Search PubMed⌕ Search

Biomedical subjects

S F Liu

Publications and source records attributed to S F Liu.

At least 55 records · Page 3Linked to original sources
PubMed1994

[Relation of effects of matrine on rat vasa deferens to activation of calcium channels].

Effective mechanisms of matrine (Mat) in contraction were observed in isolated rat vasa deferens. Mat caused a strong concentration-dependent contraction of vasa deferens, and this contraction was competitively inhibited by prazosin (Pra, 10 mumol.L-1) and nifedipine (Nif, 50 nmol.L-1), with depression of maximal responses. Their pA2 value was 5.1 and 9.29, respectively. The contraction was also inhibited by verapamil (Ver, 1 mumol.L-1) with depression of maximal responses; but this antagonism was noncompetitive. Its pD2 value was 6.07. Mat promoted CaCl2-induced contraction of vas deferens. The effect of Mat was enhanced in proportion to increase in concentrations of CaCl2. Mat markedly strengthened KCl-induced contraction of vas deferens. The results suggest that one of the mechanisms of the contractive effects of Mat within a certain range of concentrations was related to the activation of the calcium channel.

Alkaloids↗
PubMed1993

Nutrition intervention trials in Linxian, China: multiple vitamin/mineral supplementation, cancer incidence, and disease-specific mortality among adults with esophageal dysplasia.

BACKGROUND: A number of vitamins and minerals have been shown to influence carcinogenesis in experimental animals. In humans, epidemiologic evidence suggests that intake of fruits and vegetables may reduce risk of esophageal and other cancers. Vitamins and minerals in these foods may contribute to the reduced cancer risk. The people of Linxian, China, have persistently low intake of multiple nutrients and exhibit one of the world's highest rates of esophageal/gastric cardia cancer, with an exceptionally high risk of esophageal dysplasia. PURPOSE: To determine whether supplementation with multiple vitamins and minerals may reduce esophageal/gastric cardia cancer among persons with esophageal dysplasia, we conducted a 6-year prospective intervention trial in Linxian. METHODS: Mortality and cancer incidence were ascertained from May 1985 through May 1991 for 3318 persons with cytologic evidence of esophageal dysplasia who were randomly assigned to receive, throughout that period, daily supplementation with 14 vitamins and 12 minerals or placebo. Doses were typically two to three times U.S. Recommended Daily Allowances. Compliance was assessed by counting unused pills monthly for all trial participants and by assaying nutrient levels in blood collected from samples of individuals randomly selected without replacement every 3 months throughout the trial. Cancers were identified through routine surveillance and by special cytology and endoscopy screenings after 2 1/2 years and 6 years. RESULTS: A total of 324 deaths occurred during the 6-year intervention period; 167 occurred in the control (placebo) group and 157 occurred in the supplement group. Cancer was the leading cause of death (54% of all deaths); 18% were due to cerebrovascular diseases and 29% to other causes. Cumulative esophageal/gastric cardia death rates were 8% lower (relative risk [RR] = 0.92; 95% confidence interval [CI] = 0.67-1.28) among individuals receiving supplements rather than placebo, a nonsignificant (P > .10) difference. Risk of total mortality was 7% lower (RR = 0.93; 95% CI = 0.75-1.16; P > .10), total cancer 4% lower (RR = 0.96; 95% CI = 0.71-1.29; P > .10), cerebrovascular disease 38% lower (RR = 0.62; 95% CI = 0.37-1.06; P = .08), and other diseases 12% higher (RR = 1.12; 95% CI = 0.74-1.69; P > .10) among the treated group. Cumulative cancer incidence rates were nearly the same in the two groups. CONCLUSIONS: No substantial short-term beneficial effect on incidence or mortality for this type of cancer occurred following daily supplementation with multiple vitamins and minerals among adults with precancerous lesions of the esophagus. IMPLICATIONS: Although no statistically significant short-term benefits were observed, longer follow-up should be more informative about the effectiveness of this 6-year supplementation on cancer and other diseases among individuals with esophageal dysplasia.

Adult↗
PubMed1993

Cytologic screening for esophageal cancer: results from 12,877 subjects from a high-risk population in China.

