The rapid start-up of CANON process through adding partial nitration sludge to ANAMMOX system.

This study aimed to start up the completely autotrophic nitrogen removal over nitrite (CANON) process after adding partial nitration (PN) sludge to the ANAMMOX reactor, so as to help the rapid start-up and stable operation of the CANON process in practical engineering applications. There were three steps in the research: cultivating the PN sludge, building a reliable ANAMMMOX system, and finally starting and running the CANON process. The PN sludge was successfully cultivated in less than 45 days with around 90% nitrite accumulation rate. The ANAMMOX reactor enriched a significant quantity of red granular sludge within 70 days, achieving the maximum nitrogen removal rate of 1.74 kg/(m3·d). Eventually, the CANON reactor was started up successfully, which achieved 95.08% of average ammonium removal efficiency and 84.51% of average total nitrogen removal efficiency in 60 days. The residual recalcitrant nitrite-oxidizing bacteria in the CANON process was successfully inhibited by intermittent aeration and 12 mg/L free ammonia in UASB reactor. Besides, Candidatus Kuenenia, Candidatus Brocadia and Nitrosomonas were the main functional microorganisms involved in the CANON process.

Role of cGMP signals in tetramethylpyrazine induced relaxation of the isolated rat aortic strip.

In the present study, role of guanosine-3',5'-cyclic monophosphate (cGMP) in the vasodilatation of tetramethylpyrazine (TMP), one of the active ingredients of the Chinese herb Chuang-xion, was investigated. We found that the TMP could decrease the vascular tone of isolated rat aorta precontracted with phenylephrine (10(-8) M) in a concentration-dependent manner from 10(-5) M to 10(-3) M. Also, the TMP-induced relaxation was reduced by 1H-(1,2,4)-oxadiazol-(4,3-a)-quinoxalin-1-one (ODQ) or methylene blue, the inhibitor of soluble guanylyl cyclase. Moreover, the vasodilative response to TMP was enhanced significantly in the presence of sildenafil, a well-known inhibitor of phosphodiestrase type 5 that is sensitive to cGMP. In addition, TMP could increase the cGMP level in the isolated aortic rings and TMP-induced vasodilatation was deleted by cGMP-dependent protein kinases (PKG) blockade. These results suggest that relaxation of rat aortic strip by TMP is induced in the cGMP-dependent manner.

Effect of tetramethylpyrazine on potassium channels to lower calcium concentration in cultured aortic smooth muscle cells.

1. Tetramethylpyrazine (TMP) is one of the active principles contained in Ligusticum chuanxiong Hort. (Umbelliferae), a herb that has been used widely in China to treat vascular disorders. 2. In an attempt to elucidate the possible mechanisms of action of TMP, the effect of TMP on intracellular calcium concentrations ([Ca2+]i) was investigated in cultured vascular smooth muscle (A7r5) cells using the Ca(2+)-sensitive dye Fura-2 as an indicator. 3. The increase in [Ca2+]i in A7r5 cells produced by vasopressin (1 micromol/L) or phenylephrine (1 micromol/L) was attenuated by TMP in a concentration-dependent manner. Only inhibitors specific to ATP-sensitive potassium (KATP) channels or small conductance calcium-activated potassium (SKCa) channels attenuated the action of TMP (10 micromol/L) on [Ca2+]i. However, blockers of other K+ channels failed to modify the inhibitory action of TMP (10 micromol/L) on [Ca2+]i. 4. The action of TMP on membrane potential in A7r5 cells was monitored by the fluorescence of bisoxonol. Tetramethylpyrazine caused a concentration-dependent inhibition of changes in membrane potential elicited by KCl (20 mmol/L) or phenylephrine (1 micro mol/L), an effect that was totally reversed by glibenclamide (100 micromol/L) and apamin (100 nmol/L) in combination. 5. The results obtained indicate that the decrease in [Ca2+]i in A7r5 cells produced by TMP is mediated mainly by opening of KATP and/or SKCa channels.

Tetramethylpyrazine as potassium channel opener to lower calcium influx into cultured aortic smooth muscle cells.

In the present study, the effect of tetramethylpyrazine (TMP) on calcium (Ca 2+) influx was investigated in cultured vascular smooth muscle (A7r5) cells using Fura-2 as an indicator. The increase of Ca 2+ concentration in A7r5 cells produced by vasopressin or phenylephrine was attenuated by TMP from 0.01 micromol/L to 1 mmol/L. The decrease in the intracellular potassium concentration in A7r5 cells by TMP from 0.01 micromol/L to 10 micromol/L was characterized using PBFI/AM. Inhibitors specific to the small conductance calcium-activated potassium (SKCa ) channel or the ATP-sensitive potassium (K ATP ) channel abolished the actions of TMP. The obtained results indicate that the decrease of Ca 2+ influx into A7r5 cells by TMP is mainly mediated by the opening of potassium channels.

Inhibitory effects of potassium channel blockers on tetramethylpyrazine-induced relaxation of rat aortic strip in vitro.

Tetramethylpyrazine (TMP) is one of the active principles contained in Ligusticum chuanxiong Hort. (Umbelliferae), a herb that has been widely used to treat vascular disorders in China. In the present study, role of potassium channel in the vasodilatation of TMP was investigated using the effect of potassium channel blocker on TMP induced relaxation in isolated aortic rings from Wistar rats. TMP produced a concentration-dependent relaxation in the aortic rings precontracted with vasopressin or phenylephrine. Similar effect of TMP on vasoconstrictions by phenylephrine and vasopressin, induced through two different receptors, indicating the direct vasodilatation of TMP. Specific inhibitors for potassium channel were used to characterize the role of potassium channel in this action of TMP. Only the inhibitors specific to small conductance calcium-activated potassium (SK(Ca)) channel or ATP-sensitive potassium (K(ATP)) channel inhibited the action of TMP. Also, the TMP-induced relaxation was reversed by the inhibitor of soluble guanylyl cyclase in a way similar to that of K(ATP) channel blockade. The obtained results indicated that vasodilatation induced by TMP is related to the opening of SK(Ca) and K(ATP) channels.