gamma2-msh and Tachycardia

Central autonomic and neuroendocrine activities are important components of the host response to bacterial inflammation. We demonstrate that intravenous infusion of gamma(2)-melanocyte-stimulating hormone (gamma(2)-MSH), a potent autonomic regulating peptide, prevents lipopolysaccharide (LPS)-induced hypotension and tachycardia, and modulates the ACTH response to endotoxin. In the hypothalamic paraventricular nucleus, a major neuroendocrine and autonomic center, gamma(2)-MSH inhibits LPS-induced increases in CRF mRNA levels, but does not suppress LPS-augmented arginine vasopressin heteronuclear RNA expression. In the locus coeruleus, a brainstem noradrenergic center, gamma(2)-MSH inhibits LPS-induced increases in tyrosine hydroxylase mRNA levels. Gamma(2)-MSH inhibits LPS-induced IL-1beta gene expression in the brain, pituitary and thymus, and prevents increases in plasma NO levels. These findings reveal that gamma(2)-MSH attenuates systemic inflammatory responses to endotoxin and suggest that modulation of central autonomic and neuroendocrine activities by gamma(2)-MSH contributes to its anti-inflammatory effects.

Topics: Adrenocorticotropic Hormone; Animals; Arginine Vasopressin; Autonomic Nervous System; Bacterial Infections; Brain; Corticotropin-Releasing Hormone; gamma-MSH; Hypotension; Hypothalamo-Hypophyseal System; Inflammation; Interleukin-1; Lipopolysaccharides; Male; Nitric Oxide; Rats; Rats, Sprague-Dawley; RNA, Messenger; Tachycardia; Tyrosine 3-Monooxygenase