bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cyclic GMP‐independent relaxation and hyperpolarization with acetylcholine in guinea‐pig coronary artery
Authors: Eckman D.M. , Weinert J.S. , Buxton I.L.O. , Keef K.D. 
Published: July 2012

The effects of acetylcholine (ACh) on membrane potential, relaxation and cyclic GMP levels were compared to the NO donor l‐nitrosocysteine (Cys‐NO) in segments of guinea‐pig coronary artery.
ACh and Cys‐NO produced concentration‐dependent relaxations of muscles contracted with the H1 receptor agonist, 2‐(2‐aminoethyl)pyridine (AEP, 0.35 mm). The relaxation to ACh was unchanged in the presence of NG‐monomethyl‐l‐arginine (l‐NMMA; 350 μm) or indomethacin (3 μm).
Oxyhaemoglobin (HbO; 20 μm) alone or in combination with l‐NMMA increased the EC50 for ACh‐induced relaxation whereas relaxation with Cys‐NO was almost completely abolished with HbO.
Scorpion venom (SV; 8.7 μg ml−1) increased the EC50 for relaxation with ACh but not Cys‐NO. Combined l‐NMMA, HbO and SV produced nearly complete abolition of ACh‐induced relaxations.
Basal cyclic GMP levels (i.e., 20 pmol mg−1protein) were significantly increased following addition of either ACh (190 pmol mg−1protein) or Cys‐NO (240 pmol mg−1protein). l‐NMMA significantly reduced the rise of cyclic GMP with ACh but not Cys‐NO. In contrast, SV did not significantly reduce the rise in cyclic GMP produced with ACh. In the combined presence of l‐NMMA and HbO neither ACh nor Cys‐NO produced a significant increase in cyclic GMP levels.
ACh gave rise to significantly greater membrane hyperpolarization than Cys‐NO both in the presence and absence of AEP. Combined l‐NMMA and HbO did not reduce the amplitude of hyperpolarization with ACh.
These data indicate that some but not all of the actions of ACh in the coronary artery can be mimicked by the NO donor, Cys‐NO, suggesting that ACh releases NO as well as a second hyperpolarizing factor (i.e., EDHF). Release of NO results in a large increase in tissue cyclic GMP levels and minimal change in membrane potential whereas release of EDHF results in a large membrane hyperpolarization which is independent of changes in tissue cyclic GMP levels. Both of these pathways appear to contribute to relaxation throughout the entire ACh concentration‐relaxation relationship.
Depression of high‐threshold calcium currents by activation of human D2 (short) dopamine receptors expressed in differentiated NG108‐15 cells
Authors: Seabrook G.R. , McAllister G. , Knowles M.R. , Myers J. , Sinclair H. , Patel S. , Freedman S.B. , Kemp J.A. 
Published: July 2012

This study examined the regulation of calcium currents in differentiated NG108‐15 cells that had been stably transfected with cDNA encoding the short isoform of the human D2 dopamine receptor. Whole cell calcium currents were recorded by nystatin‐perforated patch clamp recording.
Transient low‐threshold calcium currents elicited by depolarizations from − 100 mV to − 20 mV were reversibly depressed by NiCl2 (84 ± 8% at 30 μm; n = 3) and by ω‐agatoxin IVA (15 ± 5%; 100 nm, n = 7). These currents were unaffected by hD2 receptor activation.
High‐threshold calcium currents elicited by depolarizations from − 80 mV to 0 mV were partly blocked by ω‐conotoxin GVIA (67 ± 6% at 100 nm, n = 4) and by the subsequent addition of the dihydropyridine, nisoldipine (94 ± 3% at 1 μm). Consistent with the presence of at least two distinct types of high‐threshold calcium channels, nisoldipine alone (38 ± 15% at 1 μm, n = 6) did not preclude the inhibition caused by ω‐conotoxin GVIA (69 ± 13% at 100 nm, n = 4). The residual current was completely blocked by 100 μm CdCl2 (98.8 ± 0.4%, n = 7).
In hD2‐transfected cells, but not untransfected cells, high‐threshold currents were depressed by quinpirole (30 ± 4% at 100 nm; n = 15) with a pEC50 of 8.61 ± 0.22 (n = 5), as well as by (−)‐noradrenaline (28 ± 5% at 1 μm, n = 9). Responses to both agonists were selectively antagonized by S‐(−)sulpiride (100 nm) but not by the α‐adrenoceptor antagonist, phentolamine (10 μm). The depression caused by (−)‐noradrenaline was positively correlated with that of quinpirole for each cell (r2= 0.91, slope = 0.99).
hD2‐receptor‐mediated inhibition of high‐threshold calcium currents was abolished by pretreatment of cells with ω‐conotoxin GVIA (100 nm; n = 4). However, a component of the high‐threshold current was reversibly depressed by ω‐conotoxin GVIA (67% to 45% depression after 10 min wash). This current was also depressed by hD2 receptor activation (59 ± 9% depression in 100 nm quinpirole, n = 3), and was completely blocked by nisoldipine (95 ± 2% at 1 μm).
These data demonstrate that activation of hD2(short) dopamine receptors can regulate both ω‐conotoxin GVIA, and dihydropyridine‐sensitive high‐threshold calcium currents in neuroblastoma cells. Morever, the ability of human D2 dopamine receptors to regulate more than one type of calcium current supports the notion that these receptors have a diverse functional role in the central nervous system.
Effects of ethanol and other aliphatic alcohols on NO‐mediated relaxations in rat anococcygeus muscles and gastric fundus strips
Authors: Rand M.J. , Li C.G. 
Published: July 2012

