The kinin receptors are classically involved in inflammation, pain and sepsis. The effects of the kinin B1 receptor agonist des-Arg9-bradykinin (DBK) and lipopolysaccharide (LPS) were investigated by comparing the membrane potential responses of aortic rings from transgenic rats overexpressing the kinin B1 receptor (B1R) in the endothelium (TGR(Tie2B1)) and Sprague Dawley (SD) rats. No difference in the resting membrane potential in the aorta's smooth muscle from the transgenic and SD rats was observed. The aorta rings from SD rats hyperpolarized only to LPS but not to DBK, whereas the aorta rings from TGR(Tie2B1) responded by the administration of both drugs. DBK and LPS responses were inhibited by the B1 receptor antagonist R715 and by iberiotoxin in both cases. Thapsigargin induced a hyperpolarization in the smooth muscle of SD rats that was not reversed by R715, but was reversed by iberiotoxin and this hyperpolarization was further augmented by DBK administration. These results show that the model of overexpression of vascular B1 receptors in the TGR(Tie2B1) rats represent a good model to study the role of functional B1 receptors in the absence of any pathological stimulus. The data also show that KCa channels are the final mediators of the hyperpolarizing responses to DBK and LPS. In addition, we suggest an interaction between the B1R and TLR4, since the hyperpolarization induced by LPS could be abolished in the presence of R715.

• MeSH
• aorta MeSH
• bradykinin * farmakologie   MeSH
• cévní endotel MeSH
• krysa rodu Rattus MeSH
• lipopolysacharidy farmakologie   MeSH
• membránové potenciály MeSH
• potkani Sprague-Dawley MeSH
• potkani transgenní MeSH
• receptor bradykininu B1 * genetika   MeSH
• techniky in vitro MeSH
• thapsigargin farmakologie   MeSH
• toll-like receptor 4 MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• bradykinin * MeSH
• lipopolysacharidy MeSH
• receptor bradykininu B1 * MeSH
• thapsigargin MeSH
• toll-like receptor 4 MeSH

Galanin and galanin receptors (GalRs) have been reported to be involved in the transmission and modulation of nociceptive information in the central nervous system (CNS). However, the underlying mechanism of the antinociception of GalRs in neuropathic pain remains unclear. This study investigated the antinociception induced by galanin receptor 1 (GalR1) via protein kinase A (PKA) signaling pathway in the nucleus accumbens (NAc) of rats with neuropathic pain. A mononeuropathy model was replicated by ligation of the left sciatic nerve, following which the expression of phospho-PKA (p-PKA) in the NAc were markedly up-regulated at 14(th) and 28(th) day after ligation of sciatic nerve, and p-PKA expression was down-regulated by intra-NAc injection of GalR1 agonist M617, but the GalR1 antagonist M35 did not have an effect. We also found that M35 in the NAc blocked the M617-induced increase in the hind paw withdrawal latencies (HWLs) of rats with mononeuropathy, but M35 alone had no effect on HWLs, and PKA inhibitor H-89 attenuated the M617-induced an increase in the HWLs. These results suggested that GalR1 induced an antinociception via inhibiting PKA activation, implying that GalR agonists may be potential and potent therapeutic options to treat chronic neuropathic pain.

• MeSH
• aktivace enzymů účinky léků   fyziologie   MeSH
• analgetika metabolismus   MeSH
• bradykinin analogy a deriváty   farmakologie   MeSH
• galanin analogy a deriváty   farmakologie   MeSH
• krysa rodu Rattus MeSH
• měření bolesti účinky léků   metody   MeSH
• neuralgie metabolismus   prevence a kontrola   MeSH
• nucleus accumbens účinky léků   metabolismus   MeSH
• peptidové fragmenty farmakologie   MeSH
• potkani Sprague-Dawley MeSH
• proteinkinasy závislé na cyklickém AMP antagonisté a inhibitory   metabolismus   MeSH
• receptor galaninu typ 1 agonisté   antagonisté a inhibitory   biosyntéza   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• analgetika MeSH
• bradykinin MeSH
• galanin MeSH
• M617 peptide MeSH Prohlížeč
• peptidové fragmenty MeSH
• proteinkinasy závislé na cyklickém AMP MeSH
• receptor galaninu typ 1 MeSH

