The endothelial barrier function is tightly controlled by a broad range of signaling cascades including nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway. It has been proposed that disturbances in NO and cGMP production could interfere with proper endothelial barrier function. In this study, we assessed the effect of interferon-gamma (IFN-gamma), a pro-inflammatory cytokine, on NO and cGMP levels and examined the mechanisms by which NO and cGMP regulate the IFN-gamma-mediated HUVECs hyperpermeability. The flux of fluorescein isothiocyanate-labeled dextran across cell monolayers was used to study the permeability of endothelial cells. Here, we found that IFN-gamma significantly attenuated basal NO concentration and the increased NO levels supplied by a NO donor, sodium nitroprusside (SNP). Besides, application of IFN-gamma also significantly attenuated both the basal cGMP concentration and the increased cGMP production donated by a cell permeable cGMP analogue, 8-bromo-cyclic GMP (8-Br-cGMP). In addition, exposure of the cell monolayer to IFN-gamma significantly increased HUVECs basal permeability. However, L-NAME pretreatment did not suppress IFN-gamma-induced HUVECs hyperpermeability. L-NAME pretreatment followed by SNP or SNP pretreatment partially reduced IFN-gamma-induced HUVECs hyperpermeability. Pretreatment with a guanylate cyclase inhibitor, 6-anilino-5,8-quinolinedione (LY83583), led to a further increase in IFN-gamma-induced HUVECs hyperpermeability. The findings suggest that the mechanism underlying IFN-gamma-induced increased HUVECs permeability is partly related to the inhibition of NO production.

• MeSH
• donory oxidu dusnatého farmakologie   MeSH
• endoteliální buňky pupečníkové žíly (lidské) účinky léků   metabolismus   MeSH
• guanosinmonofosfát cyklický analogy a deriváty   metabolismus   farmakologie   MeSH
• guanylátcyklasa antagonisté a inhibitory   MeSH
• inhibitory enzymů farmakologie   MeSH
• interferon gama farmakologie   MeSH
• kapilární permeabilita účinky léků   MeSH
• lidé MeSH
• NG-nitroargininmethylester farmakologie   MeSH
• nitroprusid farmakologie   MeSH
• oxid dusnatý metabolismus   MeSH
• permeabilita buněčné membrány MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• 8-bromocyclic GMP MeSH Prohlížeč
• donory oxidu dusnatého MeSH
• guanosinmonofosfát cyklický MeSH
• guanylátcyklasa MeSH
• inhibitory enzymů MeSH
• interferon gama MeSH
• NG-nitroargininmethylester MeSH
• nitroprusid MeSH
• oxid dusnatý MeSH

BACKGROUND: Recent results indicate a key role for cyclic guanosine monophosphate (cGMP) in the regulation of oocyte meiotic arrest in preovulatory mammalian follicles. The aim of our study was to determine whether the resumption of oocyte meiosis and expansion of cumulus cells in isolated pig cumulus-oocyte complexes (COCs) can be blocked by a high intracellular concentration of cGMP, and whether this effect is mediated by a cGMP-dependent inhibition of mitogen-activated protein kinase 3/1 (MAPK3/1). METHODS: The COCs were isolated from ovaries of slaughtered gilts and cultured in vitro in M199 supplemented with 5% fetal calf serum. The expression levels of the C-type natriuretic peptide (CNP) precursor (NPPC) and its receptor (NPR2) mRNAs during the culture of COCs were determined by real-time RT-PCR. To control the intracellular concentration of cGMP in the COCs, the culture medium was further supplemented with CNP or various concentrations of synthetic cGMP analogues; the concentration of cGMP in COCs was then assessed by ELISA. The effect of the drugs on oocyte maturation was assessed after 24 and 44 h of culture by determining nuclear maturation. The expansion of cumulus cells was assessed by light microscopy and the expression of cumulus expansion-related genes by real-time RT-PCR. A possible effect of cGMP on FSH-induced activation of MAPK3/1 was assessed by immunoblotting the COC proteins with phospho-specific and total anti-Erk1/2 antibodies. RESULTS: The COCs expressed NPPC and NPR2, the key components of cGMP synthesis, and produced a large amount of cGMP upon stimulation with exogenous CNP, which lead to a significant (P < 0.05) delay in oocyte meiotic resumption. The COCs also responded to cGMP analogues by inhibiting the resumption of oocyte meiosis. The inhibitory effect of cGMP on meiotic resumption was reversed by stimulating the COCs with FSH. However, high concentration of intracellular cGMP was not able to suppress FSH-induced activation of MAPK3/1 in cumulus cells, cumulus expansion and expression of expansion-related genes (P > 0.05). CONCLUSIONS: The findings of this study indicate that high cGMP concentrations inhibit the maturation of pig oocytes in vitro but the inhibitory mechanism does not involve the suppression of MAPK3/1 activation in cumulus cells.

