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I Zofková

Publications and source records attributed to I Zofková.

At least 55 records · Page 3Linked to original sources
PubMed1989

[The calcium signal in the regulation of insulin secretion].

In the submitted review the author pays attention to mechanisms of control of insulin secretion and the mutual interaction of other messengers (cAMP, calcium and inisitol triphosphate) with special attention to the calcium signal which plays a most important role in the stimulation of the excitable B cell. The trigger of the two-stage insulin secretion is cyclic accumulation of calcium in the cytosol of the B cell and the mutual harmony between calcium of the intra- and extracellular compartment. In the early stage of insulin secretion in particular the intracellular compartment is the source of calcium; from there the ion is released due to the action of inositol triphosphate (IP3) activated by phospholipase C. Calcium of the extracellular compartment is mobilized also in the early secretory stage by opening of the depolarization-dependent calcium channels, it plays, however, a more important part during the second stage. Activation of the other messengers, incl. the calcium signal, depends on the type of secretagogue stimulus. During systemic changes of calcium homeostasis in vivo the calcium signal of the B cell is activated or inhibited in different ways. In the course of hypercalcaemia, in particular if acute, the direct influence of calcium ions on insulin secretion is modulated by further factors, e.g. somatostatin, calcitonin, cholecystokinin, glucagon, adrenocortical hormones, opioids and other substances released into the blood stream. In chronic hypercalcaemia which is the result of primary hyperparathyroidism or vitamin D intoxication the action of calcium on the metabolic and hormonal response is enhanced by the ionophoretic action of parathormone or active vitamin D metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Use of calciotropic agents in psychiatry and neurology].

Neurotransmission of impulses is a phenomenon activated by the calcium signal. Therefore changes of calcium homeostasis in the nerve cell always influence more or less this function. Changes of calcium homeostasis in the nerve cell occur under various pathological conditions, incl. hypoxia. The cytosol of the neuron is excessively saturated with calcium ions due to a shift from the extracellular space. The affected neurons release humoral factors, so-called neurotransmitters, which by receptor-controlled activation of calcium channels enhance the calcium influx from the extracellular space. After exhaustion of defense mechanisms by which the nerve cell gets rid of excessive calcium its metabolism is affected and necrosis may occur. This toxic effect of calcium can be prevented by administration of calcium antagonists represented by 1. blockers of slow calcium currents and 2. calmodulin inhibitors. The author gives an account of antipsychotic, analgetic, myorelaxing and vasodilatating effects of some calcium antagonists, and their clinical application is discussed. The author emphasizes also some possible undesirable effects of some neuroleptics mediated by the calciotropic mechanism, in particular during long-term administration. They are manifested by increased urinary calcium losses and impaired bone mineralization. Delayed regression of myorelaxation during anaesthesia is also important and must be taken into account in patients treated for prolonged periods with blockers of calcium currents.

Calcium Channel Blockers↗
PubMed1989

Effect of calcitonin and 1,25(OH)2-vitamin D3 on the FSH, LH and testosterone secretion at rest and LHRH stimulated secretion.

The calcium signal plays an important role in the control of the secretory process of some adenohypophyseal hormones which responds to the administration of calciotropic substances by a marked change. In the submitted work the effect of calcitonin and 1,25(OH)2-vitamin D3 (1,25(OH)2D3) on FSH, LH and testosterone secretion was investigated. A single dose of 50 U synthetic salmon calcitonin did not influence the FSH, LH and testosterone secretion at rest nor stimulated secretion. 1,25(OH)2D3 administered for four days in amounts of 3 micrograms/day did not affect the LH and testosterone secretion but increased slightly the secretory response of FSH to LHRH, significantly during the 80th minute following administration of the secretagogue (P less than 0.01). The indication of bi-phasic FSH secretion was eliminated by 1,25(OH)2D3. The significant decline of PTH levels following administration of 1,25(OH)2D3 is evidence of a biologically effective level of 1,25(OH)2D3 attained by the administered dose of hormone. As compared with the marked effect of calcitonin and 1,25(OH)2D3 on thyrotropic hormone secretion, it may be concluded that the gonadotropic system is considerably less sensitive to a change of calcium homeostasis induced by calcitonin or 1,25(OH)2D3. Nevertheless a slight increase of the FSH secretion and a change of the dynamics of its secretion suggest a modulating role of 1,25(OH)2D3 in the control of FSH secretion.

