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C G Li

Publications and source records attributed to C G Li.

At least 55 records · Page 3Linked to original sources
PubMed1993

Differential effects of hydroxocobalamin on relaxations induced by nitrosothiols in rat aorta and anococcygeus muscle.

In aortic rings, hydroxocobalamin (30 microM) reduced the relaxant actions of S-nitrosocysteine (0.1-3 microM), S-nitrosoglutathione (0.1-3 microM) and S-nitroso-N-acetylpenicillamine (SNAP, 0.01-3 microM), but did not affect the relaxant action of S-nitroso-coenzyme A (0.1-3 microM). In anococcygeus muscles, hydroxocobalamin (30 microM) had little effect on relaxations produced by nitrosocysteine (0.1-3 microM) and SNAP (0.01-1 microM), and enhanced those produced by nitrosoglutathione (0.1-3 microM) and nitroso-coenzyme A (0.1-3 microM). Since hydroxocobalamin is thought to act like haemoglobin by sequestering NO, some of the effects of hydroxocobalamin were compared with those of haemoglobin. Haemoglobin (10 microM) inhibited relaxations of aortic rings produced by nitrosocysteine and nitrosoglutathione and relaxations of anococcygeus muscles produced by nitrosocysteine, nitrosoglutathione and SNAP. Thus the effects of hydroxocobalamin on nitrosothiol-induced relaxations differ between the rat aorta and anococcygeus muscle, and depend on the exact nature of the nitrosothiol; however, the effects of haemoglobin did not differ qualitatively between the two tissues. Since hydroxocobalamin reduced relaxations of rat anococcygeus muscles elicited by NO, but not those elicited by nitrergic nerve stimulation or nitrosothiols, the nitrergic transmitter more closely resembles a nitrosothiol than free NO. Of those tested, the best correspondence was with nitrosocysteine; however, there were some differences between it and the transmitter.

Animals↗
PubMed1993

Effects of hydroxocobalamin and haemoglobin on no-mediated relaxations in the rat anococcygeus muscle.

1. The effects of hydroxocobalamin (Vitamin B12a) on relaxations produced by nitric oxide (NO), some NO-donating compounds and nitrergic nerve stimulation in isolated preparations of the rat anococcygeus muscle were compared with the effects of haemoglobin. 2. Hydroxocobalamin (30 mumol/L) significantly reduced relaxations induced by NO (0.1-3 mumol/L) and sodium nitroprusside (SNP; 0.01-0.3 mumol/L) but did not affect relaxations induced by glyceryl trinitrate (GTN; 0.01-1 mumol/L), S-nitrosocysteine (0.1-0.3 mumol/L) or stimulation of nitrergic nerves. A higher concentration of hydroxocobalamin (100 mumol/L) slightly reduced nitrergic nerve stimulation-induced relaxations. 3. Haemoglobin (10 mumol/L) blocked relaxation induced by NO and reduced relaxations induced by SNP, GTN, S-nitrosocysteine and nitrergic nerve stimulation. 4. When nitrergic nerve stimulation-induced relaxations had been partially reduced by the NO synthase inhibitor L-NAME (5-10 mumol/L), hydroxocobalamin had only a weak and transient inhibitory effect. 5. Noradrenergic contractions induced by field stimulation were not affected by hydroxocobalamin (30 mumol/L), but were enhanced by haemoglobin (10 mumol/L). 6. The results suggest that the transmitter released from nitrergic nerves in anococcygeus muscles resembles NO-releasing compounds such as S-nitrosocysteine and GTN but not SNP or free NO.

Animals↗
PubMed1993

The inhibition of nitric oxide-mediated relaxations in rat aorta and anococcygeus muscle by diphenylene iodonium.

