Gender differences in contractile and relaxing responses of aortic rings from lipopolysaccharide-treated rats
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Aortic rings from male and female Sprague-Dawley rats were placed in organ chambers filled with Krebs solution, and the isometric tension was recorded. There were no gender differences in responses to potassium chloride or phenylephrine in either intact or endothelium-denuded rings from control animals. Treatment with 10 mg/kg of lipopolysaccharide (LPS) attenuated the contractile response to potassium chloride in intact, but not in endothelium-denuded rings, and suppressed the phenylephrine contractions in rings both with and without endothelium from male and female rats. Endothelium-dependent and -independent relaxation by acetylcholine and the nitric oxide donor diethylamine/NO, respectively, did not depend on gender and were equally suppressed by LPS treatment. Treatment with LPS accentuated the effects of oxyhemoglobin in rings with and without endothelium and this was significantly larger in rings from females compared to males. Thus, gender differences were present in the effect of LPS on vascular responses. LPS induced a greater increase in basal release of nitric oxide and a greater inhibition of depolarization by potassium chloride, but not receptor-activated contractions, in aortic rings from female versus male rats.Keywords:
Phenylephrine
Abstract A compromised ability to relax has been described as a characteristic of vascular smooth muscle from animal models of hypertension. Since the discovery that many vasodilators act via the release of an endothelium‐derived relaxant factor (EDRF), studies have been designed to assess whether endothelium‐dependent vs. ‐independent relaxations are impaired in the hypertensive state. A decreased maximal relaxation for such endothelium‐dependent vasodilators as acetylcholine, A23187, and histamine exists in both large conduit and resistance vessels from hypertensive animals compared to their normotensive counterparts. Endothelium‐independent vasodilators (i.e., sodium nitroprusside) typically achieve similar maximal percent relaxations in hypertensive vs. normotensive vascular preparations. This defect for endothelium‐dependent vasodilators has been described in vessels from genetic, renal, mineralocorticoid, and coarctation models of hypertension. An altered endothelium‐dependent relaxation could be a corollary of the documented structural changes which occur in hypertension although it remains to be determined if there exists an abnormal coupling between EDRF and its putative receptor in vascular smooth muscle. Several complexities hamper interpretation of altered endothelium‐dependent responses in hypertersion such as regional vascular differences, suitability of reference endothelium‐independent vasodilators, and endothelium‐dependent contractile responses elicited by acetylcholine.
Endothelium-derived relaxing factor
Sodium nitroprusside
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Phenylephrine tested on the isolated endothelium intact rat aortic strips elicited an enhanced response in the second assay when compared with the response obtained in the first trial. Removal of the endothelium and the pretreatment of the strips in the endothelium with methylene blue almost completely prevented the enhanced response to phenylephrine in the second assay. Pretreatment of the strips with lysine acetyl salicylate failed to abolish the potentiated response to phenylephrine in the second test. These data were taken as an evidence that the basal production or release of endothelium-derived relaxing factor(s) but not cyclooxygenase products of arachidonic acid from the endothelium of the rat aorta can influence the contractile effect of phenylephrine and the enhanced response to this α-adrenoceptor agonist in the second assay is probably due to the recuded production or release of these endogenously occurring endothelium-originated substance(s).
Phenylephrine
Endothelium-derived relaxing factor
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Objective To observe the effect of Tongxinlu o on endothelium-depen dent vasodilatation function in patients with CAD. Methods T he patients in exp erimental group (80 cases) were treated with Tongxinluo capsules. Endothelium-de pendent vasodilatation function was detected by ultrasound examination before an d after the treatment. The endothelium-dependent vasodilatation function in two groups was compared. Results After 12-weeks treatment, the e ndothelium-depende nt vasodilatation function increased significantly in experimental group (P 0.01 ). There was no significant difference in control group before and after treatme nt (P0.05). Conclusions Tongxinluo capsule can improve the endothelium-dependent vasodilatation function.