Linxian, China, has one of the highest esophageal-cancer mortality rates in the world. In 1983, esophageal balloon-cytology screening was performed to identify subjects eligible for 2 nutrition-intervention trials in Linxian; 12,877 subjects had cytology slides which were satisfactory for diagnosis. Of the 12,649 subjects with squamous-cell diagnoses, 31% were normal by Chinese cytologic criteria; 38% showed hyperplasia; 21% showed dysplasia 1; 6% showed dysplasia 2; 2% showed near-cancer; and 2% showed cancer. Of the 1,471 subjects with columnar-cell diagnoses, 31% were normal; 44% showed hyperplasia; 16% showed dysplasia 1; 4% showed dysplasia 2; 2% showed near-cancer; and 3% showed cancer. Squamous dysplasia and cancer were more common among females than males, while columnar dysplasia and cancer showed male predominance. The prevalence of dysplasia and cancer of both cell types increased with age. The prevalence of squamous dysplasia was significantly higher than in earlier balloon-cytology screenings in Linxian, probably reflecting changes in cytologic classification.

Adult↗
PubMed1993

The prognostic significance of positive CMV cultures during surveillance of renal transplant recipients.

Renal transplant recipients are at risk of severe morbidity and mortality from CMV disease. We have undertaken routine surveillance for CMV shedding on 133 transplant recipients, using a rapid culture technique, in order to assess the incidence of CMV infection and disease in these patients and to assess the prognostic significance of detection in whole blood, throat swab specimens, or urine. Donor CMV seropositivity was associated with posttransplant CMV infection (P < 0.05) and disease (P = 0.06). CMV infection and disease were associated with the receipt of anti-T-cell antibodies (P < 0.0001 and P = 0.08, respectively). First shedding of virus from any site occurred earlier posttransplant in those recipients who developed disease (median 39 days) than in those who did not (median 55 days)(P < 0.05). Detection of virus in blood occurred at a median time of 16 days before onset of symptoms, compared with 9 days before symptoms in urine, and 3 days after onset of symptoms from throat swab. A positive blood culture represented a relative risk of 7.1 for the subsequent development of disease, compared with 2.1 and 1.8 for positive urine and saliva cultures, respectively. The addition of urine cultures to blood cultures increased the sensitivity for identification of those at risk--however, the relative risk was reduced to 5.8. We conclude that routine surveillance for CMV shedding, especially in blood and urine, can identify recipients at high risk of CMV disease, and propose a trial in which those with asymptomatic viremia are allocated to receive ganciclovir or placebo, in order to assess the efficacy of "preemptive" therapy in this group of patients.

Antilymphocyte Serum↗
PubMed1992

Cloning and expression of the Klebsiella pneumoniae galactose operon.

The entire galactose (gal) operon of Klebsiella pneumoniae was isolated and functionally analyzed in Escherichia coli. The genes encoding galactokinase (galK), galactose-1-phosphate uridyltransferase (galT), and UDP-galactose-4-epimerase (galE) were mapped by complementation analysis. The gene order E-T-K was found to be identical to that of Salmonella spp. and E. coli. Analysis of the nucleotide sequence in the control region revealed significant homology with that of E. coli. Two major sites for transcriptional initiation, both mapped to a cytosyl residue, were identified by primer extension. When the operon is expressed in E. coli, the K. pneumoniae gal gene products make up about 30% of the total cellular proteins. The presence of a powerful promoter responsible for high level synthesis of the gal proteins was also demonstrated using beta-galactosidase as reporter.

Amino Acid Sequence↗
PubMed1992

Developmental changes in endothelium-dependent pulmonary vasodilatation in pigs.

1. We compared in vitro endothelium-dependent vasorelaxant responses to acetylcholine (ACh) and the endothelium-independent vasodilator response to sodium nitroprusside (SNP) in prostaglandin F2 alpha (PGF2 alpha)-precontracted muscular pulmonary arteries (PA) from pigs aged 5 min to 2 h (neonatal), 3-10 days, 3-8 weeks and adults. 2. In the pulmonary artery (PA) rings from neonatal animals, the vasodilator response to ACh was negligible. However, responses to ACh were present in all PA rings from older animals, being greatest at 3-10 days and then decreasing with age (P less than 0.001, ANOVA). ACh (30 microM) induced a 1 +/- 1%, 92 +/- 9%, 62 +/- 5% and 51 +/- 6% reduction of the PGF2 alpha-generated tension in neonatal, 3-10 days, 3-8 weeks and adult groups, respectively. 3. The relaxant response to SNP was present in the PA rings from all age groups and increased with age (P less than 0.001, ANOVA). SNP (1 microM)-induced relaxation was 55 +/- 9%, 73 +/- 7%, 97 +/- 5% and 93 +/- 6% in neonatal, 3-10 days, 3-8 week and adult groups, respectively. 4. Removal of the vascular endothelium abolished the relaxant response to ACh but had no effect on the response to SNP in any groups. 5. NG-monomethyl-L-arginine (30 microM), a nitric oxide synthesis inhibitor, inhibited the response to ACh but not to SNP. The lipoxygenase inhibitor, nordihydroguaiaretic acid, had no significant effect on responses to ACh or SNP in any group.6. These findings suggest that the nitric oxide pathway may not play a part in dilating the pig pulmonary arteries at birth, but may be important during the transitional period of establishing a stable post-natal pulmonary circulation. The increase in response to SNP with age parallels the increase in smooth muscle cell myofilaments to which it may be related.

