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Chiu-Yin Kwan

Publications and source records attributed to Chiu-Yin Kwan.

24 records · Page 2Linked to original sources
PubMed2002

Characterization of a novel tetrandrine-induced contraction in rat tail artery.

AIM: In an attempt to pharmacologically characterize the Chinese antihypertensive drug, tetrandrine, we observed in rat-tail arteries, an unusual contraction in tissues that were stimulated with high [KCl] and not those stimulated with phenylephrine. The characteristics of this contraction were studied. METHODS: Segments of perfused ventral rat-tail arteries (RTA) were contracted with a depolarizing concentration (120 mmol/L) of KCl or with phenylephrine (3.0 micromol/L). At peak contraction, they were exposed to tetrandrine (40 micromol/L), which caused marked relaxation in each case. Washing the RTA led to an unusual, slowly-declining contraction, hereafter referred to as tetrandrine-induced contraction (TIC) which was also observed when the tissues were exposed to 80 micromol/L, but not 10 micromol/L or 20 micromol/L of tetrandrine. RESULTS: Pretreatment with phentolamine (non-selective alpha-adrenoceptor antagonist), prazosin (selective alpha1-adrenoceptor antagonist) or 6-hydroxydopamine (for denervation), but not rauwolscine or atropine abolished the TIC. Treatment with ouabain (Na+/K+-ATPase inhibitor) did not sustain the contraction. Changing the depolarizing concentrations of KCl to 80 mmol/L or 100 mmol/L did not alter the TIC, but at 60 mmol/L, it was abolished. CONCLUSION: The data show that tetrandrine induces a K+-dependent contraction of the RTA through a neuronal mechanism involving alpha1-adrenoceptors. It is speculated that this contraction may be a factor in the reported absence of postural hypotension in the clinical use of tetrandrine.

Alkaloids↗
PubMed2002

Tetrandrine and related bis-benzylisoquinoline alkaloids from medicinal herbs: cardiovascular effects and mechanisms of action.

Tetrandrine (TET), a bis-benzylisoquinoline alkaloid purified and identified an active ingredient in a Chinese medicinal herb, radix stephanae tetrandrae, has been used traditionally for the treatment of congestive circulatory disorder and inflammatory diseases. TET, together with a few of its structural analogues, has long been demonstrated to have antihypertensive action in clinical as well as animal studies. Presumably, the primary anti-hypertensive action of TET is due to its vasodilatory properties. TET prevents or inhibits vascular contraction induced by membrane depolarization with KCl or alpha-adrenoceptor activation with phenylephrine (PE). TET (30 micromol/L) also inhibits the release of endothelium-derived nitric oxide (NO) as well as NO production by inducible NO synthase. TET apparently inhibits multiple Ca2+ entry pathways as demonstrated in cell types lacking the L-type Ca2+ channels. In cardiac muscle cells, TET inhibits both L- and T-type Ca2+ channels. In addition to its actions on cardiovascular tissues, TET may also exert its anti-hypertensive action via a Ca2+-dependent manner on other tissues intimately involved in the modulation of blood pressure control, such as adrenal glands. In adrenal glomerulosa cells, KCl- or angiotensin II-induced aldosterone synthesis is highly dependent on extracellular Ca2+. Steroidogenesis and Ca2+-influx in bovine adrenal glomerulosa cells have been shown to be potently inhibited by TET. In bovine adrenal chromaffin cells, TET inhibits Ca2+ currents via L- and N-type channels as well as other unidentified channels with IC50 of 10 micromol/L. Other than the Ca2+ antagonistic effects, TET also interacts with the alpha-adrenergic receptors and muscarinic receptors based on functional as well as radioligand binding studies. Apart from its functional effects, TET and related compounds also exert effects on tissue structures, such as remodelling of hypertrophied heart and inhibition of angiogenesis, probably by causing apoptotic responses. TET is also known for its anti-inflammatory and anti-fibrogenic actions, which make TET and related compound potentially useful in the treatment of lung silicosis, liver cirrhosis, and rheumatoid arthritis.

Adrenal Glands↗
PubMedDate not supplied

Green tea catechins evoke a phasic contraction in rat aorta via H2O2-mediated multiple-signalling pathways.