In anococcygeus muscles, ethanol (20–500 mm) slightly increased the tone and inhibited relaxations elicited by nitrergic nerve stimulation (0.5–5 Hz) in a concentration‐dependent manner.
Other aliphatic alcohols decreased the tone but had inhibitory effects similar to ethanol on stimulation‐induced relaxations, the EC50 (mm) values being: methanol 280, ethanol 80, propan‐1‐ol 20, propan‐2‐ol 55, propan 1,2‐diol 135, butan‐1‐ol 120, butan‐2‐ol 15 and pentan‐1‐ol 3.
Relaxations induced by sodium nitroprusside (SNP, 10 nm) were inhibited by ethanol (20–500 mm) in a concentration‐dependent manner and by propan‐2‐ol (100 mm). Relaxations induced by NO (1 μm) were inhibited by high concentrations of ethanol (200–300 mm) and by propan‐2‐ol (100 mm).
In gastric fundus strips, ethanol (60–200 mm) did not affect the resting tone but inhibited NO‐mediated relaxations elicited by low frequency (1 Hz) field stimulation and reduced the initial relaxation by high frequency field stimulation (10 Hz) and by SNP (50 nm). The relaxant action of isoprenaline (10 nm) was not reduced although it was slightly slower in onset. Other aliphatic alcohols tested decreased the tone and inhibited relaxations elicited by field stimulation.
Acetaldehyde (1–10 mm) inhibited relaxations elicited by field stimulation and SNP in both the rat anococcygeus muscles and gastric fundus strips. The tone of gastric fundus strips was decreased by acetaldehyde but it was transiently increased in anococcygeus muscles.
The dehydrogenase inhibitors, 4‐methylpyrazole (100 μm) and disulfiram (100 μm) did not significantly affect the inhibition by ethanol of nitrergic nerve stimulation‐induced relaxations in anococcygeus muscles, which suggests that ethanol acts directly.
The inhibition of NO‐mediated relaxations by alcohols is attributed to sequestration of NO to form nitroso‐alcohols.
Effect of PAF on rat lung vascular permeability: role of platelets and polymorphonuclear leucocytes
Authors: Sirois Martin G. , de Lima Wothan Tavares , Fernandes Artur José de Brum , Johnson Richard J. , Plante Gérard E. , Sirois Pierre 
Published: July 2012