Acetylcholine↗
PubMed1992

Role of nitric oxide and guanosine 3',5'-cyclic monophosphate in mediating nonadrenergic, noncholinergic relaxation in guinea-pig pulmonary arteries.

1. Nonadrenergic, noncholinergic (NANC) nerves mediate vasodilatation in guinea-pig pulmonary artery (PA) by both endothelium-dependent and endothelium-independent mechanisms. The transmitter(s) involved in the endothelium-independent pathway have not yet been identified. We have therefore investigated the possibility that nitric oxide (NO) and guanosine 3',5'-cyclic monophosphate (cyclic GMP) may mediate this neural vasodilator response in guinea-pig branch PA rings denuded of endothelium. 2. Electric field stimulation (EFS, 50 V, 0.2 ms) induced a frequency-dependent (1-24 Hz), tetrodotoxin-sensitive relaxation of the U44069-precontracted PA rings in the presence of adrenergic and cholinergic blockade. 3. The NO synthase inhibitors NG-monomethyl L-arginine (L-NMMA, 100 microM) and NG-nitro L-arginine methyl ester (L-NAME, 30 microM), and the guanylyl cyclase inhibitor methylene blue (5 microM) inhibited the EFS (16 Hz)-induced relaxation by 53 +/- 5, 74 +/- 9 and 82 +/- 9% respectively (n = 5-7, P < 0.01, compared with control rings). 4. Excess concentrations of L-, but not D-arginine (300 microM) completely reversed the inhibitory effect of L-NMMA. 5. The EFS-elicited relaxation (4 Hz) was potentiated by 1 microM zaprinast, a type V phosphodiesterase inhibitor which inhibits guanosine 3':5'-cyclic monophosphate (cyclic GMP) degradation, but was unaffected by 0.1 microM zardaverine, a type III/IV phosphodiesterase inhibitor which inhibits cyclic AMP degradation. 6. EFS (50 V, 0.2 ms, 16 Hz) induced a 3 fold increase in tissue cyclic GMP content, an action which was inhibited by L-NMMA (100 microM). 7. Pyrogallol (100microM), a superoxide anion generator, also inhibited the EFS-induced relaxation by 53 +/- 9%, and this effect was prevented by superoxide dismutase.8. Chemical sympathetic denervation with 6-hydroxydopamine had no effect on the relaxant response to EFS in the endothelium-denuded PA rings.9. In endothelium-denuded branch PA rings at resting tone, L-NMMA (100 microM) significantly augmented the adrenergic contractile response, an effect which was completely reversed by L-arginine,but not by D-arginine. In the same groups of vessel rings, L-NMMA had no significant effect on the matched contractile response to exogenous noradrenaline.10. These results suggest that NO may be released from intramural nerve endings other than adrenergic nerves (probably NANC nerves), and this leads to vasodilatation via activation of guanylyl cyclase.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1992

Effect of tumor necrosis factor on hypoxic pulmonary vasoconstriction.

The effects of tumor necrosis factor (TNF) on hypoxic pulmonary vasoconstriction (HPV) and endothelium-dependent relaxation were examined in a blood-perfused rat lung preparation. Lungs from TNF-treated rats (0.26 mg/kg iv 12 h before experimentation) had a significantly greater HPV and a reduced vasorelaxant response to the endothelium-dependent vasodilator acetylcholine (ACh) but a similar vasorelaxant response to the endothelium-independent vasodilator nitroprusside compared with lungs from control rats (pretreated with 0.1 ml saline iv). Pentoxifylline (20 mg/kg iv and ip 20 min before administration of TNF) had no detectable effect on either HPV or ACh-induced relaxation but completely negated the augmentation on HPV and the inhibiting action on ACh-induced relaxation caused by TNF. The TNF effect on ACh relaxation was unaffected by pretreatment with L-arginine. These results indicate that TNF induces endothelial dysfunction and enhances HPV, effects that are inhibited by pentoxifylline.

