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C G Li

Publications and source records attributed to C G Li.

At least 37 records · Page 2Linked to original sources
PubMed1998

Effect of xanthine oxidase inhibition on endothelium-dependent and nitrergic relaxations.

The effects of inhibition of xanthine oxidase on responses mediated by nitric oxide (NO) were examined using the selective xanthine oxidase inhibitors allopurinol and 4-amino-6-hydroxypyrazolo[3,4-d]pyrimidine (AHPP). In rat aortic rings precontracted with phenylephrine (1 microM), allopurinol (300 microM) and AHPP (100, 300 microM) significantly reduced tone, an effect not seen after inhibition of NO synthase with Nomega-nitro-L-arginine (NOLA 100 microM). Relaxations produced by acetylcholine (0.01-10 microM) were significantly enhanced by AHPP (100, 300 microM) but not by allopurinol. Nitrergic relaxations in the rat anococcygeus muscle (field stimulation 1 ms pulses; 1 Hz: 10 s) were not affected by either allopurinol or AHPP. However, relaxations produced by exogenous NO (0.25 microM) were significantly enhanced by AHPP, allopurinol (100 microM) and superoxide dismutase (100 U/ml). Xanthine (500 microM) partially, but significantly, reversed the enhancement produced by AHPP. These findings suggest that superoxide generated by xanthine oxidase modulates the activity of basal and stimulated NO derived from the rat aortic endothelium, but does not affect the activity of the nitrergic transmitter in the rat anococcygeus muscle, despite its ability to modulate responses to exogenous NO.

Acetylcholine↗
PubMed1998

Role of potassium channels in the nitrergic nerve stimulation-induced vasodilatation in the guinea-pig isolated basilar artery.

1. We studied the effects of various K+ channel blockers on the vasodilator responses of guinea-pig isolated basilar arteries to nitrergic nerve stimulation, the nitric oxide (NO) donor sodium nitroprusside (SNP), and the membrane permeable guanosine-3',5'-cyclic monophosphate (cyclic GMP) analogue 8-bromo-cyclic GMP (8-Br-cyclic GMP). 2. In endothelium-denuded preparations which were contracted with prostaglandin F2alpha (1 microM), electrical field stimulation (EFS, 10 Hz for 30 s) produced a vasodilatation which was totally blocked by the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester L-NAME; 100 microM) (n=3) and by the selective NO-sensitive guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ; 1 microM) (n=4). The vasodilator response to SNP (100 nM) was not reduced by L-NAME but was abolished by ODQ (1 microM) (n=4). 3. EFS-elicited vasodilatation was partly but significantly reduced by the non-selective K+ channel blockers tetraethylammonium (TEA, 1 and 3 mM) and 4-aminopyridine (4-AP, 3 mM), and by the large-conductance calcium-activated K+ channel (K(Ca) channel) blockers charybdotoxin (ChTX, 150 nM) and iberiotoxin (IbTX, 30 and 100 nM). In contrast, the ATP-sensitive K+ channel (K(ATP) channel) blocker glibenclamide (1-10 microM) and the small-conductance K(Ca) channel blocker apamin (100-500 nM) did not affect EFS-induced vasodilatation. 4. The vasodilator response elicited by SNP (10-100 nM) was significantly reduced by TEA (3 mM) and ChTX (150 nM) but not by apamin (500 nM) or glibenclamide (1 microM). The vasodilatation elicited by 8-Br-cyclic GMP (100 microM) was also reduced by TEA (3 mM) and ChTX (150 nM). 5. The results indicate that the vasodilatations induced by nitrergic nerve stimulation and the NO donor SNP in endothelium-denuded guinea-pig basilar artery depend on the formation of intracellular cyclic GMP. The increased cyclic GMP level activates large-conductance K(Ca) channels which partly mediate the vasodilator response. Neither K(ATP) channels nor apamin-sensitive small-conductance K(Ca) channels are involved in nitrergic transmitter-mediated vasodilatation.

Animals↗
PubMed1998

Serum levels of vascular endothelial growth factor (VEGF) are markedly elevated in patients with Wegener's granulomatosis.

