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Biomedical subjects

I Zofková

Publications and source records attributed to I Zofková.

At least 73 records · Page 4Linked to original sources
PubMed1986

Trifluoperazine inhibits thyrotropin-releasing hormone-stimulated TSH secretion.

In previous work changes of the thyrotropic secretion after administration of some substances affecting the calcium content in the cytosol were demonstrated. The object of the present investigation was to assess the hormonal response to the administration of trifluoperazine, a psychopharmaceutical preparation, the main mechanism of its action being the inactivation of the cytosol receptor for the calcium signal - calmodulin. The poor utilization of intracellular calcium of the secretory cell is then the factor which inhibits secretion proper. The thyrotropic secretory reserve (delta TSH) was assessed in the same subjects before and after trifluoperazine administration by the TRH test as the difference of values at rest and TRH-stimulated TSH levels during the 20th, 30th, 40th and 60th minute following intravenous administration of 200 micrograms TRH. It was revealed that this calmodulin antagonist administered for one week in amounts of 6-12 mg per day by mouth significantly inhibits the secretory response of TSH to TRH in healthy subjects during the 20th and 40th min. (P less than 0.05). The reproducibility of the TRH test repeated in a group of subjects not treated with trifluoperazine, however, under equal conditions and after the same time intervals as in the experiment with trifluoperazine was very satisfactory and thus physiological inhibition caused by repeated TRH administration could be ruled out. The inhibition of the secretory TSH response to TRH can be therefore considered the consequence of the direct effect of trifluoperazine on the thyrotropic secretory mechanism. Trifluoperazine significantly reduced serum calcium levels and raised phosphate levels, while it did not affect the blood levels of magnesium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

The effect of long-term verapamil treatment on the secretion of cortisol and aldosterone in subjects with normal and high blood pressure.

Based on their previous observations of the stimulating action of verapamil on the secretory reserve of cortisol after one-week oral administration to healthy volunteers, the author investigated the effect of this calcium entry blocker on the adrenocortical function (cortisol and aldosterone secretion) during therapeutic administration to patients with mild arterial hypertension and normotensive patients suffering from Raynaud's syndrome. Verapamil, 3-4 X 80 mg per day by the oral route, did not lead to significant changes of cortisol levels at rest nor after ACTH stimulation when assessed at the end of the first month of treatment in both groups. However, normotensive subjects with Raynaud's syndrome showed a decline of ACTH stimulated cortisolaemia during the 3rd month (p less than 0.05) and 4th month (p less than 0.01) and a reduction of cortisol secretory reserve (delta cortisol) during the 3rd month of treatment (p less than 0.05). In aldosterone secretion of normotensives with Raynaud's syndrome no significant changes were observed. In hypertensive subjects, the decline of ACTH stimulated cortisolaemia at the end of the 3rd and 4th month was not significant and delta cortisol did not change. The initial aldosterone levels before and after ACTH and delta aldosterone before treatment of hypertensives was lower as compared with normotensives (p less than 0.01, p less than 0.01 and p less than 0.05, respectively), and increased gradually during treatment in the 4th month significantly (p less than 0.05, p less than 0.01 and p less than 0.01, respectively). The hypotensive effect of verapamil persisted throughout the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1984

Hypercalcaemia and calcitonin inhibit prolactin secretion.

The authors investigated the effect of acute hypercalcaemia induced by a 2-hour intravenous infusion of calcium gluconate (8.9 mg Ca2+/kg b. w.) on the lactotrophic secretory reserve assessed by the test with insulin hypoglycaemia (delta PRL) and the effect of an intravenous bolus of 50 IU synthetic salmon calcitonin on the lactotrophic secretory reserve assessed by means of the TRH test (delta PRL). Acute hypercalcaemia inhibits PRL levels stimulated by insulin hypoglycaemia (p less than 0.01) as well as delta PRL (p less than 0.01). Calcitonin reduces PRL levels at rest and TRH stimulated levels (p less than 0.05 and p less than 0.01, respectively) as well as delta PRL (p less than 0.01). The prolactin inhibiting effect of calcitonin resembles markedly the effect of hypercalcaemia. The exact mechanism of these changes and the physiological impact of calcitonin on the regulation of PRL secretion is not known.

Adolescent↗
PubMed1984

Calcitonin inhibits TRH-induced TSH secretion.

The authors investigated in 14 healthy volunteers the effect of a single dose of 50 MRCU of synthetic salmon calcitonin on plasma levels of thyroxine (T4), triiodothyronine (T3), thyrotropin (TSH), calcium, phosphorus and magnesium and on the thyrotropic secretory reserve assessed by means of the TRH test. T4 and T3 levels did not change significantly within 120 min after administration of calcitonin. TSH levels during the 60th minute declined insignificantly. TRH stimulated TSH levels after administration of calcitonin were significantly lower, as compared with control values (p less than 0.01). The thyrotrophic secretory reserve determined as the difference of TSH values at rest and after stimulation was significantly inhibited by calcitonin (p less than 0.01). The phosphorus and magnesium levels did not change significantly after calcitonin, the calcium levels displayed only a slightly declining trend. No correlation was revealed between the secretory response of TSH and calcium, phosphorus and magnesium levels. The inhibitory action of calcitonin on TSH secretion is probably not mediated by changes in the extracellular concentration of these ions but is most probably the consequence of the direct influence on the secretory mechanism inside the thyrotrophic cell.