1. The effects of diphenylene iodonium (DPI), an inhibitor of reduced nicotinamide adenine dinucleotide phosphate-dependent oxidases (which generate superoxide anions), were studied on nitric oxide (NO)-mediated responses in isolated preparations of the rat aorta and anococcygeus muscle. 2. In aortic rings, the endothelium-dependent relaxant action of acetylcholine was reduced by DPI (0.3-10 mumol/L) in a concentration-dependent manner and abolished by the NO synthase (NOS) inhibitor L-nitro-NG-arginine methylester (L-NAME; 100 mumol/L). Relaxations induced by sodium nitroprusside (SNP) or NO were not affected by DPI or L-NAME. 3. In anococcygeus muscles, DPI (0.3-10 mumol/L) as well as L-NAME (5-100 mumol/L) produced concentration-dependent reductions of relaxations produced by nitrergic nerve stimulation. Relaxations induced by NO and SNP were not affected by either DPI or L-NAME. L-Arginine (1 mmol/L) prevented the reduction of nitrergic relaxations by L-NAME but not by DPI. 4. Contractions of anococcygeus muscles elicited by exogenous noradrenaline (1 mumol/L) were not affected or were inhibited by DPI (0.3-10 mumol/L), but the contractions elicited by noradrenergic nerve stimulation were significantly enhanced by DPI and L-NAME. When noradrenergic contractions had already been maximally enhanced by L-NAME (100 mumol/L), DPI produced no further enhancement. L-Arginine (1 mmol/L) prevented the enhancement of noradrenergic contractions by L-NAME but not by DPI. 5. The efflux of radioactivity induced by field stimulation from anococcygeus muscles previously incubated with [3H]-noradrenaline was not affected by either DPI or L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

Mediators of nicotine-induced relaxations of the rat gastric fundus.

1. Relaxations of strips of rat gastric fundus were elicited with nicotine (100 mumol/L), nitric oxide (NO; 30 mumol/L), sodium nitroprusside (SNP; 100 nmol/L) and vasoactive intestinal polypeptide (VIP; 1 nmol/L). 2. Methylene blue (30 mumol/L), an inhibitor of soluble guanylate cyclase, reduced relaxations elicited by NO and nicotine, but not those elicited by VIP. 3. Chymotrypsin (1 U/mL) abolished VIP-induced relaxations and reduced nicotine-induced relaxations, but had no effect on SNP-induced relaxations. 4. NG-nitro-L-arginine methyl ester (L-NAME; 100 mumol/L), an inhibitor of NO synthase, reduced relaxations elicited by nicotine, but not those elicited by SNP or VIP. 5. When nicotine-induced relaxations had been reduced by either L-NAME or chymotrypsin, the addition of the other agent produced a greater reduction. However, the relaxations were not abolished. 6. Nicotine-induced relaxations were abolished by tetrodotoxin (1 mumol/L) or hexamethonium (100 mumol/L), indicating that they were due to activation of neuronal nicotinic receptors. Their reduction by methylene blue and L-NAME indicates that an NO-like mediator was involved. Their reduction by chymotrypsin indicates that a VIP-like peptide was involved. However, since they were not abolished by a combination of L-NAME and chymotrypsin, it appears that at least one more as yet unidentified mediator may be involved.

Animals↗
PubMed1993

Differential effects of hydroxocobalamin on NO-mediated relaxations in rat aorta and anococcygeus muscle.

In rat aortic rings, hydroxocobalamin (10-30 microM) produced concentration-dependent reductions of the relaxant action of nitric oxide (NO) and the endothelium-dependent, NO-mediated, relaxant action of acetylcholine. In anococcygeus muscles, hydroxocobalamin (10-30 microM) reduced but also prolonged, NO-induced relaxations, but had no effect on non-adrenergic, non-cholinergic-mediated relaxations. Hydroxocobalamin had no effect on the NO-independent relaxant action of papaverine in either tissue. It is suggested that hydroxocobalamin sequesters NO by forming nitrosocobalamin. Nitrosocobalamin did not relax aortic rings, but produced a slowly developing and prolonged relaxation of anococcygeus muscles.

Acetylcholine↗
PubMed1993

Modulation of acetylcholine-induced contractions of the rat anococcygeus muscle by activation of nitrergic nerves.

