Littérature scientifique sur le sujet « Hypotensive effect of apelin »
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Articles de revues sur le sujet "Hypotensive effect of apelin"
Lee, Dennis K., Victor R. Saldivia, Tuan Nguyen, Regina Cheng, Susan R. George et Brian F. O’Dowd. « Modification of the Terminal Residue of Apelin-13 Antagonizes Its Hypotensive Action ». Endocrinology 146, no 1 (1 janvier 2005) : 231–36. http://dx.doi.org/10.1210/en.2004-0359.
Texte intégralFernandez, Kleinberg X., Conrad Fischer, Jennie Vu, Mahmoud Gheblawi, Wang Wang, Samantha Gottschalk, Xavier Iturrioz, Catherine Llorens-Cortés, Gavin Y. Oudit et John C. Vederas. « Metabolically stable apelin-analogues, incorporating cyclohexylalanine and homoarginine, as potent apelin receptor activators ». RSC Medicinal Chemistry 12, no 8 (2021) : 1402–13. http://dx.doi.org/10.1039/d1md00120e.
Texte intégralBesserer-Offroy, Élie, Patrick Bérubé, Jérôme Côté, Alexandre Murza, Jean-Michel Longpré, Robert Dumaine, Olivier Lesur et al. « The hypotensive effect of activated apelin receptor is correlated with β-arrestin recruitment ». Pharmacological Research 131 (mai 2018) : 7–16. http://dx.doi.org/10.1016/j.phrs.2018.02.032.
Texte intégralZhang, Rong, Jingyi Lu, Cheng Hu, Congrong Wang, Weihui Yu, Feng Jiang, Shanshan Tang, Yuqian Bao, Kunsan Xiang et Weiping Jia. « Associations of Common Variants atAPLNand Hypertension in Chinese Subjects with and without Diabetes ». Experimental Diabetes Research 2012 (2012) : 1–6. http://dx.doi.org/10.1155/2012/917496.
Texte intégralTrojanowicz, Bogusz, Christof Ulrich et Matthias Girndt. « Uremic Apelin and Leucocytic Angiotensin-Converting Enzyme 2 in CKD Patients ». Toxins 12, no 12 (26 novembre 2020) : 742. http://dx.doi.org/10.3390/toxins12120742.
Texte intégralПальцын, А. А., et Н. Б. Свиридкина. « Apelin ». Nauchno-prakticheskii zhurnal «Patogenez», no 2 (28 juin 2021) : 83–90. http://dx.doi.org/10.25557/2310-0435.2021.02.83-90.
Texte intégralSUZUKI, KEIKO. « Studies on estimation of hypotensive effect by hypotensive drugs. » Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 21, no 1 (1990) : 143–44. http://dx.doi.org/10.3999/jscpt.21.143.
Texte intégralAbdul-Ghani, A. S., R. Amin et M. S. Suleiman. « Hypotensive Effect ofCrataegus oxyacantha ». International Journal of Crude Drug Research 25, no 4 (janvier 1987) : 216–20. http://dx.doi.org/10.3109/13880208709055196.
Texte intégralVillar, A., M. J. Sanz et M. Paya. « Hypotensive Effect ofPistacia lentiscusL ». International Journal of Crude Drug Research 25, no 1 (janvier 1987) : 1–3. http://dx.doi.org/10.3109/13880208709060902.
Texte intégralPRIETO, Juan Carlos, Mónica QUEVEDO, Hugo F. MIRANDA et Gianni PINARDI. « Hypotensive effect of dopamine ». Acta Cardiologica 60, no 3 (1 juin 2005) : 253–57. http://dx.doi.org/10.2143/ac.60.3.2005004.
Texte intégralThèses sur le sujet "Hypotensive effect of apelin"
Alvear-Perez, Rodrigo. « Voies de signalisation activées lors de la stimulation du récepteur de l'apéline, responsables de l'effet hypotenseur de l'apéline ». Electronic Thesis or Diss., Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCB021.