The objectives of the present experiments were to assess the contribution of polymorphonuclear leucocytes (PMNLs), platelets and their products such as thromboxane A2 (TxA2), histamine and 5‐hydroxytryptamine to platelet activating factor (PAF)‐mediated protein extravasation in rat lungs.
Intravenous injection of PAF (1.0 and 5.0 μg kg−1) increased dose‐dependently (up to 7.5 fold) the vascular permeability of the trachea, upper and lower bronchi to Evans blue dye (EB), a marker of albumin extravasation. The permeability of the pulmonary parenchyma was not affected significantly by PAF.
Thrombocytopenia induced by administration of the IgG fraction of goat anti‐rat platelet serum (APS; 15 mg 100 g−1, i.p., 16–18 h) reduced by 55, 58 and 40% the effects of the lower dose of PAF (1.0 μg kg−1) and by 31, 23 and 15% the effects of the higher dose of PAF (5.0 μg kg−1) on the permeability of the trachea, upper and lower bronchi respectively to albumin.
PMNL depletion induced by administration of rabbit anti‐rat polymorphonuclear serum (ANS; 2 mg kg−1, i.v., 24 h) did not reduce significantly the effects of the lower dose of PAF (1.0 μg kg−1) on the airways, however the effects of the higher dose of PAF (5.0 μg kg−1) on the permeability of the trachea, upper and lower bronchi to albumin were reduced by 43, 25 and 23% respectively.
The injection of both the anti‐platelet and the anti‐PMNL sera reduced by 61, 62 and 96% the effects of the lower dose of PAF (1.0 μg kg−1) and by 44, 39 and 47% the effects of the higher dose of PAF (5.0 μg kg−1) on the permeability of the trachea, upper and lower bronchi respectively.
The combined injection of the TxA2‐mimetic (U‐44069; 5.0 μg kg−1) and PAF (1.0 and 5.0 μg kg−1) in thrombocytopenic rats overcame the vascular permeability decrease induced by APS treatment.
Pretreatment of the animals with a combination of antagonists to histamine (mepyramine; 3.0 mg kg−1) and 5‐hydroxytryptamine (methysergide; 2.5 mg kg−1) did not cause a significant inhibition of the effect of PAF (1.0 and 5.0 μg kg−1) on EB extravasation in the airways.
These data show that the effect of intravenous PAF on rat vascular permeability is partly modulated by polymorphonuclear leucocyte and platelet activation. Our results suggest that following its release, TxA2 could increase postcapillary hydrostatic pressure by inducing a venoconstriction and potentiate the extravasation elicited by PAF. These results do not suggest a major role for histamine and/or 5‐hydroxytryptamine on PAF‐induced albumin extravasation.
Receptor for catecholamines responding to catechol which potentiates voltage‐dependent calcium current in single cells from guinea‐pig taenia caeci
Authors: Muraki Katsuhiko , Bolton Thomas B. , Imaizumi Y. , Watanabe M. 
Published: July 2012

Single isolated cells were obtained from the taenia of the guinea‐pig's caecum by enzymic digestion and held under voltage clamp. The effects of various catecholamines, sympathomimetics and related compounds were tested for their ability to potentiate the voltage‐dependent calcium current (ICa) evoked in these cells by a depolarizing step.
ICa was potentiated by up to 60% by isoprenaline, adrenaline, and noradrenaline which were equipotent. The EC50 for isoprenaline was about 40 nm.
The racemic mixtures of the optical isomers of isoprenaline, adrenaline, and noradrenaline, and (+)‐isoprenaline, were equipotent with the (–)‐isomers of these drugs. Dopamine, l‐dopa, and catechol were equipotent with these catecholamines.
Removal or substitution of one or more of the hydroxy groups of the catechol moiety, as in phenylephrine, salbutamol, procaterol, methoxamine, terbutaline, BRL 37344, ICI 215001 or tyramine substantially reduced efficacy and/or potency.
The adrenoceptor blockers propranolol, phentolamine, dihydroergotamine, atenolol, CGP 20712A and ICI 118551, or the dopamine receptor blockers, haloperidol or flupenthixol, did not block the potentiating action of catechol or the catecholamines.
The receptor activated by catecholamines to increase ICa we suggest should be called a C‐receptor in view of its sensitivity to catechol. It may arise by enzymic modification of a conventional adrenoceptor but its transduction also involves a novel mechanism which might indicate that it is present in the muscle cells before enzyme treatment.
Characterization of 5‐hydroxytryptamine receptors mediating mucosal secretion in guinea‐pig ileum
Authors: Johnson P.J. , Bornstein J.C. , Furness J.B. , Woollard D.J. , Orrman‐Rossiter S.L. 
Published: July 2012