• MeSH
• aktivace enzymů účinky léků   MeSH
• gonadotropiny farmakologie   MeSH
• guanosinmonofosfát cyklický farmakologie   MeSH
• kultivované buňky MeSH
• kumulární buňky účinky léků   fyziologie   MeSH
• meióza účinky léků   MeSH
• mitogenem aktivovaná proteinkinasa 3 metabolismus   MeSH
• oocyty účinky léků   fyziologie   MeSH
• oogeneze účinky léků   MeSH
• Sus scrofa MeSH
• zvířata MeSH
• Check Tag
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• gonadotropiny MeSH
• guanosinmonofosfát cyklický MeSH
• mitogenem aktivovaná proteinkinasa 3 MeSH

The aim of this study was to test the hypothesis that vasorelaxing action of vasonatrin peptide (VNP) is due to activation of the large-conductance Ca(2+)-activated potassium channel (BK(Ca)) via guanylyl cyclase (GC)-coupled natriuretic peptide receptors (NPRs) in vascular smooth muscle cells (VSMCs). Contraction experiments were performed using human radial artery, whereas BK(Ca) current by patch clamp was recorded in cells from rat mesenteric artery. Contractility of rings cut from human radial artery was detected in vitro. As a result, VNP induced a dose-dependent vasorelaxation of human radial artery, which could be mimicked by 8-Br-cGMP, and suppressed by TEA, a blocker of BK(Ca), HS-142-1, a blocker of GC-coupled NPRs, or methylene blue (MB), a selective inhibitor of guanylyl cyclase. Sequentially, whole-cell K(+) currents were recorded using patch clamp techniques. BK(Ca) current of VSMCs isolated from rat mesentery artery was obtained by subtracting the whole cell currents after applications of 10(-7) mol/l iberiotoxin (IBX) from before its applications. In accordance with the results of arterial tension detection, BK(Ca) current was significantly magnified by VNP, which could also be mimicked by 8-Br-cGMP, whereas suppressed by HS-142-1, or MB. Taken together, VNP acts as a potent vasodilator, and NPRA/B-cGMP-BK(Ca) is one possible signaling system involved in VNP induced relaxation.

• MeSH
• arteria radialis cytologie   účinky léků   fyziologie   MeSH
• arteriae mesentericae cytologie   účinky léků   fyziologie   MeSH
• atriální natriuretický faktor farmakologie   fyziologie   MeSH
• guanosinmonofosfát cyklický analogy a deriváty   farmakologie   MeSH
• guanylátcyklasa fyziologie   MeSH
• krysa rodu Rattus MeSH
• lidé MeSH
• metoda terčíkového zámku MeSH
• peptidy farmakologie   MeSH
• receptory pro atriální natriuretický faktor fyziologie   MeSH
• svaly hladké cévní cytologie   účinky léků   fyziologie   MeSH
• techniky in vitro MeSH
• tetraethylamonium farmakologie   MeSH
• vápníkem aktivované draslíkové kanály s vysokou vodivostí agonisté   fyziologie   MeSH
• vazodilatace účinky léků   fyziologie   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 8-bromocyclic GMP MeSH Prohlížeč
• atrial natriuretic factor receptor A MeSH Prohlížeč
• atrial natriuretic factor receptor B MeSH Prohlížeč
• atriální natriuretický faktor MeSH
• guanosinmonofosfát cyklický MeSH
• guanylátcyklasa MeSH
• iberiotoxin MeSH Prohlížeč
• peptidy MeSH
• receptory pro atriální natriuretický faktor MeSH
• tetraethylamonium MeSH
• vápníkem aktivované draslíkové kanály s vysokou vodivostí MeSH
• ventricular natriuretic peptide, eel MeSH Prohlížeč

