive hypertension.

Original languageEnglish
Pages (from-to)962-967
Number of pages6
Issue number5
StatePublished - Nov 2003


FundersFunder number
National Heart, Lung, and Blood InstituteR01HL068871
National Institute of Diabetes and Digestive and Kidney DiseasesR01DK058812


    • Dopamine
    • Hypertension, sodium-dependent
    • Natriuretic peptides
    • Pituitary


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