The receptor subtypes through which 5‐hydroxytryptamine (5‐HT) increases electrolyte secretion across the mucosa of guinea‐pig ileum were studied.
Flat sheep preparations of guinea‐pig mucosa plus submucosa were placed in Ussing chambers and the short circuit current (ISC), an index of net electrogenic electrolyte transport across the mucosa, was measured under voltage clamp conditions.
Low concentrations of 5‐HT (10–300 nm) evoked monophasic increases in ISC which were significantly reduced by hyoscine (100 nm), tetrodotoxin (TTX, 300 nm) and the 5‐HT2 receptor antagonist, ketanserin (3–300 nm).
Higher concentrations of 5‐HT (1–10 μm) produced biphasic responses which were reduced by hyoscine (100 nm), TTX (300 nm), ketanserin (3–300 nm) and also by the 5‐HT3 receptor antagonists, granisetron (1 μm) and ICS 205–930 (100 nm).
2‐Methyl‐5‐HT (1–100 μm) and α‐methyl‐5‐HT (30 nm‐30 μm), agonists at 5‐HT3 and 5‐HT2 receptors respectively, also evoked ISC increases. These responses were reduced by hyoscine (100 nm) and abolished by TTX (300 nm) and the respective receptor antagonists, granisetron (1 μm) and ketanserin (30 nm).
The 5‐HT4 receptor antagonist, SDZ 205–557 (300 nm) had no effect on the response to 5‐HT.
The TTX‐resistant response to 5‐HT was not affected by 5‐HT23 or 4 receptor antagonists.
These results indicate that 5‐HT mediates secretion partly by an action on 5‐HT3 receptors located on cholinergic and noncholinergic secretomotor neurones, partly by an action on higher affinity ‘5‐HT2‐like’ receptors predominantly on noncholinergic neurones, and partly by a direct action on the epithelium.
Interactions between indomethacin, noradrenaline and vasodilators in the fetal rabbit ductus arteriosus
Authors: Smith Gordon C.S. , McGrath John C. 
Published: July 2012

Interactions between indomethacin, noradrenaline and vasodilators were studied in rings of ductus arteriosus isolated from fetal rabbits. The effect of incubation with prostaglandin E2 (PGE2) on the noradrenaline concentration‐contraction response curve was studied in the presence and absence of indomethacin. Also, the ductus was pre‐contracted with 10 μm noradrenaline and concentration‐relaxation response curves (CRRC) to PGE2, cicaprost, cromakalim and forskolin were obtained in the presence and absence of indomethacin.
In the absence of indomethacin, PGE2 (from 1 nm to 100 nm) decreased the pEC50 to noradrenaline to a maximum of 0.4 to 0.5 log units (i.e. an approximately three fold increase in EC50 [m]). In the presence of 1 μm indomethacin, PGE2 (0.1 nm to 100 nm) decreased the pEC50 to noradrenaline by 2.39 log units (i.e. a 245 fold increase in EC50). By comparing the control pEC50 to noradrenaline with the relationship between the pEC50 to noradrenaline and [PGE2] in 1 μm indomethacin, the effect of endogenous PGE2 synthesized in the vessel wall was estimated as being equivalent to a bath concentration of approximately 1 nm exogenous PGE2.
When the vessel was pre‐contracted with 10 μm noradrenaline, indomethacin had no effect on the CRRC to PGE2 but did alter the CRRC to other vasodilators. The sensitivity of the vessel to cicaprost, cromakalim and forskolin was decreased in 1 μm indomethacin compared with control. Forskolin caused complete relaxation in the presence and absence of indomethacin. Indomethacin decreased the maximum response to cromakalim but increased the maximum response to cicaprost. PGE2, 0.3 nm, partially reversed the effect of indomethacin on the sensitivity of the vessel to forskolin.
We conclude that under varying experimental conditions, indomethacin increased the sensitivity of the ductus to the effects of PGE2 but decreased its sensitivity to other vasodilators. Both effects can be explained by elimination of endogenous PGE2. However, indomethacin increased the maximum response to cicaprost, which cannot be explained by elimination of endogenous PGE2 but may be due to elimination of endogenous prostacyclin.
Coupling of a transfected human brain A1 adenosine receptor in CHO‐K1 cells to calcium mobilisation via a pertussis toxin‐sensitive mechanism
Authors: Iredale Philip A. , Alexander Stephen P.H. , Hill Stephen J. 
Published: July 2012

