Cardiovascular Mechanisms of Gamma (γ)<sub>2</sub>-MSH

Callahan, Michael F.; Kirby, Robert F.; Lymangrover, John R.; Johnson, Alan Kim; Gruber, Kenneth A.

doi:10.3109/10641968409046067

Cited by 19 publications

(25 citation statements)

References 5 publications

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“…In contrast, methylatropine blocked the reflex cardiodeceleration response brought by PHE-induced increase in MAP These findings, along with the results of a previous study, 8 suggest that y 2 -MSH does not cause a direct increase in sympathetic drive to the heart that can compete with baroreceptor-mediated slowing of the heart. That is, we did not observe any further increase in heart rate following cholinergic or a,-adrenergic receptor blockade.…”

Section: Discussionsupporting

confidence: 70%

“…7 - 8 We recently have demonstrated that y 2 -MSH has significant pressor actions 8 This peptide did not produce dose-dependent cardioacceleration, and the rise in mean arterial pressure (MAP) was not accompanied by a bradycardia, which suggests an inhibition of baroreceptor function. Blockade of a,-adrenergic receptors abolished the pressor response, while /3,-adrenergic blockade failed to reveal a bradycardia to the y 2 -MSH pressor response.…”

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confidence: 99%

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Sympathetic nervous system mediation of acute cardiovascular actions of gamma 2-melanocyte-stimulating hormone.

Callahan¹,

Kirby²,

Wolff³

et al. 1985

Hypertension

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SUMMARY Peptides of the pro-opiocortin class produce pronounced cardiovascular and natriuretic actions. We have investigated the acute cardiovascular effects of one of the most potent members of this class, y 2 -melanocyte stimulating hormone (y 2 -MSH), in rats. Pressor actions of y 2 -MSH administered systemicaMy were eliminated by ganglionic blockade with chlorisondamine. Peripheral cholinergic blockade failed to affect either the pressor or cardioaccelerator responses to y 2 -MSH. Administration of y r MSH (2.0-10.0 /xg) produced vasoconstriction primarily in the mesenteric and hindlimb vascular beds, while the renal bed showed little response. Infusions of phenylephrine produced pressor responses similar to those found with y 2 -MSH, which were accompanied by a decrease in heart rate and vasoconstriction in the mesenteric and renal vascular beds. Hemodynamic changes produced by y 2 -MSH and phenylephrine were blocked or attenuated by a,-adrenergic receptor blockade with pra/.osin. Direct injection of y 2 -MSH into the renal artery produced an acute renal vasoconstriction that was not attenuated by a,-adrenergic or ganglionic blockade. These findings and the results of previous publications are consistent with the hypothesis that y 2 -MSH may produce a centrally mediated activation of the sympathetic nervous system, have direct vasoconstriction actions on the renal vasculature, and inhibit baroreceptor function to produce an increase in blood pressure without an accompanying bradycardia. -10 produce pressor, cardioaccelerator, and natriuretic actions. 4 The cardiovascular actions of the peptides appear to result from direct activation of the sympathetic nervous system, in that the pressor and cardioaccelerator actions From the

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Section: Discussionsupporting

confidence: 70%

mentioning

confidence: 99%

Sympathetic nervous system mediation of acute cardiovascular actions of gamma 2-melanocyte-stimulating hormone.

Callahan¹,

Kirby²,

Wolff³

et al. 1985

Hypertension

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“…5) Pretreatment with bretylium, a compound which blocks the release of catecholamines from sympathetic nerve terminals, significantly attenuated the pressor and cardioaccelerator effect of γ 2 -MSH (Callahan et al 1988a). 6) Pretreatment with the α 1 -adrenoceptor antagonist, prazosin, in a dose of 0.5 mg/kg, reduced the effect of a single dose of 10 or 20 µg γ 2 -MSH on blood pressure by 80% (Callahan et al 1984).…”

Section: Discussionmentioning

confidence: 99%

“…It should be noted that in this latter study Callahan et al (1984) used a rather high dose of prazosin which might result in nonselective effects. In addition, these authors failed to observe the tachycardiac response which is normally seen following administration of γ 2 -MSH (cf.…”

