Search PubMed⌕ Search

Biomedical subjects

H Szmigielska

Publications and source records attributed to H Szmigielska.

At least 19 recordsLinked to original sources
PubMed1997

The cooperation between the influx of extracellular calcium and alpha1-adrenoceptor-induced translocation of protein kinase C.

Calcium ionophore A23187 or phenylephrine injected i.p. in doses of 0.05-0 .25 mg kg-1 and 0.1-1 mg kg-1, respectively, induced translocation of protein kinase C (PKC) from the cytosol to the membrane fraction of the rat frontal cortex and hippocampus. The action of A23187 was blocked in a dose-dependent manner by nifedipine and verapamil. The phenylephrine induced translocation of PKC was blocked by prazosin and in a dose-dependent manner by nifedipine and verapamil. In contrast, pre-treatment with a small, ineffective by itself, dose of A23187 (0.02 mg kg-1) potentiated the alpha1-adrenoceptor induced translocation of PKC. Thus, it seems that the influx of calcium ions through an L-type calcium channel is probably necessary for a full alpha1-adrenoceptor mediated activation and translocation of PKC.

Adrenergic alpha-Agonists↗
PubMed1986

Changed sensitivity of alpha 2-adrenoceptors mediating a decrease in protein kinase inhibitor activity in the brain of vasopressin-hypertensive rats.

Clonidine produced an increase of cGMP content and a decrease of the endogenous type II inhibitor of protein kinase in rat hypothalamic slices. When administered to rats, the effect of clonidine on type II inhibitor activity in the hypothalamus and brain-stem depended on the dose. Low doses (10-50 micrograms X kg-1 i.p.) produced an increase, probably by stimulating presynaptic alpha 2-adrenoceptors, whereas large doses (200-1000 micrograms X kg-1 i.p.) produced a decrease of type II inhibitor activity by stimulating postsynaptic receptors. The development of vasopressin hypertension was associated with a gradual reduction of the response of the type II inhibitor to low and high doses of clonidine. In vasopressin-hypertensive rats neither small nor large doses of clonidine were able to induce changes in type II inhibitor activity suggesting subsensitivity of pre- and postsynaptic alpha 2-adrenoceptors. However, clonidine appeared to be equally effective in blocking electrically stimulated [3H]noradrenaline release from hypothalamic slices of vasopressin-hypertensive and control, normotensive rats. Reduced reactivity of postsynaptic alpha 2-adrenoceptors seems to be of great importance since treatment of vasopressin-hypertensive rats with 6-hydroxydopamine resulted in a decrease of blood pressure and reappearance of the sensitivity of postsynaptic alpha 2-adrenoceptors to clonidine.

Animals↗
PubMed1984

Effect of supersensitivity of pre- and postsynaptic dopamine receptors on the activity of endogenous inhibitor of cAMP dependent protein kinase in rat striatum.

Small presynaptically active doses of apomorphine (50-100 micrograms/kg) induced an increase, while large doses (1-10 mg/kg) provoked a decrease of type I inhibitor activity in rat striatum. Supersensitivity of postsynaptic D1 receptors was produced in rats by i.c.v. injection of 6-hydroxydopamine (6-OH-DA) and supersensitivity of presynaptic dopamine autoreceptors by i.p. administration of reserpine (1 mg/kg daily for 4 days). In reserpine pretreated rats apomorphine produced an increase in type I inhibitor activity after about 5 times lower doses than in control rats. This effect of apomorphine was blocked by aminophylline and by presynaptically active doses of haloperidol. In 6-OH-DA pretreated rats small doses of apomorphine did not change the type I inhibitor activity. The apomorphine induced decrease of type I inhibitor activity was seen after about 10 times lower doses of apomorphine than in control rats. This action of apomorphine was blocked by postsynaptically active doses of haloperidol and enhanced by aminophylline. The obtained results show that supersensitivity of presynaptic D2 dopamine autoreceptors and postsynaptic D1 receptors is accompanied by changes in the reactiveness of type I inhibitor activity to apomorphine.

Aminophylline↗
PubMed1977

[Wound healing in viscera studied using a hemostatic gelatin-starch sponge of Polish manufacture].

The authors studied the reaction of liver, spleen and kidneys in rats to the implantation of Polish made hemostatic gelatin-starch sponge. The sponge under study evoked no disadvantageous tissue reactions in the case of liver; it was readily resorbed and did not inhibit the wound healing. It facilitated the healing of lienal wounds without any suturing and produced neither local nor general disadvantageous results. When dressing renal wounds, the sponge was completely resorbed within 3 weeks and the wound was completely healed. The renal wounds healed without any complications despite of a greater tissue reaction compared with that of liver and spleen.

Animals↗
PubMedDate not supplied

The study of organic nitrates, part IV. Chemical and pharmacological study of N-(1-methylethyl)-3-(1-naphthalenyloxy)-2-nitroxypropylamine--potential NO donor.