The presence of A1 adenosine receptors in CHO‐K1 cells transfected with the human brain A1 sequence was confirmed by ligand binding studies using 8‐cyclopentyl‐[3H] 1,3‐dipropylxanthine ([3H]‐DPCPX).
Alterations in intracellular calcium ([Ca2+]i) were measured with the calcium‐sensitive dye, fura‐2.
N6‐cyclopentyladenosine (CPA), the selective A1 agonist, and 5′‐N‐ethylcarboxaminoadenosine (NECA), a relatively non‐selective adenosine receptor agonist, elicited rapid, biphasic increases in [Ca2+]i which involved both mobilisation from intracellular stores and calcium entry.
The calcium response to CPA was significantly inhibited by the selective A1 antagonist DPCPX. The non‐selective adenosine receptor, xanthine amino congener (XAC), was less potent.
The calcium response to CPA was completely prevented by pretreatment of the cells with pertussis toxin implicating the involvement of Gi in the receptor‐mediated response.
In summary, we present evidence for the coupling of transfected human brain A1 adenosine receptors in CHO‐K1 cells to mobilisation of [Ca2+]i via a pertussis toxin‐sensitive G protein.
Evidence for a cooperation between adenosine A2 receptors and β1‐adrenoceptors on cardiac automaticity in the isolated right ventricle of the rat
Authors: Hernandez J. , Figueira M.A. , Ribeiro J.A. , Pinto F. 
Published: July 2012

The effects of the adenosine receptor agonists, 5′‐N‐ethyl‐carboxamidoadenosine (NECA) and 2‐[4‐(2‐carboxyethyl)phenethylamino]‐5′‐N‐ethylcarboxamidoadenosine (CGS‐21680) on ventricular automaticity induced by a local injury in the isolated right ventricle of the rat were studied.
In concentrations ranging from 0.1 to 100 nm, NECA significantly increased ventricular automaticity. This effect was more reproducible when the adenosine receptor antagonist 1,3‐dipropyl‐8‐cyclopentylxanthine (DPCPX) was present at 5 nm, a concentration that blocks A1 adenosine receptors.
The excitatory effect of NECA was not observed when DPCPX was present at a concentration of 10 μm, which antagonizes both A1 and A2 adenosine receptors, as well as when rats were reserpinized.
In reserpinized rats, NECA increased ventricular automaticity in the presence of isoprenaline and the β2‐adrenoceptor antagonist, ICI‐118,551, but not in the presence of the βradrenoceptor antagonists, bisoprolol or atenolol.
The A2a‐selective adenosine receptor agonist, CGS‐21680 (0.1 nm‐10 μm) was devoid of excitatory effect on ventricular automaticity. Binding studies of this compound to the rat ventricular membranes revealed that in the preparation there was no specific binding.
These results suggest that the excitatory effect of NECA on ectopic ventricular automaticity is dependent on endogenous catecholamines and is mediated by an A2 adenosine receptor which is in some way ‘linked’ to the β1‐adrenoceptor. These A2 receptors do not appear to be of the A2a adenosine receptor subtype.
Mediation by nitric oxide formation in the preoptic area of endotoxin and tumour necrosis factor‐induced inhibition of water intake in the rat
Authors: Calapai G. , Mazzaglia G. , Cilia M. , Zingarelli B. , Squadrito F. , Caputi A.P. 
Published: July 2012

Drinking was induced in rats by 24 h of water deprivation. Water intake (ml) was evaluated for a 1 h period.
NG‐nitro‐l‐arginine methyl ester (l‐NAME, 5–10 μg, i.c.v., 50–100 ng into the preoptic area (POA)), an inhibitor of nitric oxide (NO) synthase, and methylene blue (50–100 ng into POA), an inhibitor of guanylate cyclase activation, antagonized the inhibition of drinking induced by E. coli endotoxin (LPS, 640 μg kg−1, i.v.) and tumour necrosis factor (TNFα, 40 ng, i.c.v.) in 24 h water‐deprived rats.
l‐Arginine (25, 50 and 100 ng), the precursor aminoacid of NO, but not the stereoisomer d‐arginine (100 ng), inhibited drinking induced by water deprivation when injected into the POA 30 min before water presentation (74.4% of inhibition with the highest dose). A dose of 12.5 ng l‐arginine into the POA did not exhibit antidipsogenic effects.
TNFα (20 and 40 ng, i.c.v.; 1.25, 2.5 and 5 ng into the POA) showed a dose‐dependent and powerful inhibition of drinking behaviour in water‐deprived rats (70.4% and 80.8%, i.c.v. and into POA, with the highest doses, respectively). A dose of 10 ng of TNFα given i.c.v. had no effect on the intake of water.
LPS and TNFα, given at doses (160 μg kg−1, i.v. and 10 ng, i.c.v., respectively) that did not influence drinking in water‐deprived rats, exhibited a strong antidipsogenic effect in water‐deprived rats treated with a dose of l‐arginine (12.5 ng, into the POA) which did not modify drinking by itself. (LPS + l‐arginine: 53.6% of inhibition; TNFα + l‐arginine: 52.0% of inhibition).
These results suggest that NO into the POA: (1) acts as an inhibitory mechanism on thirst and (2) plays a role in the antidipsogenic effect of LPS and TNFα.
On the nature of the 5‐HT receptor subtype inhibiting acetylcholine release in the guinea‐pig ileum
Authors: Ramírez M.J. , Del Río J. , Cenarruzabeitia E. , Lasheras B. 
Published: July 2012