1. The contractile effects of tea polyphenols (TP) and its four principle catechins, namely (-)-epicatechin (EC), (-)-epicatechin-3-gallate (ECG), (-)-epigallocatechin (EGC) and (-)-epigallocatechin-3-gallate (EGCG), on rat aorta contractility were investigated using the isometric tension recording technique. 2. At concentrations of 5-100 mg/L, TP evoked phasic contraction of rat aorta in a concentration-dependent but endothelium-independent manner. Of the four catechins tested, EGCG and EGC (3-300 micromol/L), but not EC and ECG, mimicked the contractile response to TP, suggesting that the epigallol moiety in the B ring may be associated with the contractile effect. 3. Contractions in response to EGCG and EGC were not affected by several endogenous vasoconstrictor receptor antagonists, but could be abolished by 10 micro mol/L BAPTA-AM, a membrane-permeable Ca2+ chelator, or attenuated by removal of extracellular Ca2+, suggesting the involvement of both intracellular and extracellular Ca2+ in evoking the contraction. 4. Pretreatment with non-selective Ca2+ channel antagonists mefenamic acid (10 micro mol/L), tetrandrine (30 micro mol/L) and SKF 96365 (30 micromol/L), but not nifedipine (1 micromol/L), the selective inhibitor of voltage-dependent Ca2+ channels, inhibited the contractile responses to EGC and EGCG, indicating the involvement of Ca2+ influx via non-voltage dependent Ca2+ channels. 5. Several intracellular Ca2+ channel modulators, including procaine (5 mmol/L), dantrolene (30 micromol/L) and 2-amino ethoxydiphenyl borate (50 micromol/L; an inositol 1,4,5-trisphosphate receptor inhibitor), also inhibited EGCG- and EGC-induced contractions, thus suggesting a role of intracellular Ca2+ release in these contractions. 6. Both EGCG- and EGC-induced contractions were depressed, to different degrees, by inhibitors of several receptor-coupled enzymes, including phospholipase C, protein kinase C, phospholipase A2 and tyrosine kinase. Furthermore, both EGCG- and EGC-induced contractions were completely abolished by catalase, but not by superoxide dismutase or mannitol/dimethyl sulphoxide. 7. Taken together, these data show, for the first time, that TP and its related catechins that contain an epigallol structure in the B ring, as in EGCG and EGC, exert direct contractile effects on rat aortic smooth muscle via a H2O2-mediated pathway.

Animals↗
PubMedDate not supplied

The control of vascular smooth muscle function: my life-long learning and continuous discovery with Professor E.E. Daniel.

This communication is neither a comprehensive review of my research, nor a description about my recent new original scientific findings in smooth muscle or in cell Ca2+. For that intention, I will choose to publish via a regular channel, certainly not in this special edition. My intention is to take this opportunity to recapitulate Dr. Daniel's thoughts and spirits through the progress of my research, teaching, and personal development at McMaster University, stemming largely from Dr. Daniel's life-long interest in the regulation of Ca2+ in the control of smooth muscle function, specifically the vascular smooth muscle. Being a culturally adsorbent person, I am sure that my thoughts and behavior must have been substantially influenced by Dr. Daniel over 27 years of our collaboration. His influence may have molded me into whom and what I am today, both socially and scientifically. Equally, I may also have influenced him in some particular or peculiar way. Dr. Daniel's academic contribution is globally well known for, but not limited to, his insightful and productive research in smooth muscle, but also for his effective application of problem-based learning to education in pharmacology and his influence on students and colleagues.

Animals↗
PubMedDate not supplied

Effects of free radicals on coronary artery.

Coronary arteries supply blood to the heart and hence the control of coronary tone is pivotal to human survival. Reactive oxygen species (ROS) in specified amounts play an important role in normal metabolic and signalling processes. However, excess ROS can cause severe cardiovascular damage. For example, NO is produced by endothelium as a signal for relaxation. However, in an inflammatory response, NO from endothelium or macrophages can combine with superoxide to produce more deleterious peroxynitrite. Excess ROS have been associated with loss of coronary artery pliability--loss of contraction in some instances and relaxation in others. Atherosclerosis may also be considered an inflammatory response that leads to artery blockage, coronary disease and ischaemia-reperfusion. ROS produce various types of damage to ion channels and pumps and this damage is associated with vascular diseases such as atherosclerosis and hypertension. Endothelium and smooth muscle in the coronary artery are also affected differently by individual ROS. In fact, endothelium may act to protect the underlying smooth muscle against ROS. This review will give an overview of this field.

Cardiovascular Diseases↗