Adult↗
PubMed1983

Effect of hypercalcaemia on adrenocortical and growth hormone secretion.

The authors investigated in 19 healthy women changes in the plasma levels of cortisol and growth hormone during acute hypercalcaemia induced by a load of 8.9 mg Ca2+/kg body weight, administered as intravenous infusion and the effect of hypercalcaemia on the adrenocortical and somatotrophic secretory reserve assessed by the test with insulin hypoglycaemia. Hypercalcaemia causes a rise of the basal cortisol plasma level starting at the 90th minute from the onset of the infusion when the calcium level reaches values of 2.99 mmol/l. The adrenocortical secretory reserve is, however, significantly reduced by hypercalcaemia. Hypercalcaemia does not affect growth levels nor the somatotrophic secretory reserve.

Adolescent↗
PubMed1983

Effect of nifedipine on the adrenocortical and somatotrophic secretory reserve and TSH and thyroid hormone plasma levels.

The authors investigated the effect of one week's administration of therapeutic doses of the calcium antagonist nifedipine on the hormone homeostasis of clinically healthy subjects. The insignificant tendency towards an increase of the adrenocorticotrophic and somatotrophic secretory reserve and the unaltered levels of thyrotrophin, triiodothyronine and thyroxine rule out possible adverse side-effects of the administered therapeutic doses of nifedipine on the hormone balance of the mentioned systems. The authors discuss also the physiological impact of the assessed findings.

Adrenal Cortex Hormones↗
PubMed1983

Verapamil increases adrenocortical secretory reserve.

The authors investigated the effect of commonly used therapeutic doses of calcium antagonist verapamil on the resting cortisol level and on the adrenocortical secretory reserve assessed from the response of cortisol blood level to stimulation with ACTH in 20 healthy subjects. Verapamil increased significantly the adrenocortical secretory reserve. The resting cortisol blood levels were not affected by the investigated substance. The authors discuss the possible practical impact of the assembled findings.

Adrenal Cortex↗
PubMed1982

Effect of calcium antagonists on thyrotropin and thyroid hormone secretion.

The authors investigated the effect of one-week administration of verapamil in daily therapeutic doses of 4 X 40 mg by the oral route and the effect of nifedipine in daily therapeutic doses of 3 X 20 mg by the oral route. Verapamil and nifedipine did not affect significantly the levels of thyrotropin, triiodothyronine and thyroxine nor their response after stimulation with TRH. The theoretical and practical impact of this finding is discussed in particular with regard to possible side-effects of calcium antagonists during their therapeutic use in clinical cardiology.

Adolescent↗
PubMed1981

Effect of calcium on adrenocortical secretion.

The authors investigated the effect of calcium on the basal cortisol secretion and on the adrenocortical secretory reserve, the indicator of which is the so-called ACTH stimulation test. They revealed that during acute hypercalcaemia there is a significant increase of the basal cortisol secretion. The adrenocortical secretory reserve is significantly reduced during hypercalcaemia, this being manifested by a smaller rise of cortisolaemia after ACTH. The Synacthen test repeated after a 48-hour interval is fully reproducible under normocalcaemia. The basal values and the response to Synacthen do not differ from the control examination. The stimulatory action of calcium can be explained indirectly via other humoral factors, the production of which is enhanced by calcium but also the function of calcium which acts as the so-called "second messenger" in steroidogenesis. Calcium has, however, probably also a direct corticotropic effect, resembling that of ACTH.

Adrenal Cortex↗
PubMed1981

Hypercalcemia influences TRH-stimulated TSH and T3 response.

The influence of acute hypercalcemia induced by i.v. infusion of calcium gluconate on basal TSH and T3 levels in plasma and on their response to TRH stimulation (TRH test) was investigated in 10 healthy subjects. TRH test under normal conditions without hypercalcemia was carried out in the same subjects. Under acute hypercalcemia the basal T3 levels were evaluated markedly up to levels occurring after TRH stimulation. However, the relative increase of T3 following TRH challenge was of the same degree as in normocalcemia. Basal TSH levels did not differ from those found under normocalcemia, but the response to TRH was decreased. The results suggest that hypercalcemia affects the mechanisms regulating the levels of the thyroid hormones and TSH.

Adult↗
PubMed1981

Influence of 25-hydroxyvitamin D3 on thyrotropin and triiodothyronine plasma levels in man.

The influence of three-day oral administration of 100 microgram 25-hydroxycholecalciferol (25-HCC) on thyrotropin (TSH), triiodothyronine (T3), calcium and phosphorus plasma levels was investigated along with changes of Qet and Qat intervals on the electrocardiographic tracing. It was found that 25-HCC in an acute trial significantly elevates the TSH level and causes a slight decline of the T3 level. Changes in the calcium and phosphorus levels were not significant. No changes of the electrocardiographic tracing were found. The results suggest that 25-HCC interferes with the process of secretion (or metabolization) of TSH (and perhaps also T3), probably via changes of the calcium ion concentration in cytosol of secretory cells.

Adult↗