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141.
Tetrandrine and related bis—benzylisoquinoline alkaloids from medicinal herbs:cardiovascular effects and mechanisms of action 总被引:10,自引:1,他引:9
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 α-adrenoceptor activation with phenylephrine (PE).TET(30μmol/L) also inhibits the release of endothelium-derived nitric oxide(NO) as well as NO production by inducible NO synthase.TET apparently inhibits multiple Ca^2 entry pathways as demonstrated in cell types lacking the L-type Ca^2 channels.In cardiac muscle cells,TET inhibits both L-and T-type Ca^2 channels.In addition to its actions on cardiovascular tissues,TET may also exert its anti-hypertensive action via a Ca^2 -dependent manner on other tissues intimately involved in the modulation of blood pressure control,such as adrenal grands.In adrenal glomerulosa cells,KCl-or angiotensin II-induced aldosterone synthesis is highly dependent on extracellular Ca^2 .Steroidogenesis and Ca^2 -influx in bovine adrenal glomerulosa cells have been shown to be potently inhibited by TET.In bovine adrenal chromaffin cells,TET inhibits Ca^2 currents via L-and N-type channels as well as other unidentified channels with IC50 of 10μmol/L.Other than the Ca^2 antagonistic effects.TET also interacts with the α-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. 相似文献
142.
Anti-oxidative properties of beta-blockers and angiotensin-converting enzyme inhibitors in congestive heart failure 总被引:1,自引:0,他引:1
Chin BS Langford NJ Nuttall SL Gibbs CR Blann AD Lip GY 《European journal of heart failure》2003,5(2):171-174
BACKGROUND: Chronic elevation of plasma catecholamines and sympathetic stimulation in chronic heart failure (CHF) leads to increased production of free radicals, and so possibly to endothelial damage/dysfunction and atheroma formation. Abnormal oxidative stress may therefore be related to some of the high mortality and morbidity in CHF. The objective of the present prospective open study was to compare the effects of beta-blockers and ACE inhibitors in relation to oxidative stress and endothelial damage in CHF. METHODS: We studied 66 outpatients with CHF: 46 patients were established on an ACE inhibitor and were then started on a beta-blocker, and 20 patients not previously on ACE-inhibitors were started on lisinopril. Baseline levels of the measured parameters were compared to 22 healthy control subjects. Serum lipid hydroperoxides (LHP) and total antioxidant capacity (TAC) were determined as indices of oxidative damage and antioxidant defence, and plasma von Willebrand factor (vWf) as an index of endothelial damage/dysfunction. RESULTS: Baseline indices for the measures of oxidative damage and endothelial function in the 66 CHF patients were significantly higher than healthy control subjects [median LHP 7.5 (5.9-12.6) vs. 4.8 micromol/l, P=0.0022; TAC 428 (365-567) vs. 336 Trollox Eq. Units, P=0.0005; mean vWf 134+/-27 vs. 89+/-23 IU/dl, P<0.0001]. Following 3 months of maintenance therapy with beta-blockers, there was significant reduction in LHP levels, but not TAC or vWf. ACE inhibitor therapy also significantly reduced vWf levels, but failed to have any statistically significant effects on LHP or TAC. CONCLUSION: This pilot study suggests that oxidative stress in CHF may be due to increased free radical production or inefficient free radical clearance by scavengers. beta-Blockers, but not ACE inhibitors, reduced lipid peroxidation in patients with CHF. No relation was demonstrated between a reduction in oxidative damage and endothelial damage/dysfunction. 相似文献
143.