1. Acetylcholine-induced contractions of the rat isolated anococcygeus muscle were blocked by atropine (0.1 microM), slightly enhanced by hexamethonium (0.1 mM) and tetrodotoxin (1 microM), but little affected by prazosin (0.1 microM). 2. In the presence of the alpha 2-adrenoceptor agonist, UK14304, which raised the tone of the muscle, acetylcholine had a biphasic effect consisting of an initial relaxation followed by a contraction. 3. Atropine (0.1 microM) enhanced the relaxant component and abolished the contractile component of the response, whereas tetrodotoxin, omega-conotoxin GVIA or hexamethonium abolished or greatly reduced the relaxant component. 4. The nitric oxide synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 100 microM) increased acetylcholine-induced contractions in the absence of UK14304 and markedly reduced the relaxant component to acetylcholine in the presence of UK14304. The effects of L-NAME were annulled by L-arginine (300 microM). 5. The results suggest that acetylcholine acts concurrently on muscarinic receptors of the smooth muscle to cause contraction and nicotinic receptors of nitrergic nerves to cause relaxation. The observed response is the resultant of these two opposing effects and depends also on the prevailing tone.

Acetylcholine↗
PubMed1992

Activation of noradrenergic and nitrergic mechanisms in the rat anococcygeus muscle by nicotine.

1. Nicotine (10 mumol/L) produced rapidly developing but transient contractions of anococcygeus muscle isolated from rats. The magnitude of the response varied considerably between preparations. Tachyphylaxis occurred, such that no response was elicited by the same or a larger concentration in the continued presence of 10 mumol/L nicotine. 2. Contractions produced by nicotine were not affected by atropine, but were abolished by Hexamethonium and the alpha-adrenoceptor antagonists prazosin and phentolamine. Contractions were absent in the anococcygeus muscles of rats pretreated with reserpine. 3. The alpha 2-adrenoceptor agonist UK14304, or guanethidine, raised the tone of the anococcygeus muscle, and converted responses to field stimulation and nicotine to relaxations. Nicotine-induced relaxations were more pronounced in the presence of UK14304 than guanethidine. 4. Relaxations produced by nicotine (1-18 mumol/L) were transient, and tachyphylaxis occurred. When precautions were taken to avoid tachyphylaxis, concentration-response curves could be constructed. The relaxations elicited by nicotine were abolished or greatly reduced by hexamethonium, tetrodotoxin or omega-conotoxin GVIA. 5. The nitric oxide synthase inhibitor L-NG-nitroarginine methyl ester (90 mumol/L) enhanced contractile responses to field stimulation and nicotine, and markedly reduced relaxations elicited by field stimulation and nicotine in the presence of UK14304. These relaxations were restored by L-arginine (270 mumol/L). 6. The results suggest that nicotine acts on nicotinic receptors of noradrenergic and nitrergic nerve terminals in the rat anococcygeus muscle, resulting in the release of noradrenaline and nitric oxide respectively.

Adrenergic alpha-Agonists↗
PubMed1992

Effects of argininosuccinic acid on nitric oxide-mediated relaxations in rat aorta and anococcygeus muscle.

1. Argininosuccinic acid (ASA), a naturally occurring NG derivative of arginine, and the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) were compared for their ability to reduce responses to nitric oxide (NO) derived from endothelial cells (aorta) and nitrergic nerves (anococcygeus muscle). 2. In isolated rings of rat aorta, endothelium-dependent relaxation responses to acetylcholine were abolished by L-NAME (0.1 mmol/L) and were reduced by ASA (0.1 and 0.3 mmol/L). Relaxations induced by sodium nitroprusside (SNP) were not affected by L-NAME but were reduced by ASA. 3. In rat isolated anococcygeus muscles, relaxations elicited by nitrergic nerve stimulation at 1 Hz were abolished by L-NAME (0.1 mmol/L) but were only slightly reduced by ASA (1 mmol/L). The effect of ASA was not sustained. L-Arginine (1 mmol/L) prevented the effect of L-NAME but not that of ASA. Neither ASA or L-NAME inhibited SNP-induced relaxation in the anococcygeus muscle. 4. The results suggest that ASA inhibits NOS but this does not totally account for its effects in reducing NO-mediated relaxations produced by the endothelium-dependent vasodilator acetylcholine in rat aortic rings and stimulation of nitrergic nerves in the rat anococcygeus muscle.

Animals↗
PubMed1991

Evidence that part of the NANC relaxant response of guinea-pig trachea to electrical field stimulation is mediated by nitric oxide.

