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  • Author: R. H. Jones x
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Bradykinin stimulates phosphoinositide metabolism and prolactin secretion in rat anterior pituitary cells

T.H. Jones, B. L. Brown, and P. R. M. Dobson

ABSTRACT

Bradykinin stimulated prolactin secretion from monolayer cultures of rat anterior pituitary cells, the stimulation being greater from the cells of male rats. This stimulated secretion was accompanied by a rise in total inositol phosphate accumulation, suggesting that the action of bradykinin is mediated by phosphoinositide hydrolysis. The increase in inositol phosphate accumulation was biphasic; a further sharp rise occurred when the concentration of bradykinin exceeded 1 μmol/l. This may indicate that bradykinin acts on other cell types in the pituitary gland. Bradykinin had no effect on growth hormone secretion from cells of normal pituitary glands, or on prolactin secretion and phosphoinositide metabolism in GH3 rat pituitary tumour cells. Bradykinin receptor antagonists (both B1 and B2) had no effect on either bradykinin-stimulated inositol phosphate accumulation or prolactin secretion. Kallikreins, the enzymes responsible for the generation of kinins, are known to be present in the adenohypophysis. Therefore, the results presented here would suggest that kinins may have a role as paracrine agents in the pituitary gland.

DOI:
https://doi.org/10.1677/jme.0.0020047
Volume 2: Issue 1,
Pages:
47–53 (7 total)
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Intraperitoneal insulin is more potent than subcutaneous insulin at restoring hepatic insulin-like growth factor-I mRNA levels in the diabetic rat: a functional role for the portal vascular link

D. L. Russell-Jones, M. Rattray, V. J. Wilson, R. H. Jones, P. H. Sönksen, and C. R. Thomas

ABSTRACT

There is evidence that the hormonal control of hepatic IGF-I production is mediated by GH and insulin. To elucidate the role of these hormones further we administered s.c. or i.p. insulin (at 2·5 and 5·0 IU/day) and/or GH (0·8 IU/day) to rats made diabetic with streptozotocin 16 days previously. Hepatic IGF-I production was then assessed by quantifying hepatic IGF-I mRNA levels by autoradiography of Northern blots. Diabetes resulted in a fivefold reduction in hepatic IGF-I mRNA levels (optical density (OD) of the 0·7–1·1 kb band: controls, 1·3±0·09; diabetics, 0·28±0·08; P<0·01), which was not significantly changed by treatment with s.c. insulin (OD: low dose, 0·55±0·05; high dose, 0·58±0·05) or low dose i.p. insulin (OD: 0·40±0·03). High dose i.p. insulin enhanced hepatic IGF-I mRNA levels (OD: 0·93±0·23) compared with diabetic rats (P<0·01) and those given high dose s.c. insulin (P<0·04), despite the blood glucose values being similar in the treated groups (i.p., 4·72±0·29 mmol/l; s.c., 3·32±0·03 mmol/l). Administration of GH alone partially restored the hepatic IGF-I mRNA level (OD: GH-treated, 1·00±0·05; diabetic, 0·28±0·08; P<0·01), whilst having no effect on blood glucose values (diabetic, 36·35±0·45 mmol/l; GH-treated, 38·65±2·39 mmol/l). Additional administration of s.c. insulin completely restored IGF-I mRNA levels to those of controls (OD: low dose, 1·35±0·14; high dose, 1·27 ± 0·18). These observations indicate that insulin and GH are required for full expression of hepatic IGF-I mRNA and that insulin given i.p. is more potent than that given s.c. at stimulating hepatic synthesis of IGF-I.

DOI:
https://doi.org/10.1677/jme.0.0090257
Volume 9: Issue 3,
Pages:
257–263 (7 total)