It is established that the modulation of beta(3)-adrenoceptor function could be associated with impairment of lipolysis in white fat and be responsible for disturbed lipid metabolism. Though two isoforms of nitric oxide synthase (NOS) were reported in adipocytes, the role of nitric oxide (NO) in adipose tissue is still ambiguous. The present work was directed to study the interplay between NO production and beta-adrenoceptor/cyclic AMP (cAMP) pathway on lipid mobilization (glycerol and nonesterified fatty acids, NEFA) in cultures of rat adipocytes isolated from epididymal white adipose tissue. beta-Nonselective (isoprenaline) and beta(3)-selective (BRL-37344) agonists and the postadrenoceptor agents such as dibutyryl-cAMP, forskolin, and 3-isobutyl-1-methylxanthine significantly increased nitrite, glycerol, and NEFA levels with BRL-37344 being the most potent. Conversely, addition of beta-nonselective (propranolol) or beta(3)-selective (bupranolol) antagonist or the adenylyl cyclase inhibitor (SQ 22,536) significantly reduced beta-agonist-induced NO production and lipolysis. For beta-adrenoceptor agonists, antagonists, and their pairs, there was a positive correlation between medium nitrite and glycerol or NEFA with r(2) being 0.90 and 0.84, respectively. The possible relationship between NO and lipolysis was revealed after adipocyte treatment with nonspecific (N(omega)-nitro-l-arginine methyl ester, l-NAME) and specific (aminoguanidine) NOS inhibitors. Both l-NAME and aminoguanidine significantly inhibited the lipolytic effect of BRL-37344. Moreover, NO-donor (S-nitroso-N-acetylpenicillamine) at higher concentration increased basal glycerol and NEFA levels. 8-bromo-cyclic GMP had no effect on adipocyte lipolysis. These data suggest that beta-adrenergic lipolysis, specifically beta(3)-adrenoceptor effect, which is realized via the adenylyl cyclase/cAMP/protein kinase A signaling cascade, involves NO production downstream of beta(3)-adrenoceptor/cAMP pathway.

• MeSH
• 1-methyl-3-isobutylxanthin farmakologie   MeSH
• adenin analogy a deriváty   farmakologie   MeSH
• agonisté adrenergních receptorů farmakologie   MeSH
• agonisté beta-3-adrenergních receptorů * MeSH
• AMP cyklický metabolismus   MeSH
• donory oxidu dusnatého farmakologie   MeSH
• guanosinmonofosfát cyklický analogy a deriváty   farmakologie   MeSH
• inhibitory adenylylcyklasy MeSH
• kolforsin farmakologie   MeSH
• krysa rodu Rattus MeSH
• lipolýza * účinky léků   MeSH
• oxid dusnatý biosyntéza   MeSH
• potkani Wistar MeSH
• S-nitroso-N-acetylpenicilamin farmakologie   MeSH
• tukové buňky účinky léků   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 1-methyl-3-isobutylxanthin MeSH
• 8-bromocyclic GMP MeSH Prohlížeč
• 9-(tetrahydro-2-furyl)-adenine MeSH Prohlížeč
• adenin MeSH
• agonisté adrenergních receptorů MeSH
• agonisté beta-3-adrenergních receptorů * MeSH
• AMP cyklický MeSH
• donory oxidu dusnatého MeSH
• guanosinmonofosfát cyklický MeSH
• inhibitory adenylylcyklasy MeSH
• kolforsin MeSH
• oxid dusnatý MeSH
• S-nitroso-N-acetylpenicilamin MeSH