OBJECTIVES: Necrotizing vasculitis and granuloma formation are the predominant features of Wegener's granulomatosis (WG). We have investigated the importance of vascular endothelial growth factor (VEGF) in monitoring disease activity in WG. METHODS: Serum VEGF levels were determined in 23 patients with active WG, 21 healthy controls and 25 patients with urinary infection, by ELISA using commercially available antibodies to VEGF. RESULTS: VEGF levels were enormously elevated in patients with WG compared to both controls and patients with urinary infection (P < 0.0001). Of the 23 patients, 21 (91.3%) had VEGF levels above the cut-off value (3.3 ng/ml, calculated as the mean of the controls + 2 S.D.). Further analysis of the data showed that VEGF levels did not correlate with age, sex, incidence of classic antineutrophil cytoplasmic antibodies (c-ANCA) or duration of the disease (P > 0.05), but there was correlation with disease activity (r = 0.51, P < 0.01). VEGF levels were higher in patients with major compared to those with minor disease activity (P < 0.01). However, there was no significant correlation between VEGF levels and the Birmingham scores for vascular activity and damage. CONCLUSION: VEGF levels are raised in WG patients compared to normal controls and may be a marker of disease activity. Further studies on serial blood samples from a large cohort of patients with WG and other systemic vasculitides are needed to evaluate the specificity and usefulness of VEGF levels in monitoring disease activity.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1997

Effect of hydroxocobalamin on vasodilatations to nitrergic transmitter, nitric oxide and endothelium-derived relaxing factor in guinea-pig basilar artery.

In endothelium-denuded guinea-pig isolated basilar artery preparations, hydroxocobalamin (30, 100 and 300 microM) concentration-dependently inhibited the vasodilator responses to exogenous nitric oxide (NO), whereas the vasodilator responses to nitrergic nerve stimulation were slightly reduced by high (100 and 300 microM) but not by the low (30 microM) concentration of hydroxocobalamin. Vasodilatation in response to sodium nitroprusside (10-100 nM) was totally abolished by 300 microM hydroxocobalamin. In endothelium-intact preparations, vasodilator responses to acetylcholine (0.3-3 microM) were significantly reduced or abolished by hydroxocobalamin (30-300 microM). The mean reduction by hydroxocobalamin of relaxations to acetylcholine was significantly greater than that of the equivalent response evoked by nitrergic nerve stimulation. The findings suggest that the nitrergic transmitter in the guinea-pig basilar artery may be quantitatively less susceptible than the endothelium-derived relaxing factor to the NO scavenger hydroxocobalamin.

Acetylcholine↗
PubMed1997

Determination of nitric oxide synthase activity in rat, pig and rabbit prostate glands.

The conversion of L-arginine to L-citrulline by nitric oxide synthase and other enzymes was studied in rat, pig and rabbit prostate glands by incubating preparations of the glands with [3H]L-arginine and measuring [3H]L-citrulline formation. The nitric oxide synthase inhibitor N(G)-nitro-L-arginine, (100 microM) reduced [3H]L-citrulline production in preparations from all three species. The arginase inhibitor L-valine (60 mM) inhibited [3H]L-citrulline production in rat and pig but not in rabbit prostate preparations. Omission of calcium or NADPH significantly reduced nitric oxide synthase-like activity in preparations from all three species but arginase-like activity was not significantly affected. The results indicate that the rabbit prostate contains the greatest amount of calcium-dependent nitric oxide synthase activity, the rat and pig prostates also have arginase-like enzymatic activity and the rat prostate contains an additional unidentified enzyme that converts L-arginine to L-citrulline.

Animals↗
PubMed1997

Characterisation of excitatory and inhibitory transmitter systems in prostate glands of rats, guinea pigs, rabbits and pigs.

