Changes in calcitonin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats
To assess the role of peripheral sympathetic nerves in the regulation of calcitonin release, rats subjected to superior cervical ganglionectomy (SCGx) 16-28 h earlier were used. The time periods selected allowed us to examine C cell response during the supraliminal release of sympathetic transmitter...
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1986
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00283835_v43_n4_p498_Cardinali http://hdl.handle.net/20.500.12110/paper_00283835_v43_n4_p498_Cardinali |
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paper:paper_00283835_v43_n4_p498_Cardinali2023-06-08T14:55:00Z Changes in calcitonin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats Calcitonin Calcium homeostasis Norepinephrine Superior cervical ganglion Thyroid C cells calcitonin calcium chloride noradrenalin phenoxybenzamine propranolol radioisotope adrenergic system animal experiment autonomic nervous system c cell drug comparison drug efficacy endocrine system ganglionectomy hypercalcemia intraperitoneal drug administration nerve degeneration nervous system nonhuman peripheral nervous system rat subcutaneous drug administration superior cervical ganglion thyroid cell Animals Calcitonin Calcium Calcium Chloride Ganglia, Sympathetic Male Nerve Degeneration Norepinephrine Phenoxybenzamine Rats Rats, Inbred Strains Thyroid Gland Time Factors To assess the role of peripheral sympathetic nerves in the regulation of calcitonin release, rats subjected to superior cervical ganglionectomy (SCGx) 16-28 h earlier were used. The time periods selected allowed us to examine C cell response during the supraliminal release of sympathetic transmitter that accompanies anterograde degeneration of nerve varicosities as well as during the neural paralysis that ensues thereafter. At the time intervals examined, SCGx did not result in significant changes of basal serum calcitonin or Ca levels. The intraperitoneal administration of CaCI<inf>2</inf> brought about an impending increase of serum Ca to the same extent in SCGx and sham-operated rats. A significant depression of calcitonin release was observed in rats killed around the time of nerve terminal degeneration (16-21 h post SCGx) but not about 10 h later. Additionally a delay to achieve a maximal calcitonin response was apparent during nerve degeneration. Injection of the α-adrenoceptor blocker phenoxybenzamine significantly increased basal calcitonin levels and restored the depressed calcitonin response to hypercalcemia seen in SCGx rats. Treatment with the β-adrenoceptor blocker propranolol counteracted phenoxybenzamine activity but was unable to modify per se calcitonin release in SCGx or sham-operated rats. Basal Ca levels and their increase after intraperitoneal CaCl<inf>2</inf> were similar in all examined groups regardless of the drug injected. In an additional experiment phenoxybenzamine injected into SCGx rats in doses one-fifth those employed earlier still reversed both the depression in maximal calcitonin response as well as the delay to attain maximal release after CaCl<inf>2</inf>, but was unable to affect basal calcitonin levels. These results indicate that at the time of nerve terminal degeneration in the superior cervical ganglion territory there is a depression in C cell response to hypercalcemia. An α-adrenoceptor-mediated inhibitory influence of neropinephrine as well as a less important β-adrenoceptor-mediated stimulatory influence of the sympathetic transmitter may explain the observed results. © 1986 S. Karger AG, Basel. 1986 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00283835_v43_n4_p498_Cardinali http://hdl.handle.net/20.500.12110/paper_00283835_v43_n4_p498_Cardinali |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Calcitonin Calcium homeostasis Norepinephrine Superior cervical ganglion Thyroid C cells calcitonin calcium chloride noradrenalin phenoxybenzamine propranolol radioisotope adrenergic system animal experiment autonomic nervous system c cell drug comparison drug efficacy endocrine system ganglionectomy hypercalcemia intraperitoneal drug administration nerve degeneration nervous system nonhuman peripheral nervous system rat subcutaneous drug administration superior cervical ganglion thyroid cell Animals Calcitonin Calcium Calcium Chloride Ganglia, Sympathetic Male Nerve Degeneration Norepinephrine Phenoxybenzamine Rats Rats, Inbred Strains Thyroid Gland Time Factors |