Pig oocytes matured in vitro were parthenogenetically activated (78%) after treatment with 2 mM nitric oxide-donor (+/-)-S-nitroso-N-acetylpenicillamine (SNAP) for 24 h. Inhibition of soluble guanylyl cyclase with the specific inhibitors 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) or 6-anilino-5,8-quinolinequinone (LY83583) suppressed the SNAP-induced activation in a dose-dependent manner (23% of activated oocytes after treatment with 400 microM ODQ; 12% of activated oocytes after treatment with 40 microM LY83583). 8-Bromo-cyclic guanosine monophosphate (8-Br-cGMP), a phosphodiesterase-resistant analogue of cGMP, enhances the effect of suboptimal doses (0.1 or 0.5 mM) of the NO donor SNAP. DT3, a specific inhibitor of cGMP-dependent protein kinase (PKG, PKG), is also able to inhibit the activation of pig oocytes after NO donor treatment. Involvement of the cGMP-dependent signalling pathway is specific for NO-induced oocyte activation, because both the guanylyl cyclase inhibitor ODQ and the PKG inhibitor DT3 are unable to inhibit activation in oocytes treated with the calcium ionophore A23187. These data indicate that the activation of pig oocytes with an NO donor is cGMP-dependent and that PKG plays an important role in this mode of oocyte activation.

• MeSH
• aktivace enzymů účinky léků   MeSH
• aminochinoliny metabolismus   farmakologie   MeSH
• chinoxaliny metabolismus   farmakologie   MeSH
• digitoxin metabolismus   farmakologie   MeSH
• fosfodiesterasy metabolismus   MeSH
• guanosinmonofosfát cyklický analogy a deriváty   metabolismus   farmakologie   MeSH
• guanylátcyklasa MeSH
• inhibitory proteinkinas metabolismus   farmakologie   MeSH
• oocyty cytologie   účinky léků   enzymologie   MeSH
• oxadiazoly metabolismus   farmakologie   MeSH
• oxid dusnatý metabolismus   MeSH
• penicilamin analogy a deriváty   metabolismus   farmakologie   MeSH
• permeabilita buněčné membrány účinky léků   MeSH
• prasata metabolismus   MeSH
• proteinkinasy závislé na cyklickém GMP antagonisté a inhibitory   metabolismus   MeSH
• receptory cytoplazmatické a nukleární metabolismus   MeSH
• rozpustná guanylátcyklasa MeSH
• signální transdukce * účinky léků   MeSH
• synthasa oxidu dusnatého metabolismus   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one MeSH Prohlížeč
• 6-anilino-5,8-quinolinedione MeSH Prohlížeč
• 8-bromocyclic GMP MeSH Prohlížeč
• aminochinoliny MeSH
• chinoxaliny MeSH
• digitoxin MeSH
• fosfodiesterasy MeSH
• guanosinmonofosfát cyklický MeSH
• guanylátcyklasa MeSH
• inhibitory proteinkinas MeSH
• oxadiazoly MeSH
• oxid dusnatý MeSH
• penicilamin MeSH
• proteinkinasy závislé na cyklickém GMP MeSH
• receptory cytoplazmatické a nukleární MeSH
• rozpustná guanylátcyklasa MeSH
• S-nitro-N-acetylpenicillamine MeSH Prohlížeč
• synthasa oxidu dusnatého MeSH

The effects of nitric oxide on evoked acetylcholine (ACh) release were studied at two identified cholinergic neuro-neuronal synapses of the nervous system of the mollusc Aplysia californica. The NO-donor, 3-morpholinosydnonimine (SIN-1), decreased the amplitude of evoked inhibitory postsynaptic currents (buccal ganglion) and potentiated that of evoked excitatory postsynaptic currents (abdominal ganglion). SIN-1 acted by modulating the number of ACh quanta released. 8Br-cGMP mimicked the effects of NO on ACh release in both types of synapses thus pointing to the involvement of a NO-sensitive guanylate cyclase. Presynaptic voltage-dependent Ca2+ and K+ (IA and late outward rectifier) currents were not modified by SIN-1 suggesting another final target for NO/cGMP. The labelling of a NO-synthase by immunostaining in several neurones as well as the modulation of ACh release by L-arginine indicate that an endogenous NO-synthase is involved in the modulation of synaptic efficacy in both buccal and abdominal ganglia.

