The Secretion of Calcitonin by the Perfused Ultimobranchial Gland of the Hen

Ziegler, Ralph; Telib, M; Ef, Pfeiffer

doi:10.1055/s-0028-1096824

Cited by 32 publications

(7 citation statements)

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“…Thus, the observed effects of adrenaline, propranolol and phentolamine on CT secretion are consistent with the known effects of catecholamines in other adenyl cyclase systems. Moreover, our observations are con¬ sistent with those of Ziegler, Delling & Pfeiffer (1970) who found that noradrenaline (20 /¿m) reduced CT secretion in perfused ultimobranchial glands of the fowl, and that this inhibitory effect of noradrenaline could be prevented by 0-4 mM-phentolamine.…”

Section: Discussionsupporting

confidence: 88%

A Possible Role for the Adenyl Cyclase System in Calcitonin Release

Care¹,

Bates²,

Gitelman³

1970

Journal of Endocrinology

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A possible role of the adenyl cyclase system in calcitonin (CT) release has been investigated by measurement of the rate of CT secretion in isolated porcine thyroid glands perfused in situ. Dibutyryl cyclic AMP increased the rate of secretion of CT and this effect was enhanced by theophylline. Concentrations of glucagon as low as 1\m=.\4nm (5 ng/ml) induced a significant increase in the rate of CT secretion when precautions were taken to prevent enzymic degradation of glucagon. This stimulatory effect of glucagon on CT secretion was also increased by theophylline. Significant stimulation of CT release was demonstrated with adrenaline in the presence of \g=a\-adrenergic blockade with phentolamine and could be inhibited by \g=b\-adrenergic blockade with propranolol. In contrast, thyrotrophin, tri-iodothyronine, serotonin, parathyroid hormone and cyclic guanosine monophosphate had no significant acute effects on CT secretion. It is suggested that the C-cells of the thyroid gland contain an adenyl cyclase system similar to that described in other tissues and that physiological concentrations of glucagon and catecholamines may influence the response of the C-cell to plasma calcium concentration.

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Section: Discussionsupporting

confidence: 88%

A Possible Role for the Adenyl Cyclase System in Calcitonin Release

Care¹,

Bates²,

Gitelman³

1970

Journal of Endocrinology

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“…Depletion of secretory granules from the avian ultimobranchial cells after vitamin D treatment has also been reported by Melander et al (1971) and Swarup et al (1986-87). The present study derives support from the observations of Ziegler et al (1970;hen), Bates et al (1969;geese) and Copp et al (1970;turkeys) who have noticed increased release of calcitonin after the perfusion of ultimobranchial gland with blood of a high calcium concentration. A decrease in the staining response of the cytoplasm of ultimobranchial cells after induced hypercalcemia has also been reported from other vertebrates (Dubewar and Suryawanshi, 1977;Dubewar et al, 1978;Rani, 1991, 1992;Srivastav et al, 1994Srivastav et al, , 2008Suzuki et al, 1982Suzuki et al, , 1984 On the contrary, Gonnerman et al (1972) and Stoeckel and Porte (1972) working on chicken have not noticed hypertrophy, hyperplasia and degranulation of ultimobranchial cells when subjected to experimental hypercalcemia.…”

Section: Discussionsupporting

confidence: 89%

Ultimobranchial and parathyroid glands of the pigeon Columba livia in response to 1,25(OH)₂D₃ administration

Yadav

Srivastav

2008

Microscopy Res & Technique

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Columba livia were given daily intraperitoneal injections of 100 pmol of 1,25(OH)(2)D(3)/100 g body wt. for 15 days. Ultimobranchial and parathyroid glands were fixed on 1st, 3rd, 5th, 10th and 15th day of the experiment. Following 1,25(OH)(2)D(3) treatment, the plasma calcium levels of pigeon remain unchanged on day 1. The levels increase significantly after day 3 which progresses up to day 10. The plasma calcium level becomes normal at day 15. The plasma inorganic phosphate levels of Columba livia injected with 1,25(OH)(2)D(3) remain unaffected up to day 3. The levels exhibit a progressive increase from day 5 to day 10. The levels become normophosphatemic at day 15. Up to day 3 following 1,25(OH)(2)D(3) treatment, there is no change in the ultimobranchial gland of Columba livia. The gland exhibits an increased activity after 5 days 1,25(OH)(2)D(3) treatment which is evident by the increased nuclear volume and weak staining response of the cytoplasm of ultimobranchial cells. After day 10, the nuclear volume depicts a further increase and a few completely exhausted cells are discerned. Following 15-day 1,25(OH)(2)D(3) treatment the nuclear volume records an increase and degenerating cells have been observed at certain places. The parathyroid glands of 1,25(OH)(2)D(3)-treated Columba livia remain unaffected up to day 5. After day 10 and day 15, there is a progressive decrease in the nuclear volume of parathyroidal cells and reduced chromaticity of nuclei has been noticed. Moreover, after 15 days few degenerating cells are observed.