Texte intégralApeline is a vasoactive neuropeptide which plays a crucial role in maintaining water balance and cardiovascular functions. Laboratory studies on the effects of Aperlin-17 (K17F) and the K16P apelin fragment, corresponding to K17F deletion from phenylalanine (Phe) at its C-terminal part have shown the presence of this Phe is necessary for apelin to induce internalization of the Apelin receptor. Also cause a decrease in blood pressure. Subsequently, in the CHO cells expressing stably the murine receptor of the Apelin that the internalization of the Apelin receptor induced by K17F resulted in the activation of a second signaling pathway which is independent of the Gi protein, but dependent on beta-arrestin. This corresponds to the MAP kinase pathway (Mitogen Activator Protein Kinase), which could be involved in the hypotensive effect of the Apelin. My work consisted of characterizing a physiological model such as the rat kidney juxtamedullary afferent arterioles (JMAA), to study if the signaling pathway mediated by beta-arrestin was involved in the vasodilatory effect of K17F. Knowing that AngII induces vasoconstriction by increasing intracellular calcium mobilization ([Ca2+]i), we have showed by measuring variations in arteriolar diameter and [Ca2+]i, that when the Gi signaling pathway is blocked by pertussis toxin (PTX), the vasorelaxant effect induced by K17F is not modify. This data suggests that the vasorelaxing effect of K17F on AngII pre-contracted JMAAs is Gi-independent protein. In the presence of PTX and various internalization inhibitors the vasorelaxant effect induced by K17F on AngII-pre-contracted JMAAs is completely blocked. In addition, no significant decrease in [Ca2+]i mobilization is observed in the presence of PTX and these inhibitors, when K17F is applied to the plateau phase of the AngII-induced calcium response. This is in line with our hypothesis, that the vasorelaxing effect of K17F is Gi-independent protein and beta-arrestin-dependent. ApelineR is a potential therapeutic target for the treatment of heart failure and water retention. Knowing that the half-life of the aperitif in the bloodstream is approximatly one minute. Another aspect of my thesis was to develop metabolically stable K17F analogues by two different strategies. First, we have substituted each of the residues of the aperitif with its D-series enantiomer or a synthetic amino acid. Secondly, we added a fluoroalkyl chain to the N-terminal end of K17F. These two strategies have enabled us to obtain several compounds, the most active of which are P92 and LIT01-196. These retain pharmacological properties identical to those of K17F and have a plasma half-life significantly higher compared to the endogenous peptide. These two analogues have been shown to be active in vivo with the ability to reduce blood pressure and reduce vasopressin secretion in the blood leading to an increase in aqueous diuresis
Tran, Tung Vu. « Ocular Hypotensive Effect of the α2-Adrenergic Agonist, Lofexidine ». Thesis, University of North Texas, 1989. https://digital.library.unt.edu/ark:/67531/metadc501156/.
Texte intégralBonsu, Biggie. « The effect of high intensity interval training on the post-exercise hypotensive response in overweight/obese young women ». Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/85809.
Texte intégralENGLISH ABSTRACT: There are extensive literature on the PEH response after acute and chronic aerobic and resistance exercise, as well as a few studies on concurrent and water exercise. However, there is comparatively little evidence that high intensity interval training (HIIT) elicits similar post exercise blood pressure reductions (PEH) compared to other types of exercise. Furthermore, it is difficult to quantify the magnitude of the hypotensive response following these exercises, due to variations in exercise protocols in terms of intensity and duration. Both these training variables are considered important determinants of the magnitude and duration of the PEH response. The current study determined the magnitude of the PEH response after an acute bout and six sessions of HIIT, and the effects after two weeks of detraining in overweight/obese young women. Twenty young women (aged 21 ± 2 years) volunteered for the study. All the subjects were normotensive (SBP: 119.2 ± 5.6 mmHg and DBP: 78.8 ± 4.1 mmHg). Subjects performed six sessions of HIIT within two weeks and detrained for two weeks. SBP, DBP, MAP and HR were monitored during seated recovery after exercise for 60 min to determine the change from resting values. The overall outcome showed that an acute HIIT session resulted in a reduction of 2.9 mmHg in SBP which approached near clinical significance, while six sessions of HIIT caused a clinically significant reduction of 5.3 mmHg; this response was almost totally reversed after detraining. There were no clinically significant reductions in DBP after the acute or six sessions of HIIT (1.7 and 2.7 mmHg, respectively). However, a clinically significant hypotensive response of 3.9 mmHg was sustained after detraining following the maximal exercise capacity test. MAP also reduced by a magnitude of 2.3 and 5.6 mmHg, respectively, after the acute bout and six sessions of HIIT, and detraining values were still 2.9 mmHg lower than resting values and approached near clinical significance. The results indicate that both an acute bout and six sessions of HIIT elicited a meaningful PEH response. However, the six sessions of HIIT caused a clinically significant reduction which was approximately twice the acute session. Likewise, detraining showed clinically significant effects in DBP and MAP, but SBP returned to near baseline values. This suggests that in only two weeks, the accumulated effects of six sessions of HIIT elicited a greater hypotensive response than after an acute session of HIIT.
