Failure of Somatostatin and β-Endorphin to Affect Bovine Adrenal Cortex Cells In Vitro

Diel, F.; Holz, Josefin-Beate; Bethge, N

doi:10.1055/s-2007-1019183

Cited by 10 publications

(3 citation statements)

References 6 publications

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“…However, we were unable to observe an increase in plasma aldosterone levels by infusion of 500 g of ß-endorphin. Although ß-endorphin has been shown to stimulate aldosterone production in hypophysectomized, nephrectomized dogs (Güliner et al, 1983), other studies including humans failed to find similar effects (Kern et al, 1985;Diel et al, 1981;Szalay and Stark, 1981). Griffing et al (1985) reported increased plasma ß-endorphin level in primary aldosteronism due to adrenal hyperplasia, suggesting a pathogenetic role of ß-endorphin in this setting.…”

Section: Discussionmentioning

confidence: 99%

Pituitary Peptides other than ACTH may not be Aldosterone Secretagogue in Primary Aldosteronism

Miyamori

Koshida²,

Soma³

et al. 2009

Exp Clin Endocrinol Diabetes

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In order to elucidate whether pituitary peptides other than ACTH which are derived from the proopiomelanocortin (POMC) are involved for aldosterone secretion in primary aldosteronism, we administered ovine corticotropin releasing factor (CRF), beta-endorphin and naloxone to seven patients with aldosterone producing adenoma. One hundred micrograms of CRF produced an augmented aldosterone response in patients with aldosteronism, while 500 micrograms of beta-endorphin infusion failed to cause any significant changes in neither normal subjects nor patients. An opioid antagonist, naloxone (10 mg, iv) produced no noticeable change in plasma aldosterone in normal subjects, while it caused a slight increase in patients with primary aldosteronism. Plasma cortisol increased to a similar degree in response to CRF and naloxone in normal subjects and patients. In three patients with isolated ACTH deficiency, neither aldosterone nor cortisol responded to these stimuli. The present results indicate that POMC-derived pituitary peptides other than ACTH are unlikely to participate in the aldosterone secretion in normal subjects or in patients with primary aldosteronism.

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Section: Discussionmentioning

confidence: 99%

Pituitary Peptides other than ACTH may not be Aldosterone Secretagogue in Primary Aldosteronism

Miyamori

Koshida²,

Soma³

et al. 2009

Exp Clin Endocrinol Diabetes

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“…Animal experiments have provided evidence for a direct regulatory role of somatostatin and somatostatin receptors in the adrenal glomerulosa zone where aldosterone is released. However, this is true in rats [18][19][20][21] but not in other species [22,23]. In humans, the effect of somatostatin and octreotide on PRA has been investigated using several stimuli to increase PRA, such as head tilting, furosemide infusion and erect position [24][25][26][27][28][29].…”

Section: Discussionmentioning

confidence: 99%

Vasoactive substances in early dumping syndrome: effects of dumping provocation with and without octreotide

Vecht

Gielkens²,

Frölich

et al. 1997

Eur J Clin Investigation

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In patients after gastric surgery, early dumping symptoms can be provoked by oral glucose challenge. Octreotide effectively prevents the occurrence of dumping symptoms. We have studied plasma renin activity (PRA), aldosterone and atrial natriuretic peptide (ANP) concentrations in nine patients with early dumping, 10 surgical control subjects and nine healthy control subjects after an oral glucose challenge preceded by either placebo or 25 micrograms of octreotide subcutaneously (s.c.). In the dumping group, basal PRA was significantly (P < 0.01) higher (3.9 +/- 0.6 micrograms L-1 h-1) than in either surgical or healthy control subjects (1.1 +/- 0.3 micrograms L-1 h-1 and 1.1 +/- 0.2 micrograms L-1 h-1 respectively) and showed a significant rise after glucose ingestion to 5.4 +/- 0.9 micrograms L-1 h-1 that did not occur in control subjects. Aldosterone concentration showed a concomitant rise. In dumping patients, plasma ANP decreased after glucose ingestion from 31 +/- 6 ngL-1 to 21 +/- 5 ngL-1 (P < 0.05). This decrease did not occur in control subjects. Early dumping is associated with an activation of the renin-aldosterone axis and a decrease in plasma ANP, reflecting a hypovolaemic state. Octreotide prevents the occurrence of these changes.