Adult↗
PubMed1989

[The calcium signal in the physiology of the secretory process. II. The effect of extracellular and intracellular calcium on secretory mechanisms].

Investigations of the influence of the extra- and intracellular calcium source on secretory processes helps the understanding of the physiology and pathophysiology of secretion. The ratio of the two calcium sources in the activation of secretion depends on the type of secretory cell, on the character of the secretagogue stimulus and the phase of the secretory process. The use of intracellular sources of calcium in the early stage of secretion explains the lack of an inhibitory action of calcium current blockers on the function of some hormonal systems in short-term studies, e.g. the tyrotropic and somatotropic system, or on adrenocortical secretion. Conversely inhibition of some hormonal functions in the curse of prolonged inhibition of calcium currents indicates the importance of the inflow of calcium ions from the extracellular space into the cytosol during long-term regulation of secretion. The author gives an account of the results of investigations which by means of calcium ionophores or calcium current antagonists provide evidence of the importance of an extracellular calcium source in the control of secretion of some systems.

Animals↗
PubMed1989

[The calcium signal in the physiology of the secretory process. I].

The author gives an account of contemporary knowledge and hypotheses on the role of calcium as the second messenger signalizing stimulation of the secretory cell by a specific secretagogue stimulus. The basic structures from which calcium ions are released into the cytosol are the endoplasmatic reticulum, secretory granules and the cell membrane. The author discusses also the importance of mitochondria which act as an intracellular calcium reservoir. An important source of calcium for activation of the secretory process is also the extracellular space. Oscillation of the electric tension of the membrane of the excitable cell which causes temporary opening of the calcium channels participates also in the rise of this ion concentration in the cytosol; in the majority of endocrine systems, however, only in the second stage of the secretory process. In the reparative stage the intracellular reserves are resaturated with calcium. The ratio of the intra- and extracellular source depends probably on the type of secretory cell and the secretagogue stimulus. The author refers to some of her own clinical investigations where it did not prove possible to demonstrate the inhibiting action of calcium current blockers in the secretory process of excitable systems. Based on theoretical findings and hypotheses, she explains the inhibitory action of acute hypercalcaemia on some hormonal functions. In the review attention is paid to the function of calmodulin which is a mediator of the calcium signal and probably the site of interaction of some calciotropic substances.

Animals↗
PubMed1988

Effect of 1,25-dihydroxyvitamin D3 (calcitriol) on prolactin secretion at rest and TRH-stimulated secretion in humans.

In the submitted paper the authors investigated the effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3, calcitriol) administered by the oral route for a period of four days in amounts of 3.0 micrograms/d on prolactin secretion at rest and secretion stimulated by thyrotropin-releasing hormone (TRH) and on the lactotrophic secretory reserve assessed as the difference between values at rest and TRH-stimulated prolactin levels during the 20th, 30th, 40th and 60th minute after TRH administration (delta PRL) in 18 healthy women. The untreated control group was formed by 8 healthy women. In the subjects treated with 1,25(OH)2D3 a significant rise of the prolactin levels at rest was recorded and TRH-stimulated values and delta PRL during the 20th and 30th minute after TRH administration significantly increased as compared with control examination, while in the untreated group the values at rest and stimulated prolactin levels and delta PRL did not differ from the values recorded during the control examination. The results confirm the stimulating action of 1,25(OH)2D3 on prolactin secretion in healthy women and indicate a satisfactory reproducibility of TRH test of lactotrophic secretion.

Adult↗
PubMed1988

Influence of the interaction of calcitonin and 1,25(OH)2-vitamin D3 on prolactin secretion.

Calcitonin inhibits and 1,25(OH)2-Vitamin D3 (1,25(OH)2D3) stimulates prolactin and thyrotropin secretion. During concurrent administration of calcitonin and 1,25(OH)2D3 the action of the two calciotropic substances on thyrotropin secretion antagonizes each other. In the submitted investigation the effect of a single dose of synthetic salmon calcitonin on the prolactin secretion at rest and TRH-induced secretion was compared in untreated healthy subjects and in subjects given for four days previously 1,25(OH)2D3 in doses which have a stimulating effect on prolactin secretion (3 micrograms/d). Calcitonin, 50 U, administered by the i.v. route by infusion inhibited the secretion of prolactin at rest (p less than 0.05) and the TRH-stimulated secretion during the 20th, 30th, 40th and 60th minute after TRH administration (p less than 0.01 at all time intervals) in untreated subjects but also the secretion at rest (p less than 0.01) and TRH - stimulated secretion at times 20, 30, 40 and 60 mins following TRH administration (p less than 0.01, p less than 0.05, p less than 0.05 and p less than 0.05, respectively) in subjects pretreated with 1,25(OH)2D3. Compared with the thyrotropic system, the inhibiting effect of calcitonin on the lactotropic system is not cancelled by the administration of 1,25(OH)2D3. It is assumed that differences in the response of the lactotropic and thyrotropic system to the concurrent administration of calcitonin and 1,25(OH)2D3 are conditioned by the different ratio of the number of receptors for calcitonin and 1,25(OH)2D3 in the lactotropic and thyrotropic cell.