Acetylcholine↗
PubMed1992

Endothelin-3 is a potent pulmonary vasodilator in the rat.

The properties of endothelin-3 (ET-3) were investigated in isolated pulmonary artery rings and isolated blood-perfused lungs of the rat. ET-3 elicited a concentration-dependent relaxation of pulmonary artery rings, and effect inhibited by the nitric oxide synthesis inhibitor L-NG-monomethyl-L-arginine. At 0.1 microM, the response to ET-3 was biphasic, resulting in a sustained contraction. In the isolated lung, ET-3 caused a dose-dependent increase in pulmonary arterial pressure. In lungs ventilated with 3% oxygen, 10 nM ET-3 completely reversed the resultant hypoxic vasoconstriction (HPV) by 100 +/- 8%, an effect unchanged by either indomethacin (1 microM) or glibenclamide (10 microM). L-NG-monomethyl-L-arginine attenuated both the ET-3 dilation in prostaglandin F2 alpha-constricted lungs and the dose-dependent vasodilation of HPV by acetylcholine. ET-3 (10 nM) showed the response time to peak pulmonary arterial pressure generation by hypoxia, the size of the response being unchanged. These results demonstrate that ET-3 has both vasodilator and constrictor actions in the rat lung and that, like acetylcholine, the former is mediated in part via the release of nitric oxide. ET-3 also has the ability to modulate HPV.

Animals↗
PubMed1992

The characteristics and significance of intrathoracic and abdominal pressures during Qigong (Q-G) maneuvering.

In order to investigate the mechanism of raising the blood pressure by the Qigong (Q-G) maneuver, the changes of esophageal and gastric pressures were determined during this maneuver, and the data were compared with those from the L-1 maneuver. Eight subjects performed the Q-G maneuver at +1 Gz; their esophageal pressures (mean +/- S.D.) were -6.7 +/- 2.1 mm Hg in the inspiratory phase and 0.1 +/- 3.7 mm Hg in the expiratory phase; intragastric pressures (mean +/- S.D.) were 69.5 +/- 20.2 mm Hg and 63.4 +/- 22.6 mm Hg, respectively. In 22 centrifuge runs at +4.0 to 7.5 Gz and during Q-G maneuvering, 5 subjects had esophageal pressures of -9.0 +/- 3.3 mm Hg in the inspiratory phase and 1.6 +/- 7.2 mm Hg in the expiratory phase, and gastric pressures of 140.6 +/- 23.2 mm Hg and 138.7 +/- 29.5 mm Hg, respectively. The results showed that during Q-G maneuvering, even with a high-G load, the thoracic pressure remained negative or at low pressures while gastric pressures were remarkably raised. They both fluctuated little during respiration; therefore, a relatively large and constant pressure gradient between abdominal and thoracic pressures was maintained. Here lies the significant characteristic of blood pressure raising by the Q-G maneuver. It might possess theoretical significance for further study and development of anti-G maneuvers.

Adult↗
PubMed1992

Endothelium-dependent nonadrenergic, noncholinergic neural relaxation in guinea pig pulmonary artery.

The presence and the possible mechanism of action of the inhibitory nonadrenergic, noncholinergic nerve system (i-NANC) were investigated in guinea pig pulmonary artery (PA) precontracted with U44069 (a thromboxane analog). In the presence of alpha adrenergic blockage, electrical field stimulation induced a frequency-dependent, tetrodotoxin-sensitive relaxation. This relaxation was reduced by 9.1 +/- 1.9 and 19.4 +/- 2.8% by atropine (1 microM) and combined atropine and propranolol (both 1 microM), indicating that the main component is mediated by i-NANC neural mechanisms. In the branch PA rings, this i-NANC relaxation was unaffected by pretreatment with a cyclooxygenase inhibitor (indomethacin, 10 microM), 5-lipoxygenase inhibitor (A63162, 1 microM) or substance P desensitization, but was inhibited markedly by the P2y-purinoceptor antagonist reactive blue 2 (30 microM) and slightly potentiated by the peptidase alpha-chymotrypsin (2 U/ml). L-NG-monomethyl-arginine(L-NMMA), a nitric oxide synthesis inhibitor, caused a concentration-dependent inhibition of the i-NANC relaxation (53.9 +/- 4.1% at 100 microM), but had no effect on equivalent nitroprusside-induced relaxation. The inhibitory effect of L-NMMA was reversed completely by L-arginine (300 microM), but not by D-arginine (300 microM). Removal of vascular endothelium greatly reduced the i-NANC relaxation in the branch PA rings, but had no effect on i-NANC relaxation in main PA rings. Both in vivo capsaicinization and in vitro desensitization with capsaicin (1 microM) caused a significant reduction of the i-NANC relaxation in main PA, but had no significant effect in the branch PA.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetamides↗
PubMed1991

Endogenous nitric oxide modulates adrenergic neural vasoconstriction in guinea-pig pulmonary artery.