Excitatory and inhibitory transmitter systems were investigated in strips of prostate glands from rats, guinea pigs, pigs and rabbits. In strips from all species, electrical field stimulation (1 ms pulses at 1-30 Hz for 10 s) produced frequency-dependent contractions which were abolished by tetrodotoxin (1 microM). In strips from rats, guinea pigs and rabbits, contractions were reduced by prazosin (1 microM), guanethidine (10 microM) and atropine (2 microM), indicating the presence of noradrenergic and cholinergic mechanisms. However, the smooth muscle in the pig prostate appears to have a non-(nor)adrenergic non-cholinergic (NANC) excitatory innervation for which the transmitter was not identified. When noradrenergic and cholinergic mechanisms were blocked by guanethidine and atropine, respectively, and tone was raised with noradrenaline or methoxamine, field stimulation produced relaxations only in strips of rabbit prostate, and these were greatly reduced by N(G)-nitro-L-arginine methyl ester (L-NAME, 100 microM), providing functional evidence for a nitrergic relaxant innervation. In accord with this, nitric oxide (NO) synthase activity was considerably higher in rabbit than in rat or pig prostates.

Animals↗
PubMed1997

Glucosaminylmuramyl dipeptide (GMDP) modulates endothelial cell activities in vitro but has no effect on angiogenesis in vivo.

OBJECTIVE AND DESIGN: The aim of the study was to evaluate the effects of GMDP on angiogenesis in vivo and as a modulator of human umbilical vein endothelial cell proliferation, cell surface antigen expression and cell adhesion in vitro. MATERIALS: Human umbilical vein endothelial cells (HUVEC), fertilized white leghorn chicken eggs, antibodies against adhesion molecules and glucosaminylmuramyl dipeptide (GMDP). TREATMENT: GMDP [0.01-100 micrograms/ml] applied to cell cultures for 6-72 h and to the chick chorioallantoic membrane (CAM) for four days. METHODS: Angiogenic activity of GMDP in vivo was assessed using the CAM assay; HUVEC proliferation was measured by tritiated thymidine incorporation and cell cycle studies; cell surface antigen expression by indirect immunofluorescence and flow cytometry; cell adhesion by quantification of [3H]-thymidine labeled leukocyte adherence to HUVEC monolayers. Statistical analysis was performed using one-way ANOVA and if necessary was followed by Duncan's multiple range test for variables. RESULTS: GMDP induced [3H]-thymidine incorporation in a concentration- and time-dependent manner (p < 0.003) and significantly increased the porportion of cells in the S phase of the cell cycle (p < 0.03). It weakly augmented the expression of ICAM-1 and CD31 but not adhesion of leukocytes to HUVEC monolayers GMDP was not angiogenic in the CAM assay. CONCLUSIONS: GMDP can modulate endothelial cell activity without the induction of angiogenesis in vivo which may have implications for its use as a therapeutic agent.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1997

Mechanisms of electrical field stimulation-induced vasodilatation in the guinea-pig basilar artery: the role of endothelium.

1. The role of endothelium in neuronal vasodilatation elicited by electrical field stimulation (EFS) was investigated in preparations of the isolated guinea-pig basilar artery in which the tone was raised with prostaglandin F2 alpha. 2. In preparations with intact endothelium, EFS produced frequency-dependent dilatations which were not affected by guanethidine but were slightly yet significantly reduced by atropine (1 microM), and were blocked by tetrodotoxin (1 microM) and the nitric oxide synthase inhibitor L-NAME (10 microM). 3. Dilatations were elicited by acetylcholine (3 microM); these were blocked by L-NAME and atropine (1 microM). 4. Dilatations were elicited by nicotine (100 microM); these were blocked by L-NAME and hexamethonium (100 microM). 5. Dilation elicited by sodium nitroprusside (SNP, 3 microM) was not affected by L-NAME. 6. The inhibitory effects of L-NAME were partially prevented by L-arginine (1 microM). 7. Removal of the endothelium resulted in a significant reduction of dilatations elicited by EFS, elimination of the dilator action of acetylcholine, but enhancement of that to SNP. 8. The results suggest that EFS-induced vasodilatation is mediated in part by the nitrergic transmitter and in part endothelium derived relaxing factor (EDRF) activated by acetylcholine released from cholinergic nerves.

Animals↗
PubMed1996

Comparison of the effects of hydroxocobalamin and oxyhaemoglobin on responses to NO, EDRF and the nitrergic transmitter.