Complex regional pain syndrome (CRPS) develops after fracture. The acute CRPS phenotype resembles exaggerated inflammation, which is explained by local and systemic activation of a proinflammatory network including peptides and cytokines. Epidemiologic data suggest that inactivation of the peptidase angiotensin-converting enzyme in patients treated for hypertension increases the odds to develop CRPS. This hint leads us to investigate the serum protease network activity in patients with CRPS vs respective controls. For this purpose, we developed a dabsyl-bradykinin (DBK)-based assay and used it to investigate patients with CRPS, as well as healthy and pain (painful diabetic neuropathy [dPNP]) controls. The major result is that the degradation of DBK to fragments 1-8 and 1-5 in healthy control and dPNP is shifted to higher values for DBK1-8 and lower values for DBK1-5 at 1 hour of incubation in patients with CRPS. Using this novel reporter peptide assay, we have been able to show that the resolving protease network for mediators such as BK might be different in patients with CRPS; having a look at the clinical signs, which resemble inflammation, this resolving protease network is probably less effective in CRPS.

• MeSH
• angiotensin konvertující enzym krev   MeSH
• bolest patofyziologie   MeSH
• bradykinin farmakologie   MeSH
• cytokiny krev   MeSH
• diabetické neuropatie krev   MeSH
• dospělí MeSH
• komplexní regionální syndromy bolesti krev   patofyziologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• měření bolesti MeSH
• proteasy krev   MeSH
• Sudeckův syndrom krev   diagnóza   MeSH
• zánět farmakoterapie   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• angiotensin konvertující enzym MeSH
• bradykinin MeSH
• cytokiny MeSH
• proteasy MeSH

Exposure to repetitive low-frequency electromagnetic field (LF-EMF) shows promise as a non-invasive approach to treat various sensory and neurological disorders. Despite considerable progress in the development of modern stimulation devices, there is a limited understanding of the mechanisms underlying their biological effects and potential targets at the cellular level. A significant impact of electromagnetic field on voltage-gated calcium channels and downstream signalling pathways has been convincingly demonstrated in many distinct cell types. However, evidence for clear effects on primary sensory neurons that particularly may be responsible for the analgesic actions of LF-EMF is still lacking. Here, we used F11 cells derived from dorsal root ganglia neurons as an in vitro model of peripheral sensory neurons and three different protocols of high-induction magnetic stimulation to determine the effects on chemical responsiveness and spontaneous activity. We show that short-term (<180 sec.) exposure of F11 cells to LF-EMF reduces calcium transients in response to bradykinin, a potent pain-producing inflammatory agent formed at sites of injury. Moreover, we characterize an immediate and reversible potentiating effect of LF-EMF on neuronal spontaneous activity. Our results provide new evidence that electromagnetic field may directly modulate the activity of sensory neurons and highlight the potential of sensory neuron-derived cell line as a tool for studying the underlying mechanisms at the cellular and molecular level.

• Klíčová slova
• bradykinin receptor, electromagnetic field, ion channel, primary sensory neuron, transient receptor potential channel,
• MeSH
• bradykinin farmakologie   MeSH
• buněčné linie MeSH
• elektromagnetická pole * MeSH
• kationtový kanál TRPA1 metabolismus   MeSH
• lidé MeSH
• nervové receptory účinky léků   metabolismus   MeSH
• vápník metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• bradykinin MeSH
• kationtový kanál TRPA1 MeSH
• TRPA1 protein, human MeSH Prohlížeč
• vápník MeSH