AFRIKAANSE OPSOMMING: Daar is omvattende literatuur oor die post-oefening hipotensie (POH) na afloop van akute en kroniese aërobiese en weerstandsoefeninge, asook enkele studies oor gelyktydige krag- en uithouvermoë- en wateroefeninge. Daar is egter relatief min bewyse dat hoë intensiteit interval oefening (HIIO) soortgelyke post-oefening afnames in bloeddruk (POH) in vergelyking met ander tipes oefening veroorsaak. Voorts is dit moeilik om die omvang van die hipotensiewe respons na afloop van oefening te kwantifiseer, hoofsaaklik as gevolg van die variasies in oefeningprotokolle in terme van intensiteit en tydsduur. Beide hierdie inoefeningveranderlikes word as belangrike determinante van die omvang en die tydsduur van die POH respons beskou. Die huidige studie het die omvang van die POH respons na ʼn akute sessie en ses sessies HIIO, en die gevolge na afloop van twee weke se nie-inoefening (“detraining”) by oorgewig/vetsugtige jong dames, bepaal. Twintig jong dames (ouderdom 21 ± 2 jaar) het vrywillig ingestem om aan die studie deel te neem. Al die deelnemers was normotensief (SBD: 119.2 ± 5.6 mmHg en DBD: 78.8 ± 4.1 mmHg). Die deelnemers het ses sessies HIIO binne twee weke voltooi en het daarna vir twee weke geen inoefeningsessies gehad nie. SBD, DBD, GAD en HS is tydens ʼn sittende herstelfase vir 60 minute gemonitor om die verandering vanaf rustende waardes te bepaal. Die algehele uitkoms toon dat ʼn akute HIIO sessie ʼn afname van 2.9 mmHg in SBD tot gevolg gehad het wat aan kliniese betekenisvolheid grens, terwyl ses sessies van HIIO ʼn klinies betekenisvolle afname van 5.3 mmHg veroorsaak het; hierdie respons wat bykans volledige omgekeerd na die twee weke met geen inoefening. DBD het geen kliniese betekenisvolle afname na afloop van die akute of ses sessies van HIIO getoon nie (1.7 en 2.7 mmHg, respektiewelik). ʼn Klinies betekenisvolle hipotensiewe respons van 3.9 mmHg is egter gevind na die geen inoefeningsperiodes. GAD het ook met ʼn omvang van 2.3 en 5.6 mmHg, respektiewelik, verminder na afloop van die akute sessie en ses sessies van HIIO. Die geen inoefening waardes was steeds 2.9 mmHg laer as die rustende waardes en het aan kliniese betekenisvolheid gegrens. Die resultate toon dat beide ʼn akute sessie en ses sessies van HIIO ʼn betekenisvolle POH respons ontlok het. Ses sessies van HIIO het egter ʼn klinies betekenisvolle afname, wat ongeveer twee keer soveel as die afname van die akute sessie was, veroorsaak. In dieselde lig het ʼn twee weke geen inoefeningsperiode steeds klinies betekenisvolle veranderinge in DBD en GAD getoon, maar SBD het tot naby aan die basislyn waardes teruggekeer. Hierdie resultate suggereer dat in slegs twee weke die geakkumuleerde effekte van ses sessies van HIIO ʼn groter hipotensiewe respons as na ʼn akute sessie van HIIO ontlok het.
Chandrasekaran, Badrinathan. « The effect of cardiac resynchronisation therapy on left ventricular remodelling, plasma apelin and cytokine levels in patients with heart failure with systolic dysfunction ». Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/10726.