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“…It has been reported that somatostatin inhibits reninantiotensin-aldosterone adrenal cortex Stimulation in vivo (105)(106)(107). Since glomerulosa cells from the adrenal cortex seem to be responsible for aldosterone production (108), cells were isolated from the bovine adrenal cortex, and in vitro Stimulation by corticotropin and the influence of added Somatostatin were measured by aldosterone determination (109). The results indicated that the inhibitory effect of Somatostatin cannot be evaluated in the bovine aldosterone-producing System in vitro.…”

Section: Adrenal Glandmentioning

confidence: 99%

Somatostatin — A Regulatory Peptide of Clinical Importance

Bethge¹,

Diel²,

Kh³

1982

CCLM

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Somatostatin was first discovered in the hypothalmus and has since been located in many parts of the central and periphefal nervous System, äs well äs in the pancreas and the gastrointestinal tract. Its main biological activity is to inhibit the action of somatotropin (growth hormone, STH, GH) and a number of other hormones. The therapeutic value of somatostatin has been demonstrated in the treatment of both acute bleeding gastric ulcers and acute pancreatitis. In additioii, the measurement of somatostatin in the blood is a useful method for the screening of somatostatin-produeing tumours. This paper reviews the location, action, clinical significance and measurement of somatostatin. Somatostatin-Ein Regulatorpeptid mit klinischer Bedeutung Zusammenfassung: Somatostatin, zuerst im Hypothalamus entdeckt, ist in vielen Teilen des zentralen und peripheren Nervensystems, im Pankreas und im Gästrointestinaltrakt lokalisiert. Seine biologische Hauptwirkung ist die Hemmung von Somatotropin (GH, STH) und einer Vielzahl anderer Hormone. Der therapeutische Wert von Somatostatin konnte bei der Behandlung von akuten Magenulkusblutungen und akuter Pankreatitis gezeigt werden. Die Somatostatin-Bestimmuiig im Blut stellt eine wertvolle Methode bei der Suche nach einem somatostatinproduzierenden Tumor dar. Die Lokalisation, Wirkung, klinische Bedeutung und Bestimmung von Somatostatin wird dargestellt. hormones control ädenohypophysis hormone secretion Schally (2); Luliberin (luteinizing-hormone-releasing (fig. 2). Certain of these hormones affect more than hormone, LHRH), isolated in 1971 by Schally (3); and one pitüitary hormone: e.g., thyroliberin causes the somatostatin, reported by Guillemiii in 1973 (4) and by release of thyrotropin (thyrotropic hormone, TSH) Schally in 1976 (5). Figure l shows the chemical struc-(l, 2) and prolactin (6); luliberin releases lutropin tures of these three hormones. (luteinizing hormone, LH) and follitropin (follicle-The tuberohypophyseal neurons are believed to syn-stimulating hormone, FSH) (3,7), and somatostatin thesize, transport, and release the hypothalamic hör-inhibits the secretion of somatotropin (4) and thyromones into perivascular spaces in the median eminence tropin (8).

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Failure of Somatostatin and β-Endorphin to Affect Bovine Adrenal Cortex Cells In Vitro

Cited by 10 publications

References 6 publications

Pituitary Peptides other than ACTH may not be Aldosterone Secretagogue in Primary Aldosteronism

Pituitary Peptides other than ACTH may not be Aldosterone Secretagogue in Primary Aldosteronism

Vasoactive substances in early dumping syndrome: effects of dumping provocation with and without octreotide

Somatostatin — A Regulatory Peptide of Clinical Importance

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