• MeSH
• acetylcholin metabolismus   farmakologie   MeSH
• akční potenciály MeSH
• Aplysia MeSH
• arginin farmakologie   MeSH
• cholinergní agonisté farmakologie   MeSH
• cholinergní antagonisté farmakologie   MeSH
• draslíkové kanály účinky léků   MeSH
• ganglia bezobratlých účinky léků   metabolismus   MeSH
• ganglia parasympatická účinky léků   metabolismus   MeSH
• guanosinmonofosfát cyklický analogy a deriváty   farmakologie   MeSH
• guanylátcyklasa metabolismus   MeSH
• molsidomin analogy a deriváty   farmakologie   MeSH
• nervový přenos účinky léků   MeSH
• oxid dusnatý farmakologie   MeSH
• synapse účinky léků   metabolismus   MeSH
• synthasa oxidu dusnatého metabolismus   MeSH
• vápníkové kanály účinky léků   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 8-bromocyclic GMP MeSH Prohlížeč
• acetylcholin MeSH
• arginin MeSH
• cholinergní agonisté MeSH
• cholinergní antagonisté MeSH
• draslíkové kanály MeSH
• guanosinmonofosfát cyklický MeSH
• guanylátcyklasa MeSH
• linsidomine MeSH Prohlížeč
• molsidomin MeSH
• oxid dusnatý MeSH
• synthasa oxidu dusnatého MeSH
• vápníkové kanály MeSH

Nitric oxide (NO) is an endogenous vasodilator and inhaled NO is a promising therapeutic agent for the treatment of pulmonary hypertension. However, NO's mechanism of action is not completely understood. Previous studies have shown that NO increases intracellular levels of cyclic guanosine 3',5'-monophosphate (cGMP) and that leads to activation of calcium-gated potassium channels in vascular smooth muscle cells. Resulting cell membrane hyperpolarization causes vasorelaxation. The potassium channel activation by NO is inhibited by a blockade of cyclic nucleotide-dependent protein kinases, suggesting a key role of these enzymes in NO-induced vasodilation. To further examine this mechanism, we tested the hypothesis that pharmacological stimulation of the cGMP-dependent protein kinase will simulate the activating effect of NO on potassium channels. Indeed, we found that (Sp)-guanosine cyclic 3',5'-phosphorothioate (1 microM), a selective activator of the cGMP-dependent protein kinase, dramatically increased potassium currents measured by the whole-cell patch clamp technique in freshly dispersed pulmonary artery smooth muscle cells. These currents were inhibited by an inhibitor of calcium-gated potassium channels, charybdotoxin. Our results support the hypothesis that the effect of NO on potassium channels is mediated by the cGMP-dependent protein kinase.

• MeSH
• gating iontového kanálu účinky léků   MeSH
• guanosinmonofosfát cyklický farmakologie   MeSH
• krysa rodu Rattus MeSH
• membránové potenciály MeSH
• metoda terčíkového zámku MeSH
• oxid dusnatý farmakologie   MeSH
• potkani Sprague-Dawley MeSH
• proteinkinasy závislé na cyklickém GMP účinky léků   metabolismus   MeSH
• svaly hladké cévní účinky léků   metabolismus   MeSH
• vápníkové kanály účinky léků   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, U.S. Gov't, Non-P.H.S. MeSH
• Research Support, U.S. Gov't, P.H.S. MeSH
• Názvy látek
• guanosinmonofosfát cyklický MeSH
• oxid dusnatý MeSH
• proteinkinasy závislé na cyklickém GMP MeSH
• vápníkové kanály MeSH

Cyclic guanosine-3'5' monophosphate (cGMP) can mobilize intracellular calcium from the microsomal fraction of B-lymphocytes of the mouse spleen as a result of activation of cGMP-dependent microsomal proteinkinases. The existence of such a mechanism makes B-lymphocytes independent of extracellular calcium in response to agents whose effect on B-lymphocytes is mediated by calcium mechanisms.