Administration, Oral↗
PubMed1988

Effect of 1.25 (OH)2 vitamin D3 (calcitriol) on TRH-induced thyrotropin secretion in man.

Thyrotropin (TSH) secretion was assessed in three groups of healthy volunteers before and after four days administration of 1.25(OH)2 vitamin D3 (calcitriol) by the oral route -1.5 micrograms/d (group A), 3.0 micrograms/d (group B) or 3.0 micrograms/d combined with trifluoperazine (8-12 mg/d by mouth) (group C). The control trials and experiments proper were made in the same subjects within one month. The lower calcitriol dose did not change significantly the TRH-stimulated TSH levels nor the secretory reserve measured as the difference of TSH levels at the rest and TRH-stimulated levels (delta TSH) during the 20th, 30th, 40th and 60th minute following TRH administration. A larger calcitriol dose caused a significant increase of TSH values at rest and TRH-stimulated values during the 20th, 30th, 40th and 60th minute following TRH administration (p less than 0.05, p less than 0.05, p less than 0.05, p less than 0.05 and p less than 0.01, respectively) as well as delta TSH (p less than 0.05 at all time intervals). The intracellular calcium antagonist trifluoperazine interfered only with the stimulating effect of calcitriol on the TSH secretion at rest and on delta TSH during the 60th minute following TRH administration, while the TSH levels during the 20th, 30th, 40th and 60th minute after TRH administration were significantly higher, as compared with the control examination (p less than 0.01, p less than 0.01, p less than 0.05 and p less than 0.05, respectively) and also delta TSH was significantly elevated during 20th, 30th, and 40th minute after TRH administration during combined treatment (p less than 0.05, p less than 0.01, p less than 0.05, respectively). Calcitriol thus causes a dose-dependent increase of TSH secretion, probably partly also by a mechanism which is independent on the change of intracellular calcium homeostasis.

Adult↗
PubMed1988

Effects of calcitonin, 1,25(OH)2 vitamin D3 and trifluoperazine on thyrotropic secretion and their mutual interactions.

The effects of pharmacological doses of calcium ionophores, calcitonin and 1,25 (OH2)D3, and of the calmodulin inhibitor, trifluoperazine, on thyrotropin secretion at rest and TRH stimulated secretion were investigated as well as their mutual interactions in five groups of clinically healthy volunteers. The thyrotropic secretory response to TRH was inhibited by a single intravenous dose of 50 U synthetic salmon calcitonin or trifluoperazine administered by mouth seven days prior to the TRH test, 6-12 mg/day, and stimulated by 1,25(OH)2D3 administered by mouth four days before the TRH test -3 micrograms/day. The stimulating action of 1,25(OH)2D3 was abolished by calcitonin, administered by the intravenous route - 50 U - closely before the TRH test but not by the concomitant administration of trifluoperazine. The author expressed the hypothesis, that calcitonin and 1,25(OH)2D3 but not trifluoperazine and 1,25(OH)2D3 are mutual antagonists which act at the same subcellular level of the thyrotropic cell and that synthesis and activation of calmodulin is not the trigger of thyrotropic secretion after stimulation with 1,25(OH)2D3. An altered thyrotropin secretion must be foreseen during the therapeutic administration of the investigated calciotropic substances, the mutual interactions of which could be used in practice.

Administration, Oral↗
PubMed1987

The effects of calcitonin, somatostatin and hypercalcaemia on metabolic and hormonal indicators during an oral glucose tolerance test (OGTT).