1. The effects of ranges of concentrations of oxyhaemoglobin (0.01-30 microM) and hydroxocobalamin (1-100 microM) were compared for their abilities to reduce relaxant responses to EDRF released by acetylcholine in endothelium-intact rat aortic rings, the nitergic transmitter in rat anococcygeus muscles, and NO in aqueous solution in both tissues (aortic rings were denuded of endothelium). 2. The concentrations of oxyhaemoglobin producing 50% reduction of responses to EDRF and NO in rat aorta correspond closely, the IC50 values being 0.13 +/- 0.02 microM and 0.11 +/- 0.02 microM respectively. 3. Oxyhaemoglobin was equally effective in inhibiting responses to NO in anococcygeus muscles and in aortic rings with an IC50 of 0.14 +/- 0.05 microM. However, responses to the nitrergic transmitter were considerably less sensitive to inhibition by oxyhaemoglobin, the IC50 being 19.7 +/- 5.1 microM. 4. The IC50 values for hydroxocobalamin in inhibiting responses to EDRF and NO in aorta were 3.4 +/- 0.2 microM and 8.4 +/- 0.63 microM, respectively, but it was less effective against responses to NO in anococcygeus muscles the IC50 being 46 +/- 9.6 microM. However, even in the highest concentration used (100 microM), it did not reduce responses to the nitrergic transmitter. 5. The findings are compatible with the views that EDRF is NO, but suggest that the nitergic transmitter in the rat anococcygeus muscle does not behave like free NO.

Acetylcholine↗
PubMed1996

Inhibition of NO-medicate responses by 7-ethoxyresorufin, a substrate and competitive inhibitor of cytochrome P450.

1. The effects of 7-ethoxyresorufin (7-ER), which is a substrate for and competitive inhibitor of cytochrome P450, were studied on responses to nitric oxide (NO), the NO donors sodium nitroprusside (SNP) and glyceryl trinitrate (GTN), acetylcholine-induced endothelium-dependent relaxations of rat and rabbit aortic rings and nitrergic nerve stimulation-induced relaxations of rat anococcygeus muscles. 2. In rat and rabbit aortic rings, 7-ER (2 microM) inhibited the relaxations to acetylcholine in endothelium-intact preparations and the relaxant action of NO in endothelium-denuded preparations. Relaxant responses to SNP and GTN were inhibited by 7-ER in the rat but not rabbit aortic rings. However, the relaxant actions of papaverine and 8-bromo-cyclic GMP were not affected by 7-ER. 3. In rat anococcygeus muscles, 7ER (2 microM) inhibited the relaxant action of NO, but relaxations elicited by nitrergic nerve stimulation were only partly inhibited by a higher concentration of 7-ER (10 microM). 4. After inhibition by 7-ER, superoxide dismutase (100 u ml-1) restored NO-induced relaxations of the rat aortic rings, but not acetylcholine-, SNP or GTN-induced relaxations, and restored NO- and nitrergic nerve stimulation-induced relaxations of anococcygeus muscles. 5. Another cytochrome P450 inhibitor, troleandomycin (10-30 microM), had no effect on NO- or acetylcholine-induced relaxations of rat aortic rings and NO- or nitrergic nerve stimulation-induced relaxations of anococcygeus muscles. However, resorufin, an analogue of 7-ER, inhibited responses to acetylcholine, NO and GTN in rat aortic rings. 6. The results suggest that 7-ER inhibited responses to NO and nitrergic nerve stimulation through generation of superoxide radicals. However, an additional mechanism may be involved in the reduction in acetylcholine-induced response in aortic rings. 7. A 7-ER sensitive P450 system may be involved in the bioactivation of GTN and SNP in rat aortic rings, but not in rabbit aorta or rat anococcygeus muscles.

Acetylcholine↗
PubMed1996

Evidence for two distinct P2-purinoceptors subserving contraction of the rat anococcygeus smooth muscle.