Transient receptor potential vanilloid (TRPV1) receptors are abundant in a subpopulation of primary sensory neurons that convey nociceptive information from the periphery to the spinal cord dorsal horn. The TRPV1 receptors are expressed on both the peripheral and central branches of these dorsal root ganglion (DRG) neurons and can be activated by capsaicin, heat, low pH, and also by recently described endogenous lipids. Using patch-clamp recordings from superficial dorsal horn (DH) neurons in acute spinal cord slices, the effect of application of the endogenous TRPV1 agonist N-oleoyldopamine (OLDA) on the frequency of miniature excitatory postsynaptic currents (mEPSCs) was evaluated. A high concentration OLDA (10 microM) solution was needed to increase the mEPSC frequency, whereas low concentration OLDA (0.2 microM) did not evoke any change under control conditions. The increase was blocked by the TRPV1 antagonists SB366791 or BCTC. Application of a low concentration of OLDA evoked an increase in mEPSC frequency after activation of protein kinase C by phorbol ester (PMA) and bradykinin or in slices from animals with peripheral inflammation. Increasing the bath temperature from 24 to 34 degrees C enhanced the basal mEPSC frequency, but the magnitude of changes in the mEPSC frequency induced by OLDA administration was similar at both temperatures. Our results suggest that presumed endogenous agonists of TRPV1 receptors, like OLDA, could have a considerable impact on synaptic transmission in the spinal cord, especially when TRPV1 receptors are sensitized. Spinal TRPV1 receptors could play a pivotal role in modulation of nociceptive signaling in inflammatory pain.

• MeSH
• analýza rozptylu MeSH
• anilidy farmakologie   MeSH
• bradykinin farmakologie   MeSH
• cinnamáty farmakologie   MeSH
• dopamin analogy a deriváty   farmakologie   MeSH
• excitační postsynaptické potenciály účinky léků   MeSH
• forbolové estery farmakologie   MeSH
• kationtové kanály TRPV agonisté   antagonisté a inhibitory   MeSH
• krysa rodu Rattus MeSH
• měření bolesti metody   MeSH
• metoda terčíkového zámku metody   MeSH
• mícha cytologie   MeSH
• modely nemocí na zvířatech MeSH
• nervové receptory účinky léků   MeSH
• neurogenní zánět chemicky indukované   patofyziologie   MeSH
• novorozená zvířata MeSH
• potkani Wistar MeSH
• signální transdukce účinky léků   fyziologie   MeSH
• spinální ganglia cytologie   MeSH
• techniky in vitro MeSH
• teplota MeSH
• vazodilatancia farmakologie   MeSH
• vztah mezi dávkou a účinkem léčiva 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
• anilidy MeSH
• bradykinin MeSH
• cinnamáty MeSH
• dopamin MeSH
• forbolové estery MeSH
• kationtové kanály TRPV MeSH
• N-(3-methoxyphenyl)-4-chlorocinnamanilide MeSH Prohlížeč
• N-oleoyldopamine MeSH Prohlížeč
• Trpv1 protein, rat MeSH Prohlížeč
• vazodilatancia MeSH

Chronic volume overload (VO) on the left ventricle (LV) augments redox stress and activates matrix metalloproteinase (MMP) which causes the endocardial endothelial-myocyte (EM) disconnection leading to myocardial contractile dysfunction. VO-induced MMP-9 activation impairs cardiac functions, in part by endothelial endocardial apoptosis, but the role of MMP-9 on EM functions remains obscure. We conjecture that chronic VO activates MMP-9 and causes EM uncoupling. Arteriovenous fistula (AVF) was created in genetically identical wild type (WT) mice (FVB/NJ) and MMP-9 knockout mice (MMP-9KO, FVB.Cg-MMP9(tm1Tvu)/J). Sham-operated mice were used as controls. Before experimentation the phenotype analysis of MMP-9KO mice was carried out. In-gel-gelatin zymography for MMP-9 activation was performed on LV homogenates. The EM functions were determined on LV rings using tissue myobath. We report a decrease in MMP-9 activity in left ventricular myocardial extracts in MMP-9 deficient mice after AVF. The responses to drugs affecting cardiac functions (acetylcholine (Ach), nitroprusside and bradykinin) were attenuated in AVF mice suggesting the impairment of EM coupling. Interestingly, the EM functions were restored in the MMP-9 deficient mice after AVF. We suggest a direct cause-and-effect relationship between MMP-9 activation and EM uncoupling in LV myocardium after chronic VO and the possible involvement of MMP-9 in myocardial contractile performance.