1. Electrical field stimulation (EFS) of guinea-pig isolated pulmonary artery induced a frequency-dependent contraction. This was abolished by tetrodotoxin (1 microM) and prevented by phentolamine and prazosin (both 1 microM), indicating a role for alpha 1-adrenoceptors activated by noradrenaline (NA) released from perivascular adrenergic nerves. 2. L-NG-monomethyl arginine (L-NMMA, 0.3-100 microM) caused a concentration-dependent enhancement of the EFS-induced contraction with a 3.4 +/- 0.5 fold increase at 100 microM n = 6). The augmenting effect of 30 microM L-NMMA on the contraction to EFS was completely reversed by 100-300 microM L-arginine, but not by an identical concentration of D-arginine. 3. The contractile response to exogenous NA was similarly enhanced by 30 microM L-NMMA (2.9 +/- 0.6 fold increase, n = 5). 4. The contractile responses to exogenous phenylephrine and prostaglandin F2 alpha while matched the contraction to EFS (4 Hz) were equally augmented by 30 microM L-NMMA. 5. In vessel rings submaximally contracted with the thromboxane analogue U44069 (2 microM), the selective alpha 2-adrenoceptor agonist UK14304 induced concentration-dependent relaxation, which was abolished by removal of endothelium. NA had little relaxant effect on these precontracted vessel rings unless in the presence of prazosin (1 microM). 6. Indomethacin had no significant effect on the contractile response to EFS or NA, indicating that vasodilator cyclo-oxygenase products such as prostacyclin are not involved in modulating these responses. 7. Our results suggest that endogenous nitric oxide inhibits the contractile response to adrenergic nerve stimulation in the guinea-pig pulmonary artery by a postjunctional mechanism, but release of prostacyclin does not modulate these responses. Basal release of nitric oxide from endothelial cells may account for this inhibition.

Adrenergic alpha-Agonists↗
PubMed1991

Endothelium-derived relaxing factor inhibits hypoxic pulmonary vasoconstriction in rats.

The hypothesis that endothelium-derived relaxing factor (EDRF) modulates hypoxic pulmonary vasoconstriction (HPV) was tested in isolated, blood-perfused rat lungs ventilated with gas mixtures of 21% O2-5% CO2-74% N2 (normoxia) or of 3% O2-5% CO2-92% N2 (hypoxia); 30 microM NG-monomethyl-L-arginine (L-NMMA), an inhibitor of EDRF production, caused a reduction in the endothelium-dependent relaxant response to acetylcholine (ACh) from 62 +/- 7, 88 +/- 4, and 100 +/- 4% to 26 +/- 8, 49 +/- 12, and 75 +/- 7% at ACh concentrations of 1, 10, and 100 microM, respectively (p less than 0.05 at all concentrations), indicating that L-NMMA acts via the inhibition of EDRF production. L-NMMA induced a concentration-related augmentation in HPV of 20 +/- 5, 32 +/- 8, and 34 +/- 8% at concentrations of 30, 300, and 1,000 microM (p less than 0.05, compared with a vehicle control group at all concentrations). The pressor response to a dose of angiotensin II (A-II), which produced the same increase in pulmonary artery pressure as that induced by hypoxia, was also significantly augmented (2 +/- 0.6%), but to a lesser extent. The augmentation of HPV by 30 microM L-NMMA was completely reversed by 1 mM L-arginine (a precursor of EDRF), but not by D-arginine (an isomer of L-arginine). One and 6 mM L-arginine, but not 6 mM D-arginine caused a significant inhibition of HPV by 20 +/- 2 and 47 +/- 12% (p less than 0.05, compared with the vehicle control group) and a small but not significant reduction in A-II-mediated contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Ligustrazine is a vasodilator of human pulmonary and bronchial arteries.