Spektor M Rodriguez R Rosenbaum RS Wang HZ Melman A Christ GJ 《The Journal of urology》2002,167(6):2628-2635
PURPOSE: Recent evidence indicates that the large conductance, voltage dependent, Ca2+ sensitive K channel or Maxi-K has an important role in the modulation of human corporeal smooth muscle tone and, thus, in erectile capacity. We further clarified the contribution of the Maxi-K channel subtype to the generation of contractile responses in isolated human corporeal tissue strips. MATERIALS AND METHODS: We performed pharmacological studies of phenylephrine contracted isolated corporeal tissue strips in the presence and absence of the 2 Maxi-K channel blockers tetraethylammonium chloride (TEA) and charybdotoxin, and the Maxi-K opener NS1619. K channel treatment effects were evaluated using 2 parameters, including 1) the steady state parameter of the empirically determined peak magnitude of the steady state contractile response and 2) the kinetic parameter of time required to achieve half of the peak steady state contractile response or half-time. Electrophysiological studies in freshly isolated and cultured myocytes were performed in parallel to corroborate findings further at the tissue level. RESULTS: Pre-incubating isolated human corporeal tissue strips with 1 mM. TEA and 1 microM. charybdotoxin was associated with an approximate 20% increase in the peak steady state contractile response and a corresponding approximate 20% decrease in the half-time of the phenylephrine induced contractile response. Conversely, pre-incubation with 10 microM. NS1619 produced a significant, approximately 20% decrease in the peak steady state contractile response and an approximate 38% increase in the half-time of the phenylephrine induced contractile response. Adding 30 to 180 microM. NS1619 to phenylephrine pre-contracted smooth muscle strips resulted in a 30% to 50% reduction in steady state contractile tension. No detectable effect of NS1619 was observed in 120 mM. KCl or 100 mM. TEA pre-contracted corporeal tissue strips. Whole cell recordings of freshly isolated and cultured corporeal myocytes confirmed that 30 microM. NS1619 induced a charybdotoxin sensitive hyperpolarizing current mediated by the Maxi-K channel. CONCLUSIONS: These in vitro studies confirm and extend previous observations indicating the importance of the Maxi-K channel for regulating human corporeal smooth muscle tone, and by extension, erectile capacity and function. 相似文献
144.
145.
In clinical practice of hepatobiliary surgery,various factors, such as shock, inflammation, he patic trauma, the operations of liver and biliarytract (in case of necessities of interrupting hepaticportal), liver transplantation, are mutually relatedto commonly pathophysiological procedures,named hepatic ischemia/reperfusion injury, whichcauses Ca2+ overload of hepatocytes and hepatocel lular apoptosis and necrosis and eventually leads toliver dysfunction ( and even … 相似文献
146.
Xue-ying L 《中国医学科学杂志(英文版)》2005,20(1)
Vasovagal syncope (VVS), a clinical problem with highmorbidity, seriously affects patients' life style, therefore ap-propriate prophylaxis and treatment of VVS are imperative.Though β-blockers, theophylline, and scopolamine have sh-own curative effects on WS, their use are limited due to sideeffects. We hypothesize that irbesartan, an angiotensin Ⅱ rece-ptor antagonist, can be used to treat VVS with no limitationespecially in small dosage. 相似文献
147.
钙通道阻滞剂对缺血再灌注兔脑皮层NO和含水量及细胞内游离钙的影响 总被引:2,自引:0,他引:2
目的 探讨一氧化氮 (NO)在缺血再灌注脑损伤中的作用 ,比较两类钙通道阻滞剂的脑保护作用。方法 采用四血管夹闭法制作兔脑缺血再灌注模型。首先测定假手术及再灌注不同时间兔脑皮层NO及含水量。并将动物分为假手术组、安慰剂组、尼莫地平组、氯胺酮组、尼莫地平 +氯胺酮治疗组 ,于再灌注 30min开始持续静脉给药至再灌注 6h。测定脑皮层NO、含水量、细胞内游离钙([Ca2 + ]i)相对荧光强度。结果 再灌注后脑皮层NO、含水量逐渐升高 ,于再灌注 6h达较高水平 [分别为 (14 7± 1 7) μmol/g ,(86 7± 1 9) % ,P <0 0 5 ],NO与含水量间具有相关性 (P <0 0 1)。尼莫地平、尼莫地平 +氯胺酮组NO明显降低 [分别为 (5 1± 0 9) μmol/g、(5 1± 1 1) μmol/g ,P <0 0 1],尼莫地平、氯胺酮以及尼莫地平 +氯胺酮组含水量明显降低 [分别为 (76 3± 4 0 ) %、(81 0± 1 9) %、(78 2± 1 4 ) % ,P <0 0 1],尼莫地平组较氯胺酮组降低更明显 (P <0 0 1)。安慰剂组 [Ca2 + ]i 较假手术组明显升高 [分别为 (2 6 8± 1 4 )、(5 0± 0 4 ) ,P <0 0 1],尼莫地平、氯胺酮及尼莫地平 +氯胺酮治疗后 [Ca2 + ]i 明显降低 [分别为 (7 7± 1 1)、(13 3± 2 0 )、(9 0± 2 0 ) ,P <0 0 1]。尼莫地平组较氯胺酮 相似文献
148.