• MeSH
• acetylcholin farmakologie   MeSH
• aktivace enzymů MeSH
• arteriovenózní zkrat MeSH
• bradykinin farmakologie   MeSH
• endoteliální buňky účinky léků   enzymologie   MeSH
• fenotyp MeSH
• funkce levé komory srdeční * účinky léků   MeSH
• kontrakce myokardu * účinky léků   MeSH
• matrixová metaloproteinasa 9 nedostatek   genetika   metabolismus   MeSH
• modely nemocí na zvířatech MeSH
• myokard enzymologie   MeSH
• myši knockoutované MeSH
• myši MeSH
• nitroprusid farmakologie   MeSH
• srdeční komory enzymologie   patofyziologie   MeSH
• srdeční selhání enzymologie   patofyziologie   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH
• Názvy látek
• acetylcholin MeSH
• bradykinin MeSH
• matrixová metaloproteinasa 9 MeSH
• Mmp9 protein, mouse MeSH Prohlížeč
• nitroprusid MeSH

The impact on blood pressure of two vasodilating mechanisms, underlied by vascular smooth muscle hyperpolarization, was studied and compared to that induced by nitric oxide NO mechanism. Systemic blood pressure, after inhibitory intervention in arachidonic acid metabolism cytochrome P-450 inhibition by miconazole 0.5 mg/100 g b.w. , one of the hyperpolarizing pathways, did not change. After the inhibition of the action voltage-dependent K(+) channels operator by 4-aminopyridine 0.1 mg/100 g b.w. , the other hyperpolarizing pathway, blood pressure declined slightly from 132.3+/-3.2 mm Hg to 116.5+/-5.0 mm Hg, P<0.05 . Inhibition of nitric oxide production L-NAME 5 mg/100 g b.w. increased blood pressure considerably 123.5+/-2.7 mm Hg to 155.4+/-3.1 mm Hg, P<0.001 . After inhibition of the hyperpolarizing pathway by miconazole, hypotension induced by acetylcholine (Ach, 10 microg represented 63.0+/-1.9 mm Hg vs control value 78.6+/-5.2 mm Hg P<0.001 , by bradykinin (BK) 100 microg 59.4+/-3.9 mm Hg vs control value 71.2+/-6.1 mm Hg P<0.05 . After inhibition of the hyperpolarizing pathway by 4-aminopyridine, hypotension induced by ACh 10 microg achieved 64.6+/-2.5 mm Hg vs control value 78.4+/-2.8 mm Hg P<0.001 and that induced by BK 100 microg 56.6+/-5.3 mm Hg vs control value 72.3+/-2.5 mm Hg P<0.001 . ACh or BK hypotension after the inhibition of the above hyperpolarizing pathways was significantly attenuated. On the contrary, after NO-synthase inhibition the hypotension to ACh was significantly enhanced. Blood pressure decrease after ACh 10 microg hypotension was 91.8+/-4.1 mm Hg vs control value 79.3+/-3.3 mm Hg P<0.01 , and after BK 100 microg it was 78.4+/-7.1 mm Hg vs control value 68.3+/-5.2 mm Hg. A different basal BP response, but equally attenuated hypotension to Ach and BK, was detected after the inhibition of two selected hyperpolarizing pathways. In cotrast, the inhibition of NO production elicited an increase in systemic BP and augmentation of ACh and BK hypotension. The effectiveness of further hyperpolarizing mechanisms in relation to systemic BP regulation and nitric oxide level remains open.