The authors compared the effect of synthetic salmon calcitonin and synthetic somatostatin (SRIF) and hypercalcaemia on an oral glucose tolerance test (OGTT) in healthy subjects in relation to changes of insulin (IRI), somatotrophin (HGH) and cortisol levels. Calcitonin--100 U--in an intravenous infusion in the course of OGTT markedly altered the pattern of the blood sugar curve and of IRI levels. After the initial retardation of the rise of the blood sugar and IRI levels during the 15th and 30th min, the values of both variables increased parallel during the 120th and 180th min, as compared with the control examination after saline. SRIF--500 micrograms--administered in an intravenous infusion altered the pattern of the blood sugar and IRI curves in a similar way as calcitonin, however during the 120th and 180th minute when the blood sugar levels rose significantly the IRI levels did not rise. The curve of HGH levels on infusion with calcitonin displayed a typical three-phase course, as during the control OGTT. During infusion of SRIF the HGH levels were insignificantly but constantly reduced during the first 60 mins. of the OGTT and thus the typical three-phase shape of the curve was impaired. Calcitonin significantly raised the cortisol levels throughout the OGTT, while SRIF caused their slight decline during the 120th min. Hypercalcaemia induced by infusion of 13.3 mg Ca/kg body weight did not alter significantly the blood levels of glucose, IRI and HGH, but caused a significant rise of the cortisol level throughout the OGTT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Influence of trifluoperazine on ACTH- or angiotensin-stimulated mineralocorticoid and glucocorticoid secretion in man.

During stimulation of adrenocortical secretion the calcium--calmodulin system is activated to a different extent, depending on the secretagogue substance. In the submitted paper the influence of therapeutic doses of the calmodulin inhibitor, trifluoperazine, on aldosterone and cortisol secretion stimulated by ACTH or by activation of endogenous angiotensin by furosemide was investigated in healthy subjects. Trifluoperazine already in amounts of 6 mg/day administered for one week inhibited the "basal" aldosterone secretion assessed in a vertical position (p less than 0.01) and ACTH stimulated secretion (during the 30th minute p less than 0.05). The basal aldosterone secretion assessed in a horizontal position was not affected by trifluoperazine, similarly as it did not affect the secretory response to endogenous angiotensin activated by furosemide, regardless whether a dose of 6 mg or 12 mg/day was used. ACTH stimulated cortisol blood levels were after trifluoperazine insignificantly but constantly lower throughout the test, while they were not altered by trifluoperazine in the furosemide test. The plasma calcium level was not significantly affected by trifluoperazine. It may be concluded that trifluoperazine alters ACTH stimulated mineralocorticoid secretion, while it does not influence angiotensin stimulated secretion. The revealed differences in adrenocortical response to trifluoperazine in vivo cannot be explained merely by a different sensitivity of the calcium-calmodulin system to stimulation by two different secretagogues, but by interaction of some regulatory mechanisms influenced by trifluoperazine with adrenocortical secretion.

Adrenal Cortex↗
PubMed1987

Comparison of metabolic and hormonal effects of calcitonin and somatostatin (SRIF) in the course of oral glucose tolerance test (OGTT).

A comparison is presented of the effect of two therapeutic doses of synthetic somatostatin (250 and 500 micrograms) and salmon calcitonin (50 and 100 U) on the blood levels of sugar, insulin (IRI), somatotropin (HGH) and cortisol in healthy volunteers following peroral administration of 75 g of glucose. Calcitonin was responsible for a significant change in glycaemia as well as IRI levels: following a retarded enhancement glycaemia as well as insulinaemia through out the first 15-30 minutes of OGTT, increased levels of both indicators were persistent at minute 120 and 180, so that the course of both curves was almost parallel. The effect was similar after SRIF had been administered, with the exception of insulin secretion being more pronounced, so that at a later stage of OGTT no hyperinsulinaemia was seen. The HGH levels tended to decrease due to both hormones, the tendency being more marked after SRIF, though statistically insignificant. There was a marked difference between the hormones as regards their effect on adrenocortical secretion. While the latter was constantly stimulated throughout OGTT under calcitonin infusion, the influence of SRIF was not significant. The metabolic and hormonal changes were found after both a lower and higher dose of both hormones, the only differences being that the inhibitory effect on the initial increase in glycaemia following a lower dose of SRIF was of no statistical significance. Hence, the metabolic and hormonal effects of calcitonin and SRIF in an acute experiment display many similarities, however, they do differ in some aspects; these effects do not depend on the doses demonstrated for both lower and higher doses of the above hormones.

Adult↗