Effect of Intravenous and Intracarotid Injections of Hypertonic Fluids on the Release of Melanocyte-Stimulating Hormone From the Rat Posterior Pituitary Lobe Incubated in Situ

Cyrkowicz, A; Traczyk, W

doi:10.1677/joe.0.0660085

Cited by 9 publications

(2 citation statements)

References 17 publications

(18 reference statements)

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“…Administration of hypertonic saline in drinking water has been reported to activate the hypothalamic-neurohypophyseal axis, pro ducing an increase in the turnover of neural lobe hormones oxytocin and vasopressin [Gilman and Goodman, 1937;Friesen and Astwood, 1967;Jones and Pickering, 1969;Kleeman and Vorherr, 1974], as well as activation of MSH release [Howe and Thody, 1970;Taleisnik et al, 1972;Cyrkowicz and Traczyk, 1975]. We found that this stimulus depleted both anterior and neurointermediate lobe END levels in a significant majority of the animals after varying periods of salt loading.…”

Section: Discussionmentioning

confidence: 63%

Experimental Alterations of Endorphin Levels in Rat Pituitary

et al. 1979

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Endorphin (END) levels in rat pituitary were assessed with the opiate receptor binding assay. Procedures reported to alter hormone secretion from END-rich intermediate or anterior lobes were examined for their effect on END content. Lesions of the paraventricular nucleus (PVN) had no significant effect on END content. Ingestion of 2% NaCl reduced END levels in a significant majority of the animals. Suckling, a natural physiological stimulus, significantly elevated neurointermediate lobe END. Footshock and immobilization each evoked 40–50% reductions in anterior lobe END content. Pituitary ENDs are thus affected by many of the same stimuli that also promote release of a number of peptide hormones derived from the same biosynthetic precursor. However, separate mechanisms likely exist for control of secretion of these peptides from anterior and neurointermediate lobe.

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Section: Discussionmentioning

confidence: 63%

Experimental Alterations of Endorphin Levels in Rat Pituitary

et al. 1979

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“…Since these early reports, other investigators have found that hydromineral imbalance results in a histological appearance of PI cells suggestive of hyperactivity 20 and an increase in aMSH secretion. 21 Levitin et al 22 showed that rats bearing PI transplants had heightened natriuretic responses to volume loads. Releasing factors for PI hormones, such as serotonin agonists 23 or corticotropin-releasing factor, 24 appear to produce centrally mediated natriuresis.…”

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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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Studies on endorphin function in animals and man

Goldstein

Cox

1979

Endorphins in Mental Health Research

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Effect of Intravenous and Intracarotid Injections of Hypertonic Fluids on the Release of Melanocyte-Stimulating Hormone From the Rat Posterior Pituitary Lobe Incubated in Situ

Cited by 9 publications

References 17 publications

Experimental Alterations of Endorphin Levels in Rat Pituitary

Experimental Alterations of Endorphin Levels in Rat Pituitary

The natriuretic response to hydromineral imbalance.

Studies on endorphin function in animals and man

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