Section: Discussionmentioning

confidence: 99%

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

Bergen

Winter

Wildt

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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gamma 2-Melanocyte-stimulating hormone (gamma 2-MSH) and related melanotropins have been shown to have various cardiovascular effects, including acute, short-lasting increases in blood pressure (MAP) and heart rate (HR). gamma 2-MSH, administered intravenously, dose-dependently increased MAP and HR with an ED50 of approximately 30 nmol/kg and a maximal effect on MAP of approximately 55 mm Hg and on HR of around 70 beats per minute. Intravenous (i.v.) pretreatment with the alpha 1-adrenoceptor antagonist, prazosin, caused the dose-response curve for the effect of gamma 2-MSH on MAP to shift to the right with a decrease in slope, whereas it had no effect on the dose-response curve for the effect on HR. I.v. pretreatment with the beta 1-adrenoceptor antagonist, metoprolol, had no effect on the dose-response curve for the effect of gamma 2-MSH on MAP, but it caused the dose-response curve for the effect of the peptide on HR to shift to the right with a decrease in slope. Neither i.v. nor intracerebroventricular (i.c.v.) administration of the vasopressin V1A receptor antagonist, SR 49059 ((2S) 1-[(2R 3S)-5-chloro-3-(2-chlorophenyl)-1-(3,4-dimethoxy-benzene-sulfonyl)- 3-hydroxy-2,3-dihydro-1H-indole-2-carbonyl]-pyrrolidine-2-carboxamide), had significant effects on the dose-response curves for the effects of the peptide on either MAP or HR. The doses of prazosin, metoprolol and SR 49059 were found to be effective in counteracting the effects of agonists for these receptors (phenylephrine, isoprenaline and [Arg8]vasopressin, respectively). Taken together, these results support the postulate that the effects of gamma 2-MSH are, at least partially, due to an increase in sympathetic outflow to the periphery (Gruber and Callahan (1989), Am J Physiol 257: R681-R694), and that this increase leads to increased activation of vascular alpha 1-adrenoceptors and cardiac beta 1-adrenoceptors. If, as was suggested by these authors, gamma 2-MSH acts via activation of a central vasopressin system, it is via a vasopressin receptor subtype other than the vasopressin V1A receptor, since i.c.v. administration of a selective vasopressin V1A receptor antagonist failed to interfere with the pressor and cardioaccelerator effects of gamma 2-MSH.

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“…1) and shown to have very low melanocyte-stimulating activity compared to that of a-MSH and no pituitary hormone-releasing activity (4). In contrast, ,-MSH has been reported to have potent pressor, cardioaccelerator, and natriuretic activity (5)(6)(7). In the porcine pituitary, porcine adrenal medulla (8), and human heart (9), ,-MSH-like immunoreactivity has been demonstrated by radioimmunoassay and/or immunohistochemical staining using anti-y2-MSH antibodies, not reacting with either a-, p-, yl, or@-MSH.…”

Section: Introductionmentioning

confidence: 99%

Noncompetitive enzyme immunoassay (hetero‐two‐site enzyme immunoassay) for _γ‐melanocyte‐stimulating hormone (_γ‐msh) and measurement of immunoreactive _γ‐msh in plasma of healthy subjects

Yogi¹,

Hashida²,

Ekman³

et al. 1995

Clinical Laboratory Analysis

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A noncompetitive enzyme immunoassay (hetero-two-site enzyme immunoassay) for gamma 2-melanocyte-stimulating hormone (gamma 2-MSH) was developed. gamma 2-MSH (1-12) was biotinylated, trapped onto an anti-gamma 2-MSH (1-12) IgG-coated polystyrene bead, eluted at pH 1 after washing to eliminate other biotinylated substances, and measured using two streptavidin-coated polystyrene beads and affinity-purified anti-gamma 2-MSH (1-12) Fab'-peroxidase conjugate. The detection limit of gamma 2-MSH (1-12) was 10-30 amol (16-48 fg)/assay and 130-400 fmol (210-630 pg)/L of plasma. There was little or only slight cross reaction with alpha-MSH, beta-MSH, and gamma 1-MSH. By this immunoassay, the concentration and molecular size of immunoreactive gamma 2-MSH in plasma of healthy subjects were examined, and the results were compared with those by competitive enzyme immunoassay. Immunoreactive gamma 2-MSH measured by competitive enzyme immunoassay was a mixture of substances with high molecular weights (100-500 kDa), and its concentration was calculated to be 50-60 pmol/L using gamma 2-MSH (1-12) as standard. Immunoreactive gamma 2-MSH detected by the noncompetitive enzyme immunoassay after removal of high molecular weight substances was not homogeneous and smaller than gamma 2-MSH (1-12), and its concentration was approximately 1 pmol/L. The exact nature of these immunoreactive gamma 2-MSHs remains to be elucidated. gamma 2-MSH (1-12) added to plasma was degraded rapidly, and the concentration of gamma 2-MSH (1-12) was very low, if any, in plasma of healthy subjects.

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Cardiovascular Mechanisms of Gamma (γ)₂-MSH

Cited by 19 publications

References 5 publications

Sympathetic nervous system mediation of acute cardiovascular actions of gamma 2-melanocyte-stimulating hormone.

Sympathetic nervous system mediation of acute cardiovascular actions of gamma 2-melanocyte-stimulating hormone.

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

Noncompetitive enzyme immunoassay (hetero‐two‐site enzyme immunoassay) for _γ‐melanocyte‐stimulating hormone (_γ‐msh) and measurement of immunoreactive _γ‐msh in plasma of healthy subjects

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Cardiovascular Mechanisms of Gamma (γ)2-MSH

Cited by 19 publications

References 5 publications

Sympathetic nervous system mediation of acute cardiovascular actions of gamma 2-melanocyte-stimulating hormone.

Sympathetic nervous system mediation of acute cardiovascular actions of gamma 2-melanocyte-stimulating hormone.

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

Noncompetitive enzyme immunoassay (hetero‐two‐site enzyme immunoassay) for γ‐melanocyte‐stimulating hormone (γ‐msh) and measurement of immunoreactive γ‐msh in plasma of healthy subjects

Contact Info

Product

Resources

About

Cardiovascular Mechanisms of Gamma (γ)₂-MSH

Noncompetitive enzyme immunoassay (hetero‐two‐site enzyme immunoassay) for _γ‐melanocyte‐stimulating hormone (_γ‐msh) and measurement of immunoreactive _γ‐msh in plasma of healthy subjects