1. The nitric oxide (NO) synthesis inhibitors NG-monomethyl L-arginine (L-NMMA) and L-nitroarginine methyl ester (L-NAME) reduced relaxations of guinea-pig tracheal smooth muscle elicited by stimulation of intramural non-adrenergic, non-cholinergic (NANC) nerves, but D-NMMA had no effect. L-NAME was 10-30 times more potent than L-NMMA. Relaxations produced by sodium nitroprusside and vasoactive intestinal polypeptide (VIP) were not affected by L-NMMA or L-NAME. 2. The inhibitory effect of L-NMMA on NANC-mediated relaxations was partially reversed by L-arginine but was not affected by D-arginine. 3. VIP antibody and alpha-chymotrypsin abolished or greatly reduced the relaxant action of VIP and reduced relaxations elicited by stimulation of NANC nerves; the residual NANC relaxation was further reduced by L-NAME. 4. The results suggest that NO and VIP are mediators of NANC-induced relaxations of guinea-pig tracheal smooth muscle. We propose the term 'nitrergic' to describe transmission processes which are mediated by NO.

Animals↗
PubMed1990

Nitric oxide and vasoactive intestinal polypeptide mediate non-adrenergic, non-cholinergic inhibitory transmission to smooth muscle of the rat gastric fundus.

The nitric oxide (NO) synthesis inhibitor NG-monomethyl L-arginine (L-NMMA) reduced NANC-mediated relaxations of isolated strips of the rat gastric fundus elicited by low frequencies or short periods of field stimulation, but D-NMMA had no effect. The inhibitory effect of L-NMMA on NANC-mediated relaxations was partially reversed by L-arginine but was not affected by D-arginine. A VIP antibody abolished the relaxant response to VIP and reduced the responses to stimulation. Residual responses to stimulation in the presence of VIP antibody were further reduced by L-NMMA. The tone of the fundus strip was slightly increased by L-NMMA and slightly reduced by L-arginine. The relaxation produced by VIP was slightly reduced by L-NMMA and enhanced by L-arginine. Relaxations produced by peptide histidine isoleucine, sodium nitroprusside or isoprenaline were not affected by L-NMMA or L-arginine. The results suggest that NO as well as VIP is involved in NANC-mediated relaxations of the rat gastric fundus.

Animals↗
PubMed1990

Effects of omega-conotoxin GVIA on autonomic neuroeffector transmission in various tissues.

1. The effects of omega-conotoxin GVIA (conotoxin), a potent inhibitor of neuronal N-type Ca2+ channels, have been examined on responses to stimulation of noradrenergic, cholinergic and non-adrenergic, non-cholinergic (NANC) nerves in a range of isolated tissues to investigate the role of conotoxin-sensitive Ca2+ channels in neurotransmission. 2. Contractions elicited by field stimulation of noradrenergic nerves in rat and mouse anococcygeus muscles, rabbit ear artery and rat vas deferens (epididymal portion) were inhibited by conotoxin. Responses to noradrenaline, and to adenosine triphosphate in the vas deferens, were not affected. 3. Positive chronotropic responses to field stimulation of noradrenergic nerves were inhibited by conotoxin in rat and mouse atria, but responses to noradrenaline and tyramine were not affected. 4. The stimulation-induced release of noradrenaline was inhibited by conotoxin in the rabbit ear artery and in rat and mouse atria. 5. Relaxations in response to stimulation of the noradrenergic perivascular mesenteric nerves were reduced or abolished by conotoxin in rat and rabbit jejunum. The response to noradrenaline in rat jejunum was not affected. 6. Contractions elicited by stimulation of cholinergic nerves were inhibited by conotoxin in rat jejunum and mouse ileum (perivascular mesenteric nerves), and in guinea-pig taenia caeci (field stimulation). Responses to acetylcholine in rat jejunum and mouse ileum were not affected. 7. Contractions elicited by stimulation of the cholinergic plus NANC pelvic nerves were inhibited by conotoxin in rabbit colon, and to a lesser extent in guinea-pig colon. The stimulation-induced contraction of the guinea-pig colon was inhibited by conotoxin by a greater proportion in the presence than in the absence of atropine. Responses to acetylcholine were not affected in the rabbit colon but were slightly reduced in the guinea-pig colon. 8. Relaxations in response to field stimulation of NANC nerves were inhibited by conotoxin in guinea-pig taenia caeci and rat gastric fundus strips, and in rat anococcygeus muscle when the tone was raised by guanethidine but not when it was raised by carbachol. The relaxations produced by sodium nitroprusside in the rat gastric fundus and anococcygeus were not affected. 9. Contractions of the rat bladder elicited by stimulation of the peri-urethral nerves, which are NANC- and cholinergically mediated, were relatively insensitive to inhibition by conotoxin. The response were almost completely abolished by tetrodotoxin. 10. The conotoxin-induced inhibitions of responses to nerve stimulation developed slowly and persisted after removal of conotoxin. The responses were almost completely abolished by tetrodotoxin. 10. The conotoxin-induced inhibitions of responses to nerve stimulation developed slowly and persisted after removal of conotoxin. 11. The inhibitory effect of conotoxin was inversely proportional to the frequency of stimulation (in several preparations) and to the Ca2+ concentration in the bathing solution (in rat vas deferens). These observations suggest that the inhibition by conotoxin of the Ca2+ influx required for excitation-secretion coupling in autonomic nerve terminals is not absolute, and can be overcome by repeated stimulation or by raising the Ca2 + concentration.