The reaction of N-(1-methylethyl)-3-(1-naphthalenyloxy)-2-nitroxypropylamine (nitrate analogue of propranolol) with hydrochloride of ethyl ester of L-cysteine at pH 7.7, temp. 37 degrees C was studied. The course of the reaction was monitored by HPLC method. It was found that at these conditions the substrates react and the main product of the decomposition of the nitrate of propranolol analogue is propranolol, nitrate and nitrite ions. The reaction has been described qualitatively and quantitatively. The influence of nitrate analogue of propranolol and propranolol alone on arterial blood pressure and heart rate in normotensive and hypertensive rats (SHR) was also studied. It has been found that both compounds exert a similar effect.

Animals↗
PubMedDate not supplied

The responsiveness of D1- and D2-dopamine receptors in the striatum and hypothalamus of spontaneous and vasopressin hypertensive rats.

Low doses of apomorphine (20-50 micrograms/kg) induced an increase in the activity of an endogenous inhibitor of cAMP dependent protein Kinases (type I inhibitor) in the striatum, anterior and posterior hypothalamus of normotensive rats by stimulating D2-dopamine receptors. In contrast, high doses of the compound (2-10 mg/kg) produced a dose dependent decrease in type I inhibitor activity. In the posterior hypothalamus of vasopressin hypertensive rats and SHR the maximal increase of type I inhibitor activity was markedly higher than in normotensive animals. Moreover, apomorphine induced the increase of type I inhibitor activity in a much wider range of doses. Only as high dose of the compound as 10 mg/kg was able to decrease type I inhibitor activity. This points to a marked supersensitivity of D2 receptors and suggests the subsensitivity of D1 receptors in this brain area of hypertensive rats. In contrast, in the striatum and anterior hypothalamus of hypertensive rats the apomorphine dose response curves were similar to those in normotensive rats. Thus, it seems tha hypertension is associated with the alteration in sensitivity of D2 and D1 receptors in the posterior hypothalamus, the brain area involved in regulation of blood pressure.

Animals↗
PubMedDate not supplied

The effect of single and prolonged ethanol administration on the sensitivity of central GABA-A and benzodiazepine receptors in vivo.

The response of GABA-modulin to various doses of diazepam and muscimol was used as an index of the sensitivity of central benzodiazepine and GABA-A receptors, respectively. Diazepam and muscimol induced a dose-dependent increase in cytosol GABA-modulin activity in rat nucleus accumbens, hippocampus and cerebellum. A single dose of ethanol (1 g/kg po) potentiated the action of diazepam and muscimol. Prolonged treatment with ethanol (5 g/kg/day for 21 days) did not affect the action of diazepam. In contrast, the effect of muscimol was greatly reduced. In the rats pretreated for 21 days with ethanol five times higher doses of muscimol than in control group were necessary to induce a statistically significant increase of GABA-modulin in the cytosol of the nucleus accumbens, hippocampus and cerebellum. Those results show that a single dose of ethanol enhances GABA-ergic transmission, whereas prolonged treatment with ethanol induces subsensitivity of GABA-A but not benzodiazepine receptors in the limbic system and in cerebellum.

Animals↗
PubMedDate not supplied

The effect of prolonged ethanol administration on central alpha 2-adrenoceptors sensitivity.

The response of an endogenous inhibitor of protein kinases (type II inhibitor) to clonidine was used as an index of sensitivity of central alpha 2-adrenoceptors. Low doses of clonidine (20-50 micrograms/kg) induced an increase in type II inhibitor activity in the nucleus accumbens, hippocampus and in the anterior and posterior hypothalamus by stimulating presynaptic alpha 2-adrenoceptors. Stimulation of postsynaptic alpha 2-adrenoceptors by high doses of clonidine 0.5-1.0 mg/kg resulted in a dose-dependent decrease in type II inhibitor activity. Prolonged treatment with ethanol (5 g/kg/day po for 21 days) greatly reduced the action of high doses of clonidine in all the examined brain areas, suggesting subsensitivity of postsynaptic alpha 2-adrenoceptors lasting for at least 48 h after the last ethanol administration. A single dose of ethanol induced a short lasting subsensitivity of postsynaptic alpha 2-adrenoceptors in the anterior hypothalamus. 12 h after administration of alcohol the response of type II inhibitor to high doses of clonidine in this brain area was the same as in untreated rats.

Aminophylline↗
PubMedDate not supplied

The sensitivity of alpha-adrenoceptors in nucleus tractus solitarii, anterior hypothalamus and hippocampus of spontaneous and renal hypertensive rats.

The responsiveness of the endogenous type II inhibitor of protein kinases to clonidine was used as an index of the reactivity of alpha 2-adrenoceptors in the brain. The stimulation of postsynaptic alpha 2-adrenoceptors by clonidine resulted in a dose-dependent decrease in type II inhibitor activity. In the nucleus tractus solitarii and anterior hypothalamus of spontaneously hypertensive rats (SHR) and renal hypertensive rats (RHR) the clonidine-induced decrease in type II inhibitor activity was markedly reduced. In contrast, clonidine was equipotent in reducing type II inhibitor activity in the hippocampus of those rats and in control normotensive animals. In addition to that, in SHR and RHR the hypothermic activity of clonidine was not reduced. Thus, it seems that in experimental hypertension the decrease of the reactivity of alpha 2-adrenoceptors occurs in the brain structures responsible for the blood pressure regulation.

Animals↗