1. The effects of the P2-purinoceptor agonists, adenosine 5'-triphosphate (ATP), alpha, beta-methylene ATP (alpha, beta-MeATP), beta, gamma-methylene ATP (beta, gamma-MeATP), L-beta, gamma-methylene ATP (L-beta, gamma-MeATP), adenosine-5'-O-(2-thiodiphosphate) (ADP beta S), and 2-methylthio ATP (2-MeSATP) were investigated on the isometric tension of the rat anococcygeus muscle. 2. Non-cumulative additions of ATP (100-1500 microM), alpha, beta-MeATP (1-300 microM), beta, gamma-MeATP (10-300 microM), L-beta, gamma-MeATP (3-100 microM) and ADP beta S (1-100 microM) produced concentration-dependent contractions, whereas 2-MeSATP (1-100 microM) had no effect. The rank order of potency was alpha, beta-MeATP > L-beta, gamma-MeATP > or = ADP beta S > beta, gamma-MeATP > > ATP > 2-MeSATP. 3. Contractions to cumulative additions of ATP, alpha, beta-MeATP, beta, gamma-MeATP and L-beta, gamma-MeATP were subject to desensitization whilst those to ADP beta S were unaffected. 4. Contractions to ATP, alpha, beta-MeATP, beta, gamma-MeATP and ADP beta S were abolished by the non-selective P2X/. P2Y-purinoceptor antagonist, suramin (100 microM). In contrast, contractions to ATP, alpha, beta-MeATP and beta, gamma-MeATP were not affected by the non-selective P1-purinoceptor antagonist 8-(p-sulphophenyl)-theophylline (8SPT, 30 microM). Blockade of P2X-purinoceptors with the selective P2X-purinoceptor antagonist pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 10 microM) or desensitization with L-beta, gamma-MeATP (10 microM) abolished contractions to alpha, beta-MeATP, but enhanced those to ADP beta S. The P2Y-purinoceptor antagonist, reactive blue 2 (RB2, 100 microM) enhanced contractions to ATP and alpha, beta-MeATP but abolished those to ADP beta S. 5. Simultaneous addition of alpha, beta-MeATP and ADP beta S produced an additive contraction. 6. The findings suggest that in the rat anococcygeus, smooth muscle cells are endowed with two distinct P2-purinoceptors which subserve contractions: a P2X-purinoceptor activated by ATP and its analogues, and another type of P2-purinoceptor activated by ADP beta S.

Adenosine Diphosphate↗
PubMed1995

Discrimination by the NO-trapping agent, carboxy-PTIO, between NO and the nitrergic transmitter but not between NO and EDRF.

1. The effects of carboxy-PTIO, a scavenger of free radical nitric oxide (NO), were studied on endothelium-dependent relaxations of rat aorta and nitrergic nerve stimulation-induced relaxations of anococcygeus muscle and gastric fundus strips to test the hypothesis that endothelium-derived relaxing factor (EDRF) and the transmitter released by nitrergic nerves is free radical NO. 2. Carboxy-PTIO (10-300 microM) produced concentration-dependent reductions of relaxations elicited by exogenous NO, and relaxations mediated by EDRF released by acetylcholine and ATP in rings of rat aorta. The inhibitory effect of carboxy-PTIO was removed by washing the tissues. 3. In the rat anococcygeus muscle, carboxy-PTIO (10-300 microM) produced concentration-dependent reductions of relaxations to exogenous NO; however, in concentrations up to 2000 microM it did not reduce relaxations elicited by nitrergic nerve stimulation (1-2 Hz), in fact, concentrations of 300 microM or more slightly enhanced them. 4. In rat gastric fundus strips, carboxy-PTIO (100 and 300 microM) reduced relaxations to exogenous NO, but relaxations elicited by stimulation of the nitrergic component of non-adrenergic, non-cholinergic nerves were not affected. 5. These results suggest that EDRF is free radical NO and may be designated EDNO, but the transmitter released from nitrergic nerves does not appear to be identical to EDNO and may not be free radical NO.

Acetylcholine↗
PubMed1994

Pharmacological actions of the coenzymes NAD(H) and NADP(H) on the rat anococcygeus muscle.

