Central vasopressin system mediation of acute pressor effect of gamma-MSH

Abstract

Intravenous (iv) administration of gamma-melanocyte-stimulating hormone (gamma-MSH) produces central sympathetically mediated pressor and cardioaccelerator effects and increases the activity of hypothalamic vasopressinergic neurons. The autonomic actions are similar to infusion of vasopressin (Vp) into the hindbrain of 4th ventricle (Ven). To ascertain whether activation of the central Vp system is the proximate cause of the pressor effects of gamma-MSH, we investigated the effects of gamma-MSH in rats pre- and postblockade of central nervous system Vp receptors and in rats with a hereditary lack of vasopressin (Brattleboro strain). Central Vp receptor blockade significantly reduced (80%) the pressor effects of iv gamma-MSH. As a control, iv administration of the antagonist, while effective in blocking the pressor effect of iv Vp, had no effect on the gamma-MSH pressor response. When compared with their genetic controls (Long-Evans strain), Brattleboro rats also had greater than 80% reduction in their pressor response to iv gamma-MSH. The results indicate that circulating gamma-MSH activates the central Vp system to produce its sympathoexcitatory pressor effects.

Influence of blockade of α1-adrenoceptors, β1-adrenoceptors and vasopressin V1A receptors on the cardiovascular effects of γ2-melanocyte-stimulating hormone (γ2-MSH)

“…SR 49059. These findings question the data reported by Gruber and Eskridge (1986). It could be that [d(CH 2 ) 5 1 ,Tyr(Me) 2 ,Arg 8 ]vasopressin (Manning and Sawyer 1983) is not solely acting as a vasopressin receptor antagonist, as already discussed by Gruber and Eskridge (1986).…”

“…3) Following blockade of central vasopressin receptors with [d(CH 2 ) 5 1 ,Tyr(Me) 2 ,Arg 8 ]vasopressin, a potent vasopressin V 1 receptor antagonist (Manning and Sawyer 1983), the pressor effect of i.v. administered γ-MSH is significantly attenuated (Gruber and Eskridge 1986). 4) Following pretreatment with chlorisondamine to block ganglionic neurotransmission, the pressor action of γ 2 -MSH was eliminated (Callahan et al 1985).…”

“…In their experiments with the vasopressin V 1 receptor antagonist, [d(CH 2 ) 5 1 ,Tyr(Me) 2 ,Arg 8 ]vasopressin, Gruber and Eskridge (1986) found that i.v. administration of the antagonist, while blocking the pressor effect of i.v.…”

“…γ 2 -MSH were attenuated (Gruber and Eskridge 1986). In our experiments we used the selective vasopressin V 1A receptor antagonist, SR 49059 (Serradeil-Le Gal et al 1993), and an experimental design similar to that previously used by Gruber and Eskridge (1986), though we made complete dose-response curves for the effects of i.v. γ 2 -MSH before and after i.v.…”

Peptide hormones and the regulation of sodium excretion.

“…Higher doses of this peptide elevate blood pressure through stimulation of sympathetic nervous outflow, 108 apparently mediated by centrally acting vasopressin. 109 The function of MSH-related peptides in volume homeostasis is not established. The possiblity that y-MSH or a similar peptide could participate in the reflex control of sodium excretion has been suggested on the basis of studies of the natriuresis that occurs from the remaining kidney shortly after acute unilateral nephrectomy (AUN).…”