Natriuretic and hypertensive activities reside in a fragment of ACTH.

Gruber, Kenneth A.; Kleín, Michael C.; Hutchins, Phillip M.; Buckalew, Vardaman M.; Lymangrover, John R.

doi:10.1161/01.hyp.6.4.468

Cited by 24 publications

(9 citation statements)

References 28 publications

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“…4 -8 I M 3 We 4 8 and others 14 -l5 have presented evidence that the pressor responses of these vasoactive peptides are due to activation of the sympathetic nervous system. In Experiment 1, the pressor response to y 2 -MSH was blocked by the ganglionic blocking agent chlorisondamine.…”

Section: Discussionmentioning

confidence: 94%

mentioning

confidence: 99%

“…-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 are blocked by a,-adrenergic and /3,-adrenergic receptor blockade respectively. y-Melanocyte stimulating hormone peptides, fragments of the 16K N-terminus of pro-opiocortin 5 6 that contain an amino acid sequence analogous to ACTH 4 -10 , have been observed to be 10 to 100 times more potent than ACTH 4 …”

mentioning

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: Discussionmentioning

confidence: 94%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

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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“…We then determined that the natriuretic activity of these peptides resided in this common sequence. 17 Previous work on a natriuretic hormone had proposed aMSH (or a related peptide) as a candidate. 16 This hypothesis was based on 1) the natriuretic activity of the peptide and 2) its origin from the intermediate lobe (pars intermedia; PI) of the pituitary.…”

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confidence: 99%

“…16 We therefore concluded that if the CNS produced a natriuretic hormone it might have an aMSH-like structure (i.e., have a sequence similar to aMSH 4 " 10 ) but would not be aMSH itself. 17 During the course of our work with ACTH 4 yMSHs (see Figure 1). We showed in a rat bioassay that several peptides of the yMSH family produce a natriuresis that is qualitatively similar to ACTH 4 " 10 or aMSH, but can be demonstrated at 1/1000 the dose.…”

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confidence: 99%

The natriuretic response to hydromineral imbalance.

Gruber

1987

Hypertension

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SUMMARY Many recent investigations of the mechanism of volume-expansion natriuresis fail to appreciate that the observed renal sodium excretion may not be dependent on an increase in intravascular volume, but rather on the infused sodium load or extracellular fluid volume expansion. With this in mind, the natriuresis of isotonic volume expansion, hypertonic saline infusion, and dehydration have a common basis: they present a relative or absolute sodium load. Lesions of forebrain periventricular tissue prevent the natriuretic response to these three states of body fluid imbalance. In this review we discuss the evidence for a common central nervous system-mediated natriuretic mechanism in response to disturbances of fluid and electrolyte balance. We also propose a role for pars intermedia-derived, proopiomelanocortin-derived peptides as humoral mediators of renal sodium excretion. Evidence from our laboratory, as well as others, provides data for a testable hypothesis to explain central nervous system-mediated natriuresis, as well as an explanation of how central nervous system lesions or neurochemical perturbations affect the renal response to body fluid imbalance. ume-expansion natriuresis agree that the natriuretic response is not correlated to an increase in intravascular volume, but rather to the infused sodium load or extracellular expansion. Intravascular volume-expansion with sodium-free solutions of hyperoncotic dextran, hyperosmotic glucose, hyperoncotic albumin, or hypotonic sodium chloride produces little increase in sodium excretion. '• 2 Expansion with saline or blood, however, challenges that produce an expansion of the extracellular fluid volume and present a sodium load, results in a significant increase in urinary sodium excretion.1 -2 The hemodynamic response to "pure" intravascular expansion, isotonic saline expansion, or volume expansion with blood is quite similar. These data suggest that an increase in

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Effects of Melanocortins in the Nervous System

Adan¹

2000

The Melanocortin Receptors

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Natriuretic and hypertensive activities reside in a fragment of ACTH.

Cited by 24 publications

References 28 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.

The natriuretic response to hydromineral imbalance.

Effects of Melanocortins in the Nervous System

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