Inhibition of Frusemide-Induced Hyperreninæmia by Growth-Hormone Release-Inhibiting Hormone in Man

Rosenthal, J.; Escobar-Jiménez, Fernándo; Raptis, Sotirios A.; Pfeiffer, Ernst-Friedrich

doi:10.1016/s0140-6736(76)91611-1

Cited by 43 publications

(17 citation statements)

References 25 publications

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“…The inhibition of RAAS in octreotide-treated cirrhotic patients may arise independently of changes in systemic hemodynamics (22), supporting previous observations of a direct inhibitory effect of SMS and its analogues on the renin-aldosterone axis. Indeed, SMS significantly reduced the increase in PRA following furosemide (34), beta-adrenergic stimulation (35), or in patients with renovascular hypertension (36). Similarly, octreotide attenuated the increase in PRA induced by head-up tilting (37).…”

Section: Discussionmentioning

confidence: 93%

The Effects of Chronic Treatment with Octreotide versus Octreotide plus Midodrine on Systemic Hemodynamics and Renal Hemodynamics and Function in Nonazotemic Cirrhotic Patients with Ascites

Kalambokis

Economou

Fotopoulos

et al. 2005

Am J Gastroenterology

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Section: Discussionmentioning

confidence: 93%

The Effects of Chronic Treatment with Octreotide versus Octreotide plus Midodrine on Systemic Hemodynamics and Renal Hemodynamics and Function in Nonazotemic Cirrhotic Patients with Ascites

Kalambokis

Economou

Fotopoulos

et al. 2005

Am J Gastroenterology

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“…It has a number of actions outside the pituitary in man, which include inhibition of the secretion of insulin (Alberti et al, 1973;Mortimer et al, 1974), glucagon (Mortimer et al, 1974), gastrin and gastric acid (Bloom et al, 1974), cholecystokinin-pancreozymin (Schlegel et al, 1977), gastric inhibitory peptide, and motilin Pederson et al, 197:'5). It suppresses renin secretion (Gomez-Pan et al, 1970;Rosenthal et al, 1976). It is also known to be present in the pancreatic D cells as well as in other areas of the gut of several species including man (Luft et al, 1974;Polak et aI., 1975) where it may have a paracrine role.…”

mentioning

confidence: 99%

Development and Validation of a Specific Radioimmunoassay for Somatostatin in Human Plasma

et al. 1979

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SUMMARYLittle is known about the factors controlling somatostatin secretion in man, and data are not available on the changes in circulating levels in various human physiological or pathophysiological states. This is mainly a consequence of the technical difficulties involved in measuring somatostatin in plasma. In the presence of plasma, binding of somatostatin tracer to antibody was consistently decreased by about 20 %, and this could not be abolished by the addition of EDT A and aprotinin or by the use of specially prepared somatostatin-free plasma. Furthermore, in the presence of plasma, endogenous somatostatin does not dilute in parallel with synthetic cyclic somatostatin standard.We have, therefore, developed and validated a radioimmunoassay for somatostatin using prior extraction of the peptide onto leached silica glass. Tyrosine-II somatostatin was iodinated using lactoperoxidase and purified on ODS silica. This method is superior to iodination using chloramine-T with CMC cellulose purification, and gives a highly purified preparation with a shelf-life of at least eight weeks. Using this tracer and a specific antiserum, the limit of sensitivity of the assay was 10 pg/rnl, with an intra-assay coefficient of variation of 12 %(n = 16) and inter-assay coefficient of variation of 15% (n = 10). Parallelism has been demonstrated between standard synthetic cyclic somatostatin and all extracted plasma samples. The mean recovery of exogenous somatostatin from plasma was 78 %.

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“…This also suggests a direct effect of cysteamine on kidney growth. Somatostatin reportedly reduces the increase in PRA following frosemide [22] or beta-adrenergic [23] stimulation, and suppresses PRA in patients with essential hypertension [24]. It has also been reported that endogeneous somatostatin exerts a two-fold greater maximum tonic inhibitory effect than exogenous somatostatin on renin release by the kidneys and aldosterone secretion by the zona glomerulosa in rats [25] --a finding emphasizing the importance of manipulating endogeneous somatostatin to clarify its functions.…”

Section: Discussionmentioning

confidence: 99%

Effects of Cysteamine, a Somatostatin Depleter, on the Renin-Angiotensin-Aldosterone Axis and Glomerulosa Cell Growth in Rats.

Kikuchi¹,

Nomura²,

Toraya³

et al. 1994

Endocr J

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Abstract. Cysteamine, a specific somatostatin depleter, was given to male rats to clarify its role in relation to the renin-angiotensin-aldosterone (RAA) axis and glomerulosa cell growth. Rats received seven daily sc injections of cysteamine at doses of 50 or 150 mg/kg body weight (BW). Their adrenal weights and whole cortical thickness increased, but zona glomerulosa thickness decreased dose-responsively. Plasma renin activity (PRA) and aldosterone concentration (PAC) decreased. Similar results were observed in rats on a low or high salt diet and receiving daily doses of 150 mg/kg BW of cysteamine. In hypophysectomized rats, however, cysteamine given for seven days at daily doses of 100 mg/kg BW did not change either PRA or PAC. Adrenal weight did not change either too. Our results indicate that cysteamine suppresses the RAA axis and glomerulosa cell growth, probably through pituitary factors.

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Inhibition of Frusemide-Induced Hyperreninæmia by Growth-Hormone Release-Inhibiting Hormone in Man

Cited by 43 publications

References 25 publications

The Effects of Chronic Treatment with Octreotide versus Octreotide plus Midodrine on Systemic Hemodynamics and Renal Hemodynamics and Function in Nonazotemic Cirrhotic Patients with Ascites

The Effects of Chronic Treatment with Octreotide versus Octreotide plus Midodrine on Systemic Hemodynamics and Renal Hemodynamics and Function in Nonazotemic Cirrhotic Patients with Ascites

Development and Validation of a Specific Radioimmunoassay for Somatostatin in Human Plasma

Effects of Cysteamine, a Somatostatin Depleter, on the Renin-Angiotensin-Aldosterone Axis and Glomerulosa Cell Growth in Rats.

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