Effects of a Long-Acting Somatostatin Analogue on Pituitary-Adrenocortical Secretion in Normal Human Subjects.

Itoh, Shinji; Tanaka, Koshi; Kumage, Munehito; Shimizu, Naokata

doi:10.1507/endocrj1954.37.131

Cited by 5 publications

(3 citation statements)

References 32 publications

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“…Chronic administration also inhibits ZG cellular growth (415,421). In humans, somatostatin appears to inhibit aldosterone production stimulation by ANG II (251) but not by ACTH (246). All five known human somatostatin receptor subtypes are expressed in normal adrenal cortex and in APAs (312,532).…”

Section: Somatostatinmentioning

confidence: 99%

Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney

Stowasser

Gordon

2016

Physiological Reviews

127

134

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In the 60 years that have passed since the discovery of the mineralocorticoid hormone aldosterone, much has been learned about its synthesis (both adrenal and extraadrenal), regulation (by renin-angiotensin II, potassium, adrenocorticotrophin, and other factors), and effects (on both epithelial and nonepithelial tissues). Once thought to be rare, primary aldosteronism (PA, in which aldosterone secretion by the adrenal is excessive and autonomous of its principal regulator, angiotensin II) is now known to be the most common specifically treatable and potentially curable form of hypertension, with most patients lacking the clinical feature of hypokalemia, the presence of which was previously considered to be necessary to warrant further efforts towards confirming a diagnosis of PA. This, and the appreciation that aldosterone excess leads to adverse cardiovascular, renal, central nervous, and psychological effects, that are at least partly independent of its effects on blood pressure, have had a profound influence on raising clinical and research interest in PA. Such research on patients with PA has, in turn, furthered knowledge regarding aldosterone synthesis, regulation, and effects. This review summarizes current progress in our understanding of the physiology of aldosterone, and towards defining the causes (including genetic bases), epidemiology, outcomes, and clinical approaches to diagnostic workup (including screening, diagnostic confirmation, and subtype differentiation) and treatment of PA.

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Section: Somatostatinmentioning

confidence: 99%

Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney

Stowasser

Gordon

2016

Physiological Reviews

127

134

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“…An inhibitory effect of somatostatin or octreotide on stimulated PRA has been found by some investigators [24][25][26][27] but not by others [28,29]. Similarly, an inhibitory effect of somatostatin on aldosterone release in man, as described by Jones et al [29], was not confirmed in later studies [27,30]. Based on this information, we conclude that the observed effects of octreotide on PRA and aldosterone concentration are secondary to the alterations in haemodynamics in early dumping induced by octreotide.…”

Section: Discussionmentioning

confidence: 48%

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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“…This supports the hypothesis that growth factors or hormones regulated by somatostatin analogues play a significant role in adrenal hypertrophy (Kunjara et al 2012). However, the multifunctional properties of somatostatin include (in different clinical and experimental conditions) the depression of growth hormone (GH), IGF-I levels, IGF binding proteins, glucagon, TSH, circulating ACTH and cortisol, and this pleiotropism makes it difficult to determine the precise mode of action that is responsible for the changes (Gill et al 1982;Masuda et al 1989;Itoh et al 1990;Ørskov et al 1992;Boehm & Lustig 2002;Pokrajac et al 2009;Rutter 2009).…”

mentioning

confidence: 69%

Effects of long‐term experimental diabetes on adrenal gland growth and phosphoribosyl pyrophosphate formation in growth hormone‐deficient dwarf rats

Kunjara

Greenbaum

McLean

et al. 2012

Int J Experimental Path

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The availability of growth hormone (GH)-deficient dwarf rats with otherwise normal pituitary function provides a powerful tool to examine the relative role of hyperglycaemia and the reordering of hormonal factors in the hypertrophy-hyperfunction of the adrenal gland that is seen in experimental diabetes. Here, we examine the effects of long-term (6 months) experimental diabetes on the growth of the adrenal glands; their content of phosphoribosyl pyrophosphate (PRPP); and the activity of the PRPP synthetase, G6P dehydrogenase and 6PG dehydrogenase enzymes in GH-deficient dwarf rats compared to heterozygous controls. These parameters were selected in view of the known role of PRPP in both de novo and salvage pathways of purine and pyrimidine synthesis and in the formation of NAD, and in view of the role of the oxidative enzymes of the pentose phosphate pathway in both R5P formation and the generation of the NADPH that is required in reductive synthetic reactions. This study shows that GH deficiency prevents the increase in adrenal gland weight, PRPP synthetase, PRPP content and G6P dehydrogenase and 6PG dehydrogenase. This contrasts sharply with the heterozygous group that showed the expected increase in these parameters. The blood glucose levels of the groups of long-term diabetic rats, both GH-deficient and heterozygous, remained at an elevated level throughout the experiment. These results are fully in accord with earlier evidence from studies with somatostatin analogues which showed that the GH-insulin-like growth factor I (IGF-I)-axis plays a key role in the adrenal diabetic hypertrophy-hyperfunction syndrome.

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Effects of a Long-Acting Somatostatin Analogue on Pituitary-Adrenocortical Secretion in Normal Human Subjects.

Cited by 5 publications

References 32 publications

Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney

Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney

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

Effects of long‐term experimental diabetes on adrenal gland growth and phosphoribosyl pyrophosphate formation in growth hormone‐deficient dwarf rats

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