• MeSH
• 4-aminopyridin farmakologie   MeSH
• acetylcholin farmakologie   MeSH
• arteriae carotides účinky léků   metabolismus   MeSH
• biologické faktory metabolismus   MeSH
• blokátory draslíkových kanálů farmakologie   MeSH
• bradykinin farmakologie   MeSH
• draslíkové kanály řízené napětím účinky léků   metabolismus   MeSH
• inhibitory cytochromu P450 MeSH
• inhibitory enzymů farmakologie   MeSH
• krevní tlak účinky léků   MeSH
• krysa rodu Rattus MeSH
• kyselina arachidonová metabolismus   MeSH
• mikonazol farmakologie   MeSH
• NG-nitroargininmethylester farmakologie   MeSH
• potkani Wistar MeSH
• svaly hladké cévní účinky léků   metabolismus   MeSH
• synthasa oxidu dusnatého antagonisté a inhibitory   metabolismus   MeSH
• systém (enzymů) cytochromů P-450 metabolismus   MeSH
• vazodilatancia farmakologie   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH
• Názvy látek
• 4-aminopyridin MeSH
• acetylcholin MeSH
• biologické faktory MeSH
• blokátory draslíkových kanálů MeSH
• bradykinin MeSH
• draslíkové kanály řízené napětím MeSH
• endothelium-dependent hyperpolarization factor MeSH Prohlížeč
• inhibitory cytochromu P450 MeSH
• inhibitory enzymů MeSH
• kyselina arachidonová MeSH
• mikonazol MeSH
• NG-nitroargininmethylester MeSH
• synthasa oxidu dusnatého MeSH
• systém (enzymů) cytochromů P-450 MeSH
• vazodilatancia MeSH

Two exogenous NO donors were used to act as substitutes for impaired endogenous nitric oxide (NO) production due to inhibition of NO synthase in rats. Six weeks' lasting inhibition of NO synthase by NG-nitro-L-arginine methyl ester (L-NAME) induced stabilized hypertension. Simultaneously administered isosorbide-5-mononitrate did not prevent the development of hypertension. Molsidomine, administered concomitantly with L-NAME, significantly attenuated the BP increase. However, BP was still found to be moderately increased compared to the initial values. Remarkable alterations in the geometry of the aorta, carotid and coronary artery found in NO-deficient hypertension were prevented in rats administered L-NAME plus molsidomine at the same time. In spite of 6 weeks' lasting inhibition of NOS, the NOS activators acetylcholine and bradykinin induced BP decrease; the maximum hypotensive value did not differ from the values recorded in the controls or in animals treated with L-NAME plus molsidomine. Notably enough, the hypotension was similar to that found in rats administered L-NAME alone for six weeks. After NO synthase inhibition, Isosorbide-5-mononitrate does not substitute and molsidomine substitute only partially the impaired endogenous NO production.

• MeSH
• acetylcholin farmakologie   MeSH
• aktivace enzymů účinky léků   MeSH
• bradykinin farmakologie   MeSH
• donory oxidu dusnatého farmakologie   MeSH
• hypertenze farmakoterapie   metabolismus   MeSH
• inhibitory enzymů farmakologie   MeSH
• isosorbiddinitrát analogy a deriváty   farmakologie   MeSH
• krevní tlak účinky léků   MeSH
• krysa rodu Rattus MeSH
• molsidomin farmakologie   MeSH
• NG-nitroargininmethylester farmakologie   MeSH
• oxid dusnatý biosyntéza   MeSH
• potkani Wistar MeSH
• synthasa oxidu dusnatého metabolismus   MeSH
• vazodilatancia farmakologie   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
• acetylcholin MeSH
• bradykinin MeSH
• donory oxidu dusnatého MeSH
• inhibitory enzymů MeSH
• isosorbiddinitrát MeSH
• isosorbide-5-mononitrate MeSH Prohlížeč
• molsidomin MeSH
• NG-nitroargininmethylester MeSH
• oxid dusnatý MeSH
• synthasa oxidu dusnatého MeSH
• vazodilatancia MeSH