• MeSH
• B-lymfocyty účinky léků   metabolismus   MeSH
• fosforylace MeSH
• guanosinmonofosfát cyklický farmakologie   MeSH
• mikrozomy účinky léků   enzymologie   metabolismus   MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• proteinkinasy metabolismus   MeSH
• sarkoplazmatické retikulum účinky léků   metabolismus   MeSH
• vápník metabolismus   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• guanosinmonofosfát cyklický MeSH
• proteinkinasy MeSH
• vápník MeSH

We studied the effects of cyclic nucleotides and theophylline on growth activity of Chinese hamster V79-1A cells after extracellular application. Cyclic AMP inhibited the growth activity of V79-1A cells only at extracellular concentrations higher than 10-3 M and dibutyryl cAMP only at extracellular concentrations higher than 10-4 M. Theophylline inhibited V79-1A cell growth at concentrations higher than 10-4M. We demonstrated that cAMP or dibutyryl cAMP applied together with theophylline exerted a synergistic inhibitory effect on V79-1A cell growth. The synergistic inhibitory effect of cAMP and cGMP was found, too. Cyclic AMP at extracellular concentration of 10-10M was able to stimulate the growth of V79-1A cells slightly. Cyclic CMP slightly stimulated the proliferation of V79-1A cells at a concentration of 10-8 M. Cyclic GMP applied alone was not demonstrated as V79-1A cell growth stimulator. However, 10-6 M cGMP applied together with 10-5 M theophylline exerted a small but recognizable stimulatory effect.

• MeSH
• AMP cyklický farmakologie   MeSH
• buněčné dělení účinky léků   MeSH
• buněčné linie MeSH
• CMP cyklický farmakologie   MeSH
• Cricetulus MeSH
• dibutyryl cyklický AMP farmakologie   MeSH
• guanosinmonofosfát cyklický farmakologie   MeSH
• křečci praví MeSH
• nukleotidy cyklické farmakologie   MeSH
• synergismus léků MeSH
• theofylin farmakologie   MeSH
• zvířata MeSH
• Check Tag
• křečci praví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• AMP cyklický MeSH
• CMP cyklický MeSH
• dibutyryl cyklický AMP MeSH
• guanosinmonofosfát cyklický MeSH
• nukleotidy cyklické MeSH
• theofylin MeSH

Cyclic AMP has a radioprotective effect and its aministration results in a significant increase in LD50/30 values in Chinese hamsters. The efficiency of these radioprotective effects is comparable to that of such radioprotective compounds as AET and cystamine + mexamine. Cyclic GMP is responsible for significant radiosensitizing effects. Changes in radiosensitivity after administration of cyclic nucleotides are both immediate and delayed and correlate closely with dose and time of administration.

• MeSH
• 5-methoxytryptamin farmakologie   MeSH
• AMP cyklický farmakologie   MeSH
• beta-aminoethylisothiomočovina farmakologie   MeSH
• cystamin farmakologie   MeSH
• dibutyryl cyklický AMP farmakologie   MeSH
• guanosinmonofosfát cyklický farmakologie   MeSH
• křečci praví MeSH
• nukleotidy cyklické farmakologie   MeSH
• radioprotektivní látky farmakologie   MeSH
• theofylin farmakologie   MeSH
• tolerance záření * MeSH
• zvířata MeSH
• Check Tag
• křečci praví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• 5-methoxytryptamin MeSH
• AMP cyklický MeSH
• beta-aminoethylisothiomočovina MeSH
• cystamin MeSH
• dibutyryl cyklický AMP MeSH
• guanosinmonofosfát cyklický MeSH
• nukleotidy cyklické MeSH
• radioprotektivní látky MeSH
• theofylin MeSH