1. The pharmacological actions of the oxidized and reduced forms of nicotinamide-adenosine dinucleotide (NAD, NADH) and nicotinamide-adenosine dinucleotide phosphate (NADP, NADPH) were studied on rat isolated anococcygeus muscles. 2. The actions of the two nucleotides were different, but there were no apparent qualitative differences between the oxidized and reduced forms of each. 3. In fully relaxed anococcygeus muscles, NADP(H) produced transient contractions that were subject to desensitization, but NAD(H) had no effect. 4. NADP(H) slightly enhanced contractions elicited by noradrenergic nerve stimulation. In contrast, noradrenergic contractions were inhibited by NAD(H). NADH reduced the stimulation-induced release of noradrenaline, but enhanced contractions elicited by exogenous noradrenaline. 5. In anococcygeus muscles partly contracted with guanethidine, NAD(H) produced a further sustained increase in tone; in contrast, NADP(H) mainly produced transient relaxations to which there was immediate desensitization. 6. Relaxations of anococcygeus muscle elicited by nitrergic nerve stimulation were not affected by NAD. In contrast, NADP(H) reduced them. 7. The actions of NAD(H) were generally the same as those of adenosine and can be attributed to activation of P1-purinoceptors since they were blocked by the selective antagonist 8-sulphophenyltheophylline. 8. The actions of NADP resembled those of the P2-purinoceptor agonist ATP to some extent, but there were some differences. As suggested by others, NADP may act on a unique receptor.

Adenosine↗
PubMed1994

Inhibition by ethacrynic acid of NO-mediated relaxations of the rat anococcygeus muscle.

1. The effects of ethacrynic acid were studied on relaxations elicited by nitric oxide (NO), the NO-donors sodium nitroprusside (SNP) and glyceryl trinitrate (GTN), nitrergic nerve stimulation and the NO-independent agent papaverine in isolated preparations of rat anococcygeus muscles. 2. Ethacrynic acid (100 mumol/L) produced complete relaxation of partially contracted anococcygeus muscles, but the tone recovered after the ethacrynic acid was washed out. Following exposure to ethacrynic acid, the relaxant responses to NO, SNP, GTN and nitrergic nerve stimulation were abolished or markedly reduced; however, the response to papaverine was only slightly reduced. 3. The presence of 3 mmol/L L-cysteine during the period of exposure to ethacrynic acid prevented the inhibition of the relaxing effects of SNP, GTN and nitrergic nerve stimulation almost completely, but did not affect the slight reduction in responses to papaverine. 4. The addition of L-cysteine (3 mmol/L) after incubation with ethacrynic acid did not significantly affect the inhibited responses to SNP and GTN; however, the inhibited responses to nitrergic nerve stimulation were slightly but significantly increased. 5. The results suggest that endogenous sulphydryl groups are required for the actions of NO, NO-donating drugs and the nitrergic transmitter in the rat anococcygeus muscle and possibly for the synthesis or release of the nitrergic transmitter.

Amino Acid Oxidoreductases↗
PubMed1994

Effects of ethanol and other aliphatic alcohols on NO-mediated relaxations in rat anococcygeus muscles and gastric fundus strips.

1. 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. 2. 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. 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 microM) were inhibited by high concentrations of ethanol (200-300 mM) and by propan-2-ol (100 mM). 4. 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. 5. 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. 6. The dehydrogenase inhibitors, 4-methylpyrazole (100 MicroM) and disulfiram (100 MicroM) did not significantly affect the inhibition by ethanol of nitrergic nerve stimulation-induced relaxations in anococcygeus muscles, which suggests that ethanol acts directly.7. The inhibition of NO-mediated relaxations by alcohols is attributed to sequestration of NO to form nitroso-alcohols.

Acetaldehyde↗
PubMed1994

[Pharmacognostical identification and investigation of commercial product of traditional Chinese drug jiuyanduhuo].

Through investigation on original plants and commercial products of the traditional Chinese drug Jiuyanduhuo, the authors have ascertained its botanical origin and present medicinal usage, and found out that Aralia cordata is the main species of Jiuyanduhuo, and A. fargesii is another species that has come into use due to short supply of the main species, and A. henyri is used only in Sichuan and Hubei Provinces. Principal identification features of the original plants and crude drugs with 2 keys have been given, and TLC identification for 3 kinds of Jiuyanduhuo have also been carried out.

China↗