We have investigated the dilator effect of ligustrazine, the semisynthetic principle of a traditional Chinese herbal remedy, on human pulmonary and bronchial arteries in vitro. Ligustrazine caused a concentration-dependent relaxation of human small pulmonary arteries, which was independent of endothelium. Although ligustrazine was equally potent in inducing dilatation of pulmonary and bronchial arteries, it was about 10 times more potent in relaxing small pulmonary arteries (300-500 microns i.d.) compared with lobar pulmonary arteries (7-8 mm i.d.). By contrast, the relaxant responses of small and lobar pulmonary arteries to sodium nitroprusside was not significantly different. Ligustrazine was equally potent in relaxing prostaglandin F2 alpha- or 5-hydroxytryptamine-precontracted pulmonary arteries, suggesting that it is not a prostaglandin F2 alpha or 5-hydroxytryptamine antagonist. Preincubating the vessels with propranolol (1 microM) or indomethacin (10 microM) had no significant effect on the ligustrazine-induced vasodilatation. However, ligustrazine caused concentration-dependent inhibition of calcium-evoked contraction when applied to rat aorta in calcium-free K(+)-depolarizing medium. We conclude that ligustrazine is a dilator of human pulmonary and bronchial arteries, which is endothelium-independent and that ligustrazine preferentially relaxes pulmonary resistance vessels rather than large conduit pulmonary arteries.

Animals↗
PubMed1990

Effect of histamine on human bronchial arteries in vitro.

Histamine caused a concentration-dependent relaxation at lower concentrations (1 pmol/l-1 mumol/l) and contraction at higher concentrations (0.01-1 mmol/l) of isolated precontracted human bronchial arteries. In the vessels at resting tension only concentration-dependent contraction was evoked by histamine (0.01-1 mmol/l). Both the contractile and relaxant responses were significantly antagonised by mepyramine (1 mumol/l), with an estimated pKB value of 8.4, but not by cimetidine (100 mumol/l). Our results indicate that histamine induces biphasic effects on human bronchial arteries via H1-receptors.

Adult↗
PubMed1990

Inhibitory role of endothelium-derived relaxing factor in rat and human pulmonary arteries.

1. The inhibitory role of endothelium-derived relaxing factor was studied in both rat and human pulmonary arteries in vitro by inhibiting its synthesis with the L-arginine analogue NG-monomethyl-L-arginine (L-NMMA). 2. In rat pulmonary arteries, L-NMMA pretreatment (10-300 microM) dose-dependently inhibited acetylcholine-induced relaxation (which is endothelium-dependent). NG-monomethyl-D-arginine (D-NMMA, 100 microM) was without effect. L-Arginine, but not D-arginine, dose-dependently reversed this inhibition. L-NMMA had no effect on relaxation induced by sodium nitroprusside. 3. In human small pulmonary arteries L-NMMA (100 microM) pretreatment similarly inhibited the acetylcholine-induced relaxation but had no effect on the sodium nitroprusside-induced relaxation. 4. In both rat and human pulmonary arteries, L-NMMA, but not D-NMMA, always caused contraction of preconstricted tissues whereas it had no effect on baseline tone. In the rat this contraction was completely prevented by prior treatment with L-arginine. 5. L-NMMA (100 microM) pretreatment mimicked the effect of endothelium removal on phenylephrine-induced vasoconstriction, both resulting in an increase in tension development at each concentration of phenylephrine. This enhancement was greatest at low concentrations of phenylephrine but was still present even at the highest concentrations. Pretreatment with L-NMMA (100 microM) also significantly increased the responses to single doses of phenylephrine. 6. These results suggest that endothelium-derived relaxing factor from endothelial cells both mediates the relaxation response to acetylcholine and also acts as a physiological brake against vasoconstriction in pulmonary vessels.

Acetylcholine↗
PubMed1990

[Relationship between the positive inotropic action of matrine and extracellular calcium].

Matrine (Ma) was extracted from the seed and leaves of Sophora alopecuroides L. Ma showed positive inotropic actions in isolated guinea pig left atrium and rat vas deferens under electric stimulation. The positive inotropic actions were markedly inhibited by verapamil (1 mumol/L). Isolated rat vas deferens under the action of Ma showed rhythmic contraction. High K+ (KCl 40 mmol/L) augmented the frequency of rhythmic contraction induced by Ma; conversely, Ma may also augment the increased tension produced by high K+. These results suggest that, the positive inotropic actions of Ma is relevant to its activation of Ca2+ channels.

Alkaloids↗