Texte intégralBernardes, Milton Junio Cândido. « Efeito hipotensor de Aspidosperma subincanum Mart. em ratos e o seu mecanismo de vasodilatação em artérias isoladas ». Universidade Federal de Goiás, 2012. http://repositorio.bc.ufg.br/tede/handle/tede/7219.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Aspidosperma subincanum Mart. is a medicinal herb that is known to be useful for the treatment of cardiovascular-related illnesses. However, its effects and pharmacological mechanisms of action have not been studied. The aim of the present study was to determine the effect of an ethanol extract of Aspidosperma subincanum Mart. (EEAS) on blood pressure (in vivo) and vascular tension (in vitro) in the rat thoracic aorta. Catheters were inserted into the right femoral vein and artery of anesthetized rats for EEAS infusion and the measurement of blood pressure, heart rate and aortic blood flow (flow probes were placed around the aorta). Moreover, the vasodilator effect of EEAS in isolated pre-contracted rat aortas was examined. Intravenous infusion of EEAS resulted in significant and dose-dependent hypotension, bradycardia and increased aortic blood flow. In isolated arteries, EEAS (0-27μg/mL) induced a concentration-dependent relaxation of pre-contracted aortic rings; endothelial denudation potentiated this effect. Pre-treatment of the aortic rings with ODQ, an inhibitor of soluble guanylyl cyclase (sGC); MDL-12,330A, an inhibitor of adenylyl cyclase (AC); or CPA, a SERCA inhibitor, reduced EEAS-induced vasorelaxation. Treatment with an EEAS impaired contractions induced by phenylephrine (an adrenergic agonist) and Bay K 8644 (an L-type Ca(2+) channel activator). The blockade of K(+) channels with tetraethylammonium, clotrimazole, glibenclamide or 4-aminopyridine reduced the relaxation stimulated by EEAS. These findings suggest that EEAS induces hypotension associated with bradycardia. EEAS induces endothelium-independent vascular relaxation. The sGC/cGMP and AC/cAMP pathways, SERCA activation and Ca(2+) and K(+) flux across the sarcolemma, are likely involved in this relaxation.
O Aspidosperma subincanum Mart. é uma planta medicinal que é conhecida por ser utilizada para o tratamento de doenças relacionadas com o sistema cardiovascular. No entanto, seus efeitos e mecanismos de ação farmacológicos não estão muito bem elucidados. O objetivo do presente estudo foi determinar o efeito do Extrato Etanólico do Aspidosperma Subincanum Mart. (EEAS) sobre a pressão arterial (in vivo) em ratos anestesiados e da pressão arterial (in vitro) em artéria aorta torácicas de ratos. Para a realização do protocolos experimentais foram inseridos cateteres na veia e artéria femural direita de ratos anestesiados para que pudesse ser realizada a infusão do EEAS e a verificação da pressão arterial, frequência cardíaca e fluxo sanguíneo aórtico; foram inseridas sondas de fluxo e posicionadas em torno da aorta. Além da pressão foi verificado o efeito vasodilatador do EEAS em anéis de aortas isoladas de ratos pré-contraídas com vasoconstritor. A infusão intravenosa do EEAS resultou em significativa hipotensão, bradicardia e aumento do fluxo aórtico dose-dependente. Em artérias isoladas, o EEAS (0-27μg/mL) induziu relaxamento concentração-dependente em anéis de aorta pré-contraídas com agonista contrátil; foi potencializado o relaxamento nos anéis de aorta sem endotélio. O pré-tratamento dos anéis isoladas de aorta com ODQ, um inibidor da guanilato clicase solúvel (sGC), MDL – 12,330A um inibidor da adenilato ciclase (AC) e CPA um inibidor da bomba do retículo sarcoplasmático, reduziram o vasorelaxamento induzido pelo EEAS. O EEAS foi capaz de diminuir o efeito ocasionado pelo tratamento com fenilefrina (um agonista adrenérgico) e Bay K 8644 (ativador dos canais de Calcio do tipo L) de forma concentração-dependente. O bloqueio dos canais de K+ com tetraetilamonio, clotrimazol, glibenclamida ou 4-aminopiridina reduziu o relaxamento estimulado pelo EEAS. Estes achados sugerem que o EEAS induz hipotensão associada à bradicardia e o relaxamento independente do endotélio vascular. As vias do cGMP/sGC e cAMP/AC foram ativadas e a SERCA e os canais de K+ possivelmente estão envolvidos neste relaxamento.
Der-Shiang, Tsai, et 蔡德祥. « Hypotensive Effect of Scutellaria baicalensis Georgi (huangqin) on Spontaneously Hypertensive Rats ». Thesis, 2000. http://ndltd.ncl.edu.tw/handle/40653214872639846238.