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Objective To measure the endothelium dependent vasodilatation in patients with essential hypertension (EH) and normal subjects (NPs) and to observe the effect of foods rich in high fat or arginine on endothelium dependent vasodilatation. Methods Thirty one patients with EH and 10 NPs were studied.All of them received a single high fat meal, the endothelium dependent vasodilatation was assessed in the brachial artery by high resolution ultrasound technique with Color Doppler Power Imaging at fasting and 4 hours after high fat meal. And then, 14 patients with EH and 10 NPs received foods rich in arginine while another 17 patients with EH received, the ordinary foods. Endothelium dependent vasodilatation was assessed again after 1 week of eating foods rich in arginine or foods as usual.Results After high fat meal, the endothelium dependent vasodilatation in patients with EH and NPs was significantly reduced before eating foods rich in arginine [EH:(12.9±5.7)% vs (3.3±5.2)%, P 0.01; NPs:(16.5± 9.4 )% vs (5.5±5.9)%, P 0.05]; and after 1 week of eating foods rich in arginine, the endothelium dependent vasodilatation after high fat meal of NPs increased, but no significant difference was observed [(5.5±5.9)% vs ( 13.1 ± 4.1)%, P 0.05], However, it was significantly increased in patients with EH [(3.3±5.2)% vs (13.3±5.7)%, P 0.01], Endothelium dependent vasodilatation of patients with EH without having foods rich in arginine after 1 week wasn't significantly different from that after high fat meal [(6.0±5.0)% vs (5.8±4.1)%, P 0.05 ].Conclusion Endothelium dependent vasodilatation after high fat meal in patients with EH and NPs reduces obviously, but it can be corrected by foods rich in arginine.
Brachial artery
Endothelial Dysfunction
Epicardial Fat
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The present study aimed to examine whether there is any change in vascular responsiveness to phenylephrine and KC1 during exercise, and whether the vascular endothelium plays a role in these changes. Adult male rats were subjected to a swimming schedule every day for 5–6 weeks. Studies were performed in vitro on thoracic aortae. Maximum contractile response to phenylephrine of endothelium‐intact thoracic aortic rings (passive tension 1.0 g) obtained from swimming rats (1.2 ±0.2 g, n = 8) was lower than that of sedentary control rats (2.1 ±0.2 g, n = 8). When the endothelium was removed, however, the dose‐response curves of both groups of rats were shifted to the left with an increase in maximum responses and they were no longer significantly different (max. tension, swimming rats: 3.2 ±0.3 g, n = 6, control rats: 3.4 ±0.4 g, n = 5). Indomethacin did not significantly alter the dose‐response curves. A similar effect to that obtained by removal of the endothelium was observed when methylene blue and indomethacin were both added. Passive tension in the range of 2.5‐3.0 g, caused a significant increase in active tension developed to phenylephrine (1 μ m for endothelium‐intact and 0.1 μ m for endothelium‐denuded) of thoracic aortic rings of both swimming and sedentary control rats compared to their corresponding groups when using passive tension of 1.0–1.5 g. The reduction in responses to phenylephrine of endothelium‐intact thoracic aortic rings of swimming rats persisted with the use of a passive tension of 3.0 g. The presence of 300 μ m N G ‐nitro‐L‐arginine (L‐NOARG) caused a significant leftward shift of the curve with an increase in maximum responses when a passive tension of either 1.0 or 3.0 g was applied to the rings. However, for the rings with a passive tension of 1.0 g, L‐NOARG caused a smaller increase in maximal contractile responses to phenylephrine of the rings of sedentary controls than those of swimming rats. There was no difference in the dose‐response curves to depolarizing concentrations of KC1 (20, 40, 80 and 120 mM) of endothelium‐intact thoracic aortic rings from swimming and sedentary control rats. When the endothelium was removed, however, the dose‐response curves of both groups of animals were shifted to the left with an increase in maximum responses. Moreover, the responses to KC1 of endothelium‐denuded thoracic aortic rings of swimming rats were greater than those of sedentary control rats. These results suggest that there were changes in vascular responsiveness to phenylephrine and KC1 during exercise. The fall in sensitivity to phenylephrine with no change in KC1 responses, and the increase in maximum responses to phenylephrine in the presence of L‐NOARG in endothelium‐intact aortae (passive tension 1.0 g) from swimming rats, were due to an increase in spontaneous release and upregulation of phenylephrine‐stimulated release of EDRF/NO, and may not be a consequence of an increase in prostaglandins or a decrease in the production of endothelial constrictors by vascular endothelium. EDRF/NO may play an important role in modulating local vasodilatation.
Phenylephrine
Thoracic aorta
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AIM:To make hyperglycemia models to observe the effects of hyperglycemia on vascular endothelium relaxative function in rats.METHODS:Used vascular function detection,tissue culture and radioactivity analysis.RESULTS:NO - 2 content,NOS activity and vasodilatory response in hyperglycemia group was lower than control group.CONCLUSION:It was possible that hyperglycemia reduced vasodilatory function by inducing a disturbance of endothelium endothelium-derived relaxing factor /NO system.