The hypotensive response to acetylcholine and bradykinin was studied in rats with NO synthase activity inhibited for a short period of 2 h or a long period of 6 weeks. N(G)-nitro-L-arginine-methyl ester (L-NAME) was used as NO synthase inhibitor (given in a dose of 50 mg/kg either into the jugular vein, or daily in drinking water). Blood pressure was measured in the right carotid artery by a Statham pressure transducer in acute experiments, and on the tail artery by the plethysmographic method weekly in chronic experiments. During both the short- and long-lasting NO synthase inhibition blood pressure rose significantly. The heart rate decreased significantly in rats treated with L-NAME for 6 weeks. Surprisingly, the hypotensive responses to acetylcholine and bradykinin were present in both experimental groups. Paradoxically, the hypotensive responses to all three doses of acetylcholine were remarkably enhanced in rats with NO synthase inhibition lasting 6 weeks, in comparison to both age-matched controls and to rats subjected to short-lasting NO synthase inhibition. The blockade of muscarinic receptors by atropine abolished the hypotensive response to acetylcholine but not to bradykinin. The hypothetical mechanisms underlying this unexpected paradoxical phenomenon of cardiovascular control are discussed.

• MeSH
• acetylcholin aplikace a dávkování   farmakologie   MeSH
• antagonisté muskarinových receptorů farmakologie   MeSH
• atropin farmakologie   MeSH
• bradykinin aplikace a dávkování   farmakologie   MeSH
• hypertenze patofyziologie   MeSH
• inhibitory enzymů farmakologie   MeSH
• krevní tlak účinky léků   MeSH
• krysa rodu Rattus MeSH
• NG-nitroargininmethylester farmakologie   MeSH
• oxid dusnatý fyziologie   MeSH
• potkani Wistar MeSH
• srdeční frekvence účinky léků   MeSH
• synthasa oxidu dusnatého antagonisté a inhibitory   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
• acetylcholin MeSH
• antagonisté muskarinových receptorů MeSH
• atropin MeSH
• bradykinin MeSH
• inhibitory enzymů MeSH
• NG-nitroargininmethylester MeSH
• oxid dusnatý MeSH
• synthasa oxidu dusnatého MeSH

Doubly transfected human embryonal kidney cells (clone E2M11 of the HEK 293 cell line) expressing both thyrotropin-releasing hormone (TRH) receptors and G11alpha protein in high amounts were used to analyze the desensitization phenomenon of the Ca2+-mobilizing pathway. Quite unexpectedly, we did not observe any significant desensitization of the [Ca2+]i response to TRH in these cells after repeated or prolonged incubation with the hormone (up to 5 h). Under the same conditions, the TRH-induced [Ca2+]i response was completely desensitized in the parent cell line (293-E2 cels) expressing TRH receptors alone. In both cell lines, inositol phosphate response was desensitized after TRH exposure, although basal levels of inositol phospates in TRH-pretreated cells were much higher than in "naive" TRH-unexposed cells. These data suggest a significant role of the G protein G11alpha in desensitization of the Ca2+-mobilizing pathway occuring after repeated or long-term exposure of target cells to TRH-receptor agonists.

• MeSH
• blokátory kalciových kanálů farmakologie   MeSH
• bradykinin farmakologie   MeSH
• buněčné linie MeSH
• časové faktory MeSH
• EGTA farmakologie   MeSH
• exprese genu MeSH
• hormon uvolňující thyreotropin agonisté   antagonisté a inhibitory   farmakologie   MeSH
• inositolfosfáty metabolismus   MeSH
• krysa rodu Rattus MeSH
• lidé MeSH
• nifedipin farmakologie   MeSH
• proteiny vázající GTP antagonisté a inhibitory   genetika   metabolismus   MeSH
• receptory thyroliberinu agonisté   antagonisté a inhibitory   genetika   fyziologie   MeSH
• suramin farmakologie   MeSH
• thapsigargin farmakologie   MeSH
• transfekce MeSH
• vápník metabolismus   farmakologie   MeSH
• vápníková signalizace účinky léků   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
• blokátory kalciových kanálů MeSH
• bradykinin MeSH
• EGTA MeSH
• hormon uvolňující thyreotropin MeSH
• inositolfosfáty MeSH
• nifedipin MeSH
• proteiny vázající GTP MeSH
• receptory thyroliberinu MeSH
• suramin MeSH
• thapsigargin MeSH
• vápník MeSH