The nature of the 5‐hydroxytryptamine (5‐HT) receptor subtype controlling acetylcholine release and contraction induced by stimulation of the neurokinin NK3 receptor has been studied in the longitudinal muscle‐myenteric plexus preparation from guinea‐pig ileum.
In preparations preloaded with [3H]‐choline, the selective NK3 agonist, senktide, produced a concentration‐dependent increase in tritium overflow, an index of [3H]‐acetylcholine release. Low concentrations of neurokinin B, also markedly increased tritium efflux.
The senktide‐induced acetylcholine release was markedly increased by the same concentration of methysergide and mesulergine. The 5‐HT2A/2C agonist DOI (1 μm) inhibited the tritium overflow while 8‐OH‐DPAT, sumatriptan and ketanserin (1 μm each) were without effect on the senktide‐induced tritium efflux.
The contractile response to senktide in the guinea‐pig ileum was attenuated by atropine, 0.1 μm. Methysergide, a 5‐HT1/2 receptor antagonist, and mesulergine, a 5‐HT2A/2B/2C receptor antagonist, (1 μm each), enhanced the contractile effect of the NK3 receptor agonist.
It is concluded that the acetylcholine release induced by a NK3 receptor agonist is inhibited by stimulation of a 5‐HT receptor, possibly of the 5‐HT2C or 5‐HT2B subtype.
Pharmacological characterization of rabbit corpus cavernosum relaxation mediated by the tissue kallikrein‐kinin system
Authors: Lopes‐Martins Rodrigo A.B. , Antunes Edson , Oliva Maria Luiza V. , Sampaio Cláudio A.M. , Burton James , de Nucci Gilberto 
Published: July 2012

The roles of the tissue kallikrein‐kinin system and nitric oxide (NO) release in Phoneutria nigriventer venom‐induced relaxations of rabbit corpus cavernosum (RbCC) smooth muscle have been investigated by use of a bioassay cascade.
Phoneutria nigriventer venom (10–30 μg), porcine pancreatic kallikrein (100 mu), rabbit urinary kallikrein (10 mu), bradykinin (BK, 0.3–3 nmol), acetylcholine (ACh, 0.3–30 nmol) and glyceryl trinitrate (GTN, 0.5–10 nmol) caused relaxations of the RbCC strips. Captopril (1 μm) substantially potentiated Phoneutria nigriventer venom‐ and BK‐induced RbCC relaxations without affecting those elicited by GTN.
The bradykinin B2 receptor antagonist, Hoe 140 (d‐Arg‐[Hyp3, Thi5,d‐Tic7, Oic8]‐BK, 50 nm), aprotinin (10 μg ml−1) and the tissue kallikrein inhibitor, Pro‐Phe‐Aph‐Ser‐Val‐Gln‐NH2 (KIZD‐06, 1.3 μm) significantly inhibited Phoneutria nigriventer venom‐induced RbCC relaxations, without affecting those provoked by GTN and ACh. The B1 receptor antagonist, [Leu9]des Arg10BK (0.5 μm) and soybean trypsin inhibitor (SBTI, 10 μg ml−1) had no effect on Phoneutria nigriventer venom‐induced RbCC relaxations.
The relaxations induced by Phoneutria nigriventer venom, porcine pancreas kallikrein, BK and ACh were significantly inhibited by Nω‐nitro‐l‐arginine methyl ester (l‐NAME, 10 μm) but not by d‐NAME (10 μm). l‐NAME did not affect GTN‐induced relaxations. l‐Arginine (300 μm), but not d‐arginine (300 μm), significantly reversed the inhibitory effect of l‐NAME.
Our results indicate that Phoneutria nigriventer venom activates the tissue kallikrein‐kininogen‐kinin system in RbCC strips leading to NO release and suggest a functional role for this system in penile erection.