Aim of the study was to test the effect of nicotine (NIC) and kainic acid (KA) co-treatment in immature rats. Male Wistar albino rats (two different age groups) were chosen for the study. Experiments started on postnatal day (PD) 8 or 21 and animals were treated twice a day for three days with nicotine, fourth day KA was administered. Animals at PD12 (PD25 respectively) were examined electrophysiologically for cortical epileptic afterdischarges (ADs). First cortical ADs in PD12 animals were longer, when compared to PD25 rats (group treated with both substances). Nor NIC or KA treatment affected the length of discharges in PD12 rats. Older experimental group exhibited the shortening of the first ADs (group treated with NIC and KA, compared with groups exposed to single treatment). Few changes were found in KA treated group – 2nd and 4th ADs were shorter when compared with first ADs. These results demonstrate that NIC treatment played minor role in seizure susceptibility of PD12 rats, sensitivity to NIC differs during ontogenesis and subconvulsive dose of KA influenced the length of discharges only in PD25 animals., V. Riljak ... [et al.]., and Obsahuje seznam literatury
The first part of the article outlines Bohr's complementary way of thinking with which he amongst others approached the solution of atomic events in his three famous articles On the constitution of atoms and molecules from 1913. It also shows Bohr not only as a physicist, but as an interdisciplinary thinker and philanthropist. The second part gives a summary of the conference commemorating the centenar of the Bohr model of the atom, which claims to at least to partially for some gaps in the perception of this remarkable figure., Výklad stability atomu podal Niels Bohr ve svých třech stěžejních článcích nazvaných O konstituci atomů a molekul v roce 1913. V nich jedinečným způsobem aplikoval na Rutherfordův model atomu dosud nespojované předpoklady (klasické předpoklady a Planckovu kvantovou hypotézu nebo Balmerovu-Rydbergovu konstantu). To mu umožnilo podat vysvětlení čárového spektra (nejenom) vodíku a v neposlední řadě ho jeho teorie dovedla až k revolučnímu pojetí struktury molekul. V české odborné a laicky zainteresované veřejnosti tak přetrvává představa Bohra především jako fyzika nebo jen strůjce modelu atomu vodíku. Takový obraz o Bohrovi je velmi zavádějící. Ve fyzice Bohr dosáhl řady dalších významných příspěvků a současně byl interdisciplinárním myslitelem, jenž se zabýval filosofií, psychologií, biologií nebo jazykem. Nárokem konference ke stému výročí Bohrova modelu atomu tak bylo alespoň zčásti zaplnit některá bílá místa ve vnímání této pozoruhodné osobnosti., Patrik Čermák, Filip Grygar., and Obsahuje seznam literatury
High blood pressure (BP) of spontaneously hypertensive rats (SHR) is maintained by enhanced activity of sympathetic nervous system (SNS), whereas that of Ren-2 transgenic rats (Ren-2 TGR) by increased activity of renin-angiotensin system (RAS). However, both types of hypertension are effectively attenuated by chronic blockade of L-type voltage-dependent calcium channel (L-VDCC). The aim of our study was to evaluate whether the magnitude of BP response elicited by acute nifedipine administration is proportional to the alterations of particular vasoactive systems (SNS, RAS, NO) known to modulate L-VDCC activity. We therefore studied thes e relationships not only in SHR, in which mean arterial pressure was modified in a wide range of 100-210 mm Hg by chronic antihypertensive treatment (captopril or hydralazine) or its withdrawal, but also in rats with augmented RAS activity such as homozygous Ren-2 TGR, pertussis toxin- treated SHR or L-NAME-treated SHR. In all studied groups the magnitude of BP response to nifedipine was proportional to actual BP level and it closely correlated with BP changes induced by acute combined blockade of RAS and SNS. BP response to nifedipine is also closely related to the degree of relative NO deficiency. This was true for both SNS- and RAS-dependent forms of genetic hypertension, suggesting common mechanisms responsible for enhanced L-VDCC opening and/or their upregulation in hypertensive animals. In conclusions, BP response to nifedipine is proportional to the vasoconstrictor activity exerted by both SNS and RAS, indicating a key importance of these two pressor systems for actual L-VDCC opening necessary for BP maintenance., J. Zicha ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Maintenance of norepinephrine (NE)-induced contraction is dependent on Ca2+ influx through L-type voltage-dependent Ca2+ channels (VDCC), which is opposed by nitric oxide. Adrenergic receptors are coupled with different G proteins, including inhibitory G proteins (Gi) that can be inactivated by pertussis toxin (PTX). Our study was aimed to investigate the effects of endothelium removal, PTX pretreatment and acute VDCC blockade by nifedipine on the contractions of femoral arteries stimulated by norepinephrine. We used 12-week-old male WKY, half of the rats being injected with PTX (10 μg/kg i.v., 48 h before the experiment), which considerably reduced their blood pressure (BP). Contractions of isolated arteries were measured using Mulvany-Halpern myograph. NE dose-response curves determined in femoral arteries from PTX-treated WKY rats were shifted to the right compared to those from control WKY. On the contrary, removal of endothelium augmented NE dose-response curves shifting them to the left. Acute VDCC blockade by nifedipine (10-7 M) abolished all differences in NE dose-response curves which were dependent on the presence of either intact endothelium or functional Gi proteins because all NE dose-response curves were identical to the curve seen in vessels with intact endothelium from PTX-treated animals. We can conclude that BP reduction after PTX injection is accompanied by the attenuation of NE-induced contraction of femoral arteries irrespective of endothelium presence. Moreover, our data indicate that both vasodilator action of endothelium and Gi-dependent vasoconstrictor effect of norepinephrine operate via the control of Ca2+ influx through VDCC., S. Líšková, J. Kuneš, J. Zicha., and Obsahuje bibliografii a bibliografické odkazy