Animals↗
PubMed1989

Prejunctional inhibition of non-adrenergic non-cholinergic transmission in the rat anococcygeus muscle.

The muscarinic agonist McN-A-343 did not affect the tone or nitroprusside-induced relaxations of the rat anococcygeus, but inhibited non-adrenergic non-cholinergic (NANC) relaxations. Atropine, pirenzepine and gallamine blocked the McN-A-343 inhibition of NANC relaxations. Agonists of alpha 1-(methoxamine) or alpha 2-adrenoceptors (clonidine, rilmenidine) increased tone and reduced NANC relaxations. Carbachol also increased tone but produced a greater reduction of NANC relaxations. The findings suggest that activation of prejunctional muscarinic receptors on NANC terminals inhibits transmitter release, but there is no evidence for prejunctional alpha-adrenoceptors.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1989

Evidence for a role of nitric oxide in the neurotransmitter system mediating relaxation of the rat anococcygeus muscle.

1. The nitric oxide (NO) synthesis inhibitor NG-monomethyl-L-arginine (L-NMMA), but not D-NMMA, inhibited the NANC-mediated relaxations of the rat anococcygeus muscle, but did not affect the relaxation produced by sodium nitroprusside. 2. The inhibitory effect of L-NMMA was reversed by L-arginine but not by D-arginine, and prior exposure to L-arginine blocked the effect of L-NMMA. 3. The noradrenergically mediated contractions of the anococcygeus elicited by field stimulation were slightly enhanced by L-NMMA, but the response to noradrenaline was not affected. 4. The results suggest that NANC transmission in the rat anococcygeus muscle involves the generation of NO from arginine.

Animals↗
PubMed1989

Rilmenidine differs from clonidine in that it lacks histamine-like activity.

Studies were carried out to determine whether rilmenidine, a recently introduced antihypertensive agent with a similar mechanism of action of clonidine, possesses histamine-like activity on tissues responding to histamine H2-receptor agonists. In guinea-pig isolated atria, both histamine and clonidine caused concentration-dependent positive chronotropic effects which were blocked by the histamine H2-receptor antagonist cimetidine (5 microM); in contrast, rilmenidine produced a concentration-dependent negative chronotropic effect which was not altered by cimetidine. In stilboestrol-treated rat isolated uterus contracted by KCl, histamine and clonidine produces concentration-dependent relaxations which were blocked by cimetidine (5 microM); rilmenidine also produced relaxation, but this was not affected by cimetidine (5 microM). These findings suggest that rilmenidine, unlike clonidine, does not activate histamine H2-receptors in either guinea-pig atria or rat uterus.

Adrenergic alpha-Agonists↗
PubMed1989

[Histopathologic observation on the therapeutic effect of Tripterygium wilfordii in treating experimental allergic encephalomyelitis].