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“…Enhanced activity/secretion of CT from the fish UBG has been reported in the past by several investigators in response to experimentally induced hypercalcemia (Lopez et al 1968, Lopez & Bagot 1971, Chan 1972, Lopez 1973, Peignoux-Deville et al 1975, Swarup & Srivastav 1984, Fouchereau-Peron et al 1986, Suzuki et al 1999, Kaida & Sasayama 2003. Hyperactivity of ultimobranchial gland after induced hypercalcemia has also been reported from non-piscine vertebrates (Ziegler et al 1970, Dubewar et al 1978, Suzuki et al 1982, Srivastav & Rani 1991, 1992, Srivastav et al 1994. It is concluded from this study that (i) CT provokes hypocalcemia in fish only when they are kept in a medium which can reduce the circulating levels of CT, (ii) the UBG of normal fish respond to CT administration by depicting inactivity, and (iii) UBG gets activated when the fish is kept in calcium-rich medium and this activity of UBG is not influenced by administration of CT.…”

Section: Discussionmentioning

confidence: 84%

Ultimobranchial gland of freshwater catfish, Heteropneustes fossilis, in response to calcitonin administration

et al. 2009

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The absence o!!f a hypocalcemic effect of calcitonin (CT) in fishes has been suggested due to exceedingly high plasma levels of CT; the fish may be saturated with respect of circulating CT and therefore unable to respond to exogenously administered CT. Earlier it has been suggested that a hypocalcemic action of injected CT may be obscured by changes in the release of endogenous CT and other calcium regulating hormones. In this study we have used artificial freshwater, calcium-deficient freshwater and calcium-rich freshwater and injected the fish with CT. The aim behind selecting these media were (i) in calcium-deficient medium there would be reduced circulating levels of CT, (ii) in calciumrich medium there would be diminished secretion of prolactin (this hormone is hypercalcemic in fish), and (iii) by keeping the fish in calcium-rich medium we can test the antihypercalcemic action of CT. Moreover, the present study would reveal the changes in the ultimobranchial gland (UBG) after keeping the fish in all the above three media and/or injecting the fish with CT. Freshwater catfish, Heteropneustes fossilis, were administered intraperitoneally daily with vehicle or 0.5 U/100g body wt of salmon calcitonin (CT) and kept in artificial freshwater, calcium-rich freshwater and calcium-deficient freshwater for 10 days. Blood samples were collected on 1, 3, 5, and 10 days following the treatment and analyzed for serum calcium levels. The ultimobranchial gland (UBG) was also fixed for histological studies on these intervals. In artificial freshwater there was no change in the serum calcium levels of calcitonin-injected fish. The ultimobranchial gland of calcitonin-injected fish exhibited a progressive decrease in the nuclear volume from day 5 onwards. On day 10 vacuolization in the gland was also noticed. In vehicle-injected fish (control) kept in calcium-rich freshwater hypercalcemia has been noticed which persists till the end of the experiment. In calcitonin-treated fish maintained in calcium-rich freshwater there is no change in serum calcium level as compared to vehicle-injected fish. In vehicleinjected fish the UBG depicts decreased staining response and increased nuclear volume at day 5. On day 10 the nuclear volume is further increased and few degenerating cells have been noticed. Calcitonin fails to induce any histological change in the UBG as compared to control. In vehicle-injected fish kept in calcium-deficient freshwater the serum calcium levels decrease from day 1 to day 3. The levels exhibit hypercalcemia on day 10. CT treatment to the fish kept in calcium-deficient freshwater evokes a decrease in the calcium levels on day 1 and day 3. A significant hypercalcemia has been noticed on day 5 and day 10. In vehicle-injected fish kept in calcium-deficient freshwater the UBG reveals a decreased staining response on day 10. In CT-injected fish maintained in calcium-deficient freshwater the UBG depicts an increased nuclear volume and few exhausted cells on day 10. It can be concluded that CT can provoke hypocalcemia o...

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The Secretion of Calcitonin by the Perfused Ultimobranchial Gland of the Hen

Cited by 32 publications

References 0 publications

A Possible Role for the Adenyl Cyclase System in Calcitonin Release

A Possible Role for the Adenyl Cyclase System in Calcitonin Release

Ultimobranchial and parathyroid glands of the pigeon Columba livia in response to 1,25(OH)₂D₃ administration

Ultimobranchial gland of freshwater catfish, Heteropneustes fossilis, in response to calcitonin administration

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The Secretion of Calcitonin by the Perfused Ultimobranchial Gland of the Hen

Cited by 32 publications

References 0 publications

A Possible Role for the Adenyl Cyclase System in Calcitonin Release

A Possible Role for the Adenyl Cyclase System in Calcitonin Release

Ultimobranchial and parathyroid glands of the pigeon Columba livia in response to 1,25(OH)2D3 administration

Ultimobranchial gland of freshwater catfish, Heteropneustes fossilis, in response to calcitonin administration

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Ultimobranchial and parathyroid glands of the pigeon Columba livia in response to 1,25(OH)₂D₃ administration