Tzivoni D 《Clinical cardiology》2001,24(2):102-106
In recent years, much attention has been given to end organ protection by antihypertensive, anti-heart failure, and anti-ischemic medications. This review describes the available information on end organ protection by calcium-channel blockers (CCBs). In normotensive patients and patients with hypertension treated with long-acting dihydropyridines, medial thickness was thinner than in patients treated with atenolol or in untreated hypertensive patients. Long-term treatment was associated with significant reduction in left ventricular mass. Calcium-channel blockers also improved endothelial-dependent relaxation and reversed the vasoconstrictive response to nitric oxide inhibitors. In diabetic patients, CCBs were effective in preserving kidney function and microalbuminurea. The combination of angiotensin-converting enzyme (ACE) inhibitors and CCBs was more effective than ACE inhibitors alone in preserving kidney function. In animal experiments, CCBs prevented development of coronary atheroschlerosis; however, in humans only limited data are available on their antiatherogenic effect. Some studies suggest that CCBs exert antiplatelets properties and may therefore be beneficial in patients with coronary artery disease. 相似文献
149.
MN-9202对兔血小板聚集、5-HT释放、TXB_2合成及Ca~(2 )转运的影响(英文) 总被引:2,自引:0,他引:2
目的:研究新二氢吡啶类钙拮抗剂MN-9202对兔血小板激活的影响,并探讨其作用机制。方法:以Fu-ra-2 AM为荧光探针,采用时间扫描方式记录血小板内Ca~(2 )的变化;分别用HPLC/ECD和放射免疫测定法检测5-HT及TXB_2。结果:MN-9202剂量依赖地抑制ADP或凝血酶诱导的血小板聚集,抑制TXA_2的释放并且能有效阻滞激活血小板胞内Ca~(2 )水平的增加。MN-9202 1μmol·L~(-1)能抑制胶原15mg·L~(-1)诱导的5-HT释放反应,但对胶原45mg·L~(-1)诱导的反应无抑制作用。结论:MN-9202阻滞血小板Ca~(2 )内流并抑制血小板花生四烯酸代谢及激活反应。 相似文献
150.
AIMS: A recent report has raised concern that nifedipine may be associated with an increased risk of aplastic anaemia. This large population-based study evaluated the risk of idiopathic aplastic anaemia in users of calcium channel blockers compared with that of other antihypertensive drugs. METHODS: The study was based on information derived from the General Practice Research Database. We conducted a follow-up study with a nested case-control analysis of 322 448 subjects who received antihypertensive drugs. Cases were people who had a first-time diagnosis of aplastic anaemia during January 1, 1988 through September 30, 1997. The risk estimate of aplastic anaemia was calculated for all antihypertensive drugs. For the nested case-control analysis, six controls were matched to each case on age, sex and general practice attended. Odds ratios compared the risk of idiopathic aplastic anaemia for all antihypertensive drugs relative to nonusers. RESULTS: There were 13 cases of newly diagnosed idiopathic aplastic anaemia. The estimated risk of aplastic anaemia per 100 000 users was 0.8 (95% CI 0.1, 4.7) for calcium channel blockers, 1.4 (95% CI 0.5, 4.1) for beta-adrenoceptor blockers, 2.3 (95% CI 0.6, 8.6) for angiotension-converting enzyme (ACE) inhibitors and 5.9 (95% CI 1.6, 21.5) for users of other antihypertensive drugs. In the case-control analysis of 13 cases and 77 controls, the odds ratio was 0.3 (95% CI 0.02, 3.3) for calcium channel blockers, 0.5 (95% CI 0.1, 2.5) for beta-adrenoceptor blockers, 0.7 (95% CI 0.1, 5.6) for ACE inhibitors, 1.2 (95% CI 0.1, 11.8) for users of other antihypertensive drugs and 0.7 (95% CI 0.1, 7.2) for users of multiple drugs with a calcium channel blocker compared with nonusers. CONCLUSIONS: The present study suggests that the use of calcium channel blockers is not associated with an increased risk of aplastic anaemia. 相似文献