The Tripterygium wilfordii (TW) was used to treat experimental allergic encephalomyelitis (EAE) in guinea-pig. The morphological change was observed by using light microscope. Lymphocytic histochemical staining was performed on the spinal cord from EAE in guinea-pig. The results were: The incidence of inflammatory reaction, neuraxial swelling, break and neuronal necrosis in the treatment group was lower than that in the control group (P less than 0.01-0.005); the variation of incidence of neurofibrillar demyelinating in the treatment group was smaller than that in the control group (P less than 0.025). The result of ANAE and ALP staining for lymphocytes in the spinal cord from EAE was T-cell. It showed TW could inhibit the allergic action and decrease tissular injury.

Animals↗
PubMed1988

Rilmenidine acts as a partial agonist at prejunctional alpha 2-adrenoceptors in guinea-pig atria.

1. The present study was carried out to determine whether rilmenidine, a recently introduced antihypertensive agent which acts on alpha 2-adrenoceptors, has partial agonist activity on prejunctional alpha 2-adrenoceptors in guinea-pig atria. 2. Isolated preparations of guinea-pig atria were incubated with [3H]-noradrenaline and the efflux of radioactivity induced by stimulation of intramural sympathetic nerves was used as an index of release of transmitter noradrenaline. 3. Rilmenidine (1 mumol/l) inhibited noradrenaline release evoked by short trains (five, 20 and 50 pulses) of sympathetic nerve stimulation and this inhibitory effect of rilmenidine was antagonized by the alpha 2-adrenoceptor antagonists, idazoxan (0.1 and 0.3 mumol/l) and rauwolscine (0.3 mumol/l) whereas it was not affected by the alpha 1-adrenoceptor antagonist prazosin (0.1 mumol/l). 4. On the other hand, rilmenidine (1 mumol/l) enhanced noradrenaline release evoked by long trains (150 and 300 pulses) of stimulation and this effect was also abolished by idazoxan (0.1 mumol/l). 5. These findings suggest that the effects of rilmenidine on transmitter release depend on the degree of auto-inhibition: when the concentration of noradrenaline in the biophase of the prejunctional alpha 2-adrenoceptors is low, rilmenidine acts as an agonist, but when the concentration is high it acts as an antagonist. Thus, rilmenidine, like clonidine, is a partial agonist on prejunctional alpha 2-adrenoceptors in guinea-pig atria.

Adrenergic alpha-Agonists↗
PubMed1988

Facilitation of noradrenaline release from sympathetic nerves in rat anococcygeus muscle by activation of prejunctional beta-adrenoceptors and angiotensin receptors.

1. Isolated preparations of rat anococcygeus muscle were incubated with [3H]-noradrenaline and the efflux of radioactivity induced by stimulation of intramural sympathetic nerves was used as a measure of release of transmitter noradrenaline. Isometric contractile responses were also measured. 2. Angiotensin I (0.03 microM) and angiotensin II (0.03 microM) produced non-sustained contractile responses and enhanced the stimulation-induced (S-I) effluxes of radioactivity as well as the contractile responses to electrical stimulation. These effects were blocked by the angiotensin II receptor antagonist saralasin (0.03 microM), and the effect of angiotensin I, but not angiotensin II, was blocked by the angiotensin converting enzyme inhibitor captopril (0.1 microm). 3. The findings indicate that there are both pre- and postjunctional receptors for angiotensin II and that angiotensin I is converted to angiotensin II in the anococcygeus muscle preparation. 4. Isoprenaline (0.1 microM) slightly enhanced the S-I efflux of radioactivity, and produced a greater enhancement after neuronal uptake blockade with desipramine (0.03 microm) and alpha-adrenoceptor blockade with phentolamine (1 microM). 5. The facilitatory effect of isoprenaline on S-I efflux of radioactivity was abolished by propranolol (0.3 microM), but was not affected by low concentrations of saralasin (0.03 microM) or captopril (0.1 microM) which abolished the effect of angiotensin I. The findings suggest that isoprenaline acts directly on prejunctional beta-adrenoceptors to enhance S-I noradrenaline release, rather than indirectly by releasing angiotensin II from within the tissue. Higher concentrations of saralasin (0.1 microM) or captopril (5 microM) did block the facilitatory effect of isoprenaline. The significance of this finding is not clear.

Angiotensin I↗