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To investigate the effect of fluvastatin on the endothelium dependent vasodilatation function in elder hypertensives. Endothelium dependent vasodilatation and non-endothelium dependent vasodilatation function was determined in brachial artery in 51 elderly hypertensives (17 cases each in glade 1–3), 15 normotensives served as control. Endothelium-dependent vascular function (Δ;Dia-P) was determined by the percentage changes in vessel diameter after 5 min compression using Acuson 128X110 sonography. It was found that endothelium dependent vasodilatation function was markedly decreased in three hypertensive group as compared with normotensives (P<0.01), though there was no significant differences among three hypertensive groups.No significant difference of non-endothelium dependent vasodilatation function was noted between hypertensives and normotensives. Endothelium dependent vasodilatation function was markedly ameliorated after an average of 5 months treatment with 20–40 mg daily fluvastatin (9.16 ± 5.32% vs5.93 ± 3.51%). Multiple stepwise regression analysis showed that systolic blood pressure was an only independent factor for brachial endothelium dependent vasodilatation function (R2 =0.359,df=65;P<0.001). It is concluded that hypertension per se is an independent risk factor for the deterioration of vascular endothelial function in elder hypertensives. Endothelium dependent vasodilatation function was markedly ameliorated after fluvastatin treatment in elderly hypertensives.
Brachial artery
Fluvastatin
Endothelial Dysfunction
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Aims Nitroglycerin (or glyceryl trinitrate, GTN) has been long considered an endothelium‐independent vasodilator because GTN vasodilation is intact in the absence of the endothelium and in the presence of endothelial dysfunction. However, in animal and in vitro models, GTN has been shown to stimulate the release of certain endothelium‐derived vasodilators such as nitric oxide (NO) and prostacyclin (PGI 2 ). In addition, chronic GTN therapy leads to endothelial dysfunction. In this series of experiments, we explored how GTN might interact with the vascular endothelium in normal humans, without cardiovascular disease or risk factors associated with abnormalities in vascular function. Methods We examined the effect of inhibition of NO, PGI 2 , and epoxyeicosatrienoic acids (EETs, a class of endothelium‐derived hyperpolarizing factor) on GTN‐mediated vasodilation. We measured arterial blood flow responses to brachial artery infusions of GTN in the absence and presence of L‐NMMA ( n = 13), ketorolac ( n = 14) and fluconazole ( n = 16), which are inhibitors of endothelium‐derived NO, PGI 2 and EETs, respectively, in healthy volunteers. Results Our results demonstrate that inhibition of endothelium‐dependent vasodilator mechanisms does not alter forearm resistance vessel responses to GTN. Conclusion We conclude that GTN‐mediated dilation of forearm resistance vessels is largely independent of vascular endothelium.
Brachial artery
Endothelial Dysfunction
Endothelium-derived hyperpolarizing factor
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Reduced availability of nitric oxide leads to dysfunction of endothelium which plays an important role in the development of cardiovascular diseases.The aim of the present study was to determine whether the dietary supplement L-arginine improves the endothelial function of microvessels by increasing nitric oxide production.We undertook experiments on 51 healthy male volunteers, divided into 4 groups based on their age and physical activity since regular physical activity itself increases endothelium-dependent vasodilation. The skin laser Doppler flux was measured in the microvessels before and after the ingestion of L-arginine (0.9 g). The endothelium-dependent vasodilation was assessed by acetylcholine iontophoresis and the endothelium-independent vasodilation by sodium nitroprusside iontophoresis. In addition, we measured endothelium-dependent and endothelium-independent vasodilation in 81 healthy subjects divided into four age groups.After the ingestion of L-arginine, the endothelium-dependent vasodilation in the young trained subjects increased (paired t-test, p < 0.05), while in the other groups it remained the same. There were no differences in the endothelium-independent vasodilation after ingestion of L-arginine. With aging endothelium-independent vasodilation decreased while endothelium-dependent vasodilation remained mainly unchanged.Obtained results demonstrated that a single dose of L-arginine influences endothelium-dependent vasodilation predominantly in young, trained individuals.
Sodium nitroprusside
Iontophoresis
Endothelial Dysfunction
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Vascular response to exogenously administered nitroglycerine, an index of endothelium-independent vasodilation, has been used as a control test for the assessment of endothelium-dependent vasodilation (endothelial function) in humans. However, evidence has been accumulating that not only endothelium-dependent vasodilation but also endothelium-independent vasodilation per se is impaired in individuals with cardiovascular risk factors and cardiovascular disease. Impaired endothelium-independent vasodilation is associated with structural vascular alterations and alterations in vascular smooth muscle cells. Several methods, including assessment of vascular responses to vasoactive agents using angiography in a coronary artery and vascular responses to vasoactive agents using venous occlusion plethysmography and ultrasonography in a peripheral artery, are used to assess endothelium-independent vasodilation in humans. Measurement of endothelium-independent vasodilation is also useful for assessment of atherosclerosis and may be a predictor of future cardiovascular events. In this review, we focus on assessment of endothelium-independent vasodilation from methodology aspects to clinical perspectives.
Brachial artery
Endothelial Dysfunction
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