Texte intégral國防醫學院
生理學研究所
88
Scutellaria baicalensis (huangqin) is one of the widely used Chinese herbs to treat symptoms of hypertension in traditonal Chinese medicine. Though being therapeutically effective in hypertension, the mechanism of its hypotensive function has not been well clarified. Previous reports proposed that huangqin might reduce blood pressure via a direct vasodilator effect. Recently, it was shown to potentiate the interferon-stimulated release of nitric oxide (NO) from macrophages. On the other hand, it is well established that NO activates soluble guanylyl cyclase in cells, producing cGMP which in turn mediates relaxation of vascular smooth muscle. These observations prompted us to examine the hypotensive effect of huangqin and to further investigate the involvement of NO in this hypotensive effect. Spontaneously hypertensive rats (SHR) were subjected to intragastric administration of huangqin (0.7gm/kg/day) for 5 consecutive weeks and the systolic blood pressure was significantly lower than that of age-matched control rats. The aortic ring derived from huangqin-treated SHR showed a decreased contractile response to norepinephrine (NE) and an increased dilator response to acetylcholine (ACh) as compared with that from control rats. However, pretreatment with L-NAME or methylene blue (MB) abolished the difference between the two groups. The aortic samples derived from SHR were pretreated with huangqin followed by measuring the response to NE or ACh so as to determine whether huangqin has direct effect on blood vessels. Pretreatment with huangqin markedly decreased the contractile response to NE and increased the dilator response to ACh. Also, the direct vasodilator effect of huangqin was observed. Pretreatment with wogonin, one of the major components of huangqin, reduced the contractile response to NE and enhanced the dilation response to ACh compared with control group. In contrast, pretreatment with L-NAME, MB and ODQ abolished the difference between wogonin-treated and control groups. The wogonin-induced vasorelaxation was also abated by pretreatment with L-NAME, MB, ODQ or endothelium-denuded. Furthermore, the combined effect of YC-1 (an activator of soluble guanyl cyclase) and wogonin was equal to the sum of the effect of each agent given alone, suggesting that wogonin might be able to selectively activate soluble guanylyl cyclase. In conclusion, treatment with huangqin in vivo significantly reduces the systolic blood pressure in SHR. Huangqin and wogonin induce vasodilation, decrease contractile response to NE and increases dilation response to ACh, all of which are presumably related to the increment of nitric oxide production.
Su, Yu-ting, et 蘇渝庭. « Modulation of central hypotensive effect of resveratrol in fructose-fed rats ». Thesis, 2012. http://ndltd.ncl.edu.tw/handle/77931604424697904965.
Texte intégral國立中山大學
生物醫學研究所
100
Recent studies demonstrated that fructose intake can increase blood pressure in experimental animals. Oxidative stress has emerged as an important pathogenic factor in the development of hypertension. It has been reported that increased superoxide production in fructose-fed rat mediated through nicotinamide adenine dinucleotide phosphate NAD(P)H oxidase. Superoxide dismutase (SOD) is one of the most important enzymes against oxidative stress. However, the signaling mechanisms of fructose which induce hypertension through superoxide remain unclear. Nucleus tractus solitarii (NTS) is the integrative center for baroreflex. Our previous study had revealed that accumulation of superoxide in the NTS can induce hypertension. As an important antioxidant in red wine, resveratrol is likely to contribute to the potential of red wine to prevent cardiovascular disease. At pharmacological doses, resveratrol increases vascular nitric oxide (NO) levels and improves NO bioavailability in animal models. Resveratrol is a potent activator of AMPK in neuronal cell lines, primary neurons, and the brain. Recent reports have indicated that metformin targets AMPK which activates nNOS and eNOS. Therefore, we hypothesized that resveratrol causes blood pressure decrease through regulating nitric oxide and superoxide production in the NTS of fructose-fed rats. There were three specific aims: 1. To investigate whether fructose induce superoxide production and causes hypertension in the NTS. 2. To investigate which signaling pathway is involved in fructose-induced hypertension. 