| spellingShingle |
Calcitonin Calcium homeostasis Norepinephrine Superior cervical ganglion Thyroid C cells calcitonin calcium chloride noradrenalin phenoxybenzamine propranolol radioisotope adrenergic system animal experiment autonomic nervous system c cell drug comparison drug efficacy endocrine system ganglionectomy hypercalcemia intraperitoneal drug administration nerve degeneration nervous system nonhuman peripheral nervous system rat subcutaneous drug administration superior cervical ganglion thyroid cell Animals Calcitonin Calcium Calcium Chloride Ganglia, Sympathetic Male Nerve Degeneration Norepinephrine Phenoxybenzamine Rats Rats, Inbred Strains Thyroid Gland Time Factors Changes in calcitonin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats |
| topic_facet |
Calcitonin Calcium homeostasis Norepinephrine Superior cervical ganglion Thyroid C cells calcitonin calcium chloride noradrenalin phenoxybenzamine propranolol radioisotope adrenergic system animal experiment autonomic nervous system c cell drug comparison drug efficacy endocrine system ganglionectomy hypercalcemia intraperitoneal drug administration nerve degeneration nervous system nonhuman peripheral nervous system rat subcutaneous drug administration superior cervical ganglion thyroid cell Animals Calcitonin Calcium Calcium Chloride Ganglia, Sympathetic Male Nerve Degeneration Norepinephrine Phenoxybenzamine Rats Rats, Inbred Strains Thyroid Gland Time Factors |
| description |
To assess the role of peripheral sympathetic nerves in the regulation of calcitonin release, rats subjected to superior cervical ganglionectomy (SCGx) 16-28 h earlier were used. The time periods selected allowed us to examine C cell response during the supraliminal release of sympathetic transmitter that accompanies anterograde degeneration of nerve varicosities as well as during the neural paralysis that ensues thereafter. At the time intervals examined, SCGx did not result in significant changes of basal serum calcitonin or Ca levels. The intraperitoneal administration of CaCI<inf>2</inf> brought about an impending increase of serum Ca to the same extent in SCGx and sham-operated rats. A significant depression of calcitonin release was observed in rats killed around the time of nerve terminal degeneration (16-21 h post SCGx) but not about 10 h later. Additionally a delay to achieve a maximal calcitonin response was apparent during nerve degeneration. Injection of the α-adrenoceptor blocker phenoxybenzamine significantly increased basal calcitonin levels and restored the depressed calcitonin response to hypercalcemia seen in SCGx rats. Treatment with the β-adrenoceptor blocker propranolol counteracted phenoxybenzamine activity but was unable to modify per se calcitonin release in SCGx or sham-operated rats. Basal Ca levels and their increase after intraperitoneal CaCl<inf>2</inf> were similar in all examined groups regardless of the drug injected. In an additional experiment phenoxybenzamine injected into SCGx rats in doses one-fifth those employed earlier still reversed both the depression in maximal calcitonin response as well as the delay to attain maximal release after CaCl<inf>2</inf>, but was unable to affect basal calcitonin levels. These results indicate that at the time of nerve terminal degeneration in the superior cervical ganglion territory there is a depression in C cell response to hypercalcemia. An α-adrenoceptor-mediated inhibitory influence of neropinephrine as well as a less important β-adrenoceptor-mediated stimulatory influence of the sympathetic transmitter may explain the observed results. © 1986 S. Karger AG, Basel. |
| title |
Changes in calcitonin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats |
| title_short |
Changes in calcitonin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats |
| title_full |
Changes in calcitonin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats |
| title_fullStr |
Changes in calcitonin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats |
| title_full_unstemmed |
Changes in calcitonin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats |
| title_sort |
changes in calcitonin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats |
| publishDate |
1986 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00283835_v43_n4_p498_Cardinali http://hdl.handle.net/20.500.12110/paper_00283835_v43_n4_p498_Cardinali |
| _version_ |
1768541694676959232 |