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In the 15 years since the identification and characterisation of the extracellular calcium-sensing receptor (CaR), it has become increasingly apparent that this cationic binding receptor is found in many tissues, not associated with the control of plasma calcium. One of these tissues is the pancreatic islet where insulin secretion provides the basis of energy regulation. It seems inherently unlikely that the islet responds to alterations in systemic calcium and a more plausible and intriguing possibility is that the CaR mediates cell-to-cell communication through local increases in the concentration of extracellular Ca2 +, co-released with insulin. This short article explores this possibility and suggests that this novel mechanism of cell communication, along with direct coupling via gap junctions and other local paracrine regulators helps explain why the glucose responsiveness of the intact islet is greater than the sum of the composite parts in isolation.
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SUMMARY
1. Relaxin administered to intact female rats at oestrus stimulated an increase in 24 hr. uptake of 131I by the thyroid gland.
2. In oestrogen-treated spayed rats, relaxin stimulated increases in 24 hr. thyroidal uptake of 131I, thyroid weight and plasma PB131I to levels which were significantly higher than in the oestrogen treated controls.
3. The effect of relaxin on the thyroid was not observed in oestrogen-treated hypophysectomized female rats or in hypophysectomized rats on a maintenance dose of TSH.
4. It is concluded that relaxin causes an increase in size of the thyroid and uptake of radioactive iodine (RAI) in oestrogen-primed animals by means of an increased production of TSH. Two mechanisms by which TSH production may be stimulated under these experimental conditions are discussed.
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Search for other papers by S. J. RICHARDSON in
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SUMMARY
The effect of relaxin on the thyroid weights of intact, oophorectomized and hypophysectomized female Sprague-Dawley rats, intact and castrated male rats, and male and female guinea-pigs has been described.
Relaxin caused significant increases in thyroid weights in the presence of oestrogen or the ovaries and an intact pituitary. This effect of relaxin on the thyroid was not found to be significant in the presence of the testes or testosterone.
Evidence is presented that the response observed in the thyroid was due to relaxin and not to a contaminant of the relaxin extract.
A theory of action is described.