3. To investigate which signaling pathway is involved in resveratrol modulates blood pressure. Male Wistar Kyoto rats (WKY) were divided into two groups: control group and fed with 10% fructose water group for 1 week. After one-week treatment, the systolic blood pressure and superoxide production increased significantly and the nitrate level in the NTS was significantly decreased. Immunoblotting showed that administration of fructose significantly increased NADPH oxidase subunits p22-phox, p67-phox activity, RAGE activity and reduce SOD2 activity in the NTS. Based on our previous studies, male Wistar-Kyoto rats (WKY) were divided into five groups: Group I: Control group; Group II: fructose-fed rats (FFR) fed with 10% fructose for 4 weeks; Group III: Control + resveratrol (R) rats received a gavage of resveratrol; Group IV: FFR+ resveratrol (FR) fed with 10% fructose and resveratrol ; Group V: FFR + 2weeks resveratrol (F2R) fed with 10% fructose and received a gavage of resveratrol 2 weeks. We found that systolic blood pressure measured by tail-cuff method in F group rats and F2R group rats revealed a significantly increased than C group rats continuously through week 0 to week 2 but R group rats and FR group rats were no difference with C group. However, received a gavage of resveratrol (10 mg/kg/d) 2 weeks, F2R group revealed a significantly decrease in SBP than the F group continuously through week 2 to week 4. Fructose-induced hypertension increased NADPH oxidase activity and SOD2 activity related to inhibit the production of NO in the regulation of blood pressure. These results suggest that in the NTS, intake of fructose induces NADPH oxidase activity and reduces SOD2 activity to increase blood pressure. Resveratrol can not only reverse fructose-induced hypertension but also prevent fructose-induced hypertension.
Sarvaiya, Sushil R. « Studies on hypertension with special references to hypotensive effect of ocimum sanctum ». Thesis, 1986. http://hdl.handle.net/2009/5067.
Texte intégralHung, Chih-Peng, et 洪志鵬. « Clinical observation of the immediate hypotensive effect of acupuncture on essential hypertensive patients ». Thesis, 2003. http://ndltd.ncl.edu.tw/handle/01677167001045134828.
Texte intégral中國醫藥學院
中西醫結合研究所
91
The immediate hypotensive effect of acupuncture on essential hypotensive patients Graduate student:Chih-Peng Hung Institute of Integration of Chinese and Western Medicine,China Medical College ABSTRACT Acupuncture has certain accommodation effects on physiological abnormalities. In order to compare the immediate hypotensive effect with hemodynamic change of low frequency 5 Hz electro-acupuncture, acupuncture and bed rest at bilateral Neiguan(P6) and Zu-San-Li(S36) acupoints, 23 essential hypertensive patients are involved in this study. Each patient received these 3 different treatments for about 20mins on three individual days. We collect 4 time sections of BP HR and hemodynamic changes, which include data of pre-treatment, treatment for 10min, treatment for 20min, and post-treatment 10min. All of these data were collected by dynapulse. Our result shows: In the groups we find both electro-acupuncture and acupuncture groups could cause hypotensive effect and heart rate decrease (P<0.05), whereas in the bed rest group no such effects were found. The differences between groups are as following: At first, electro-acupuncture group has more apparent heart rate decrease effect on post-acupuncture 10min than bed rest group (P<0.05). The hypotensive effect of systolic pressure at time course of post-acupuncture 20min and 10 min after removing acupuncture needles in both electro-acupuncture and acupuncture groups are more explicit than the bed rest group (P<0.05). Secondly, in the analysis of hemodynamic change, acupuncture group significant decrease cardiac out and cardiac index after treatment time course; furthermore, electro-acupuncture group is superior in increasing systemic vascular compliance. Lastly, in the post-treatment questionnaire we find both acupuncture and electro-acupuncture group have significant improvement of hypertension associated symptoms (F=10.62,P=0.02). As a result, no significant differences between acupuncture and electro-acupuncture groups were found from the evaluation of heart rate, BP change, post-treatment and the survey result﹒ Keywords:essential hypertension, electro-acupuncture, Neiguan(P6), Zu-San-Li(S36), dynapulse, heart rate, blood pressure, hemodynamic change
Roddy, Gabrielle. « The hypotensive effect of exercise on IOP : an interaction of physical fitness and parasympathetic efficacy ». Thèse, 2015. http://hdl.handle.net/1866/13504.
Texte intégralAfter over 100 papers on post exercise reductions in IOP it is known that under a vast number of exercise protocols, of differing intensities and durations, the hypotensive effects of exercise on IOP are attenuated in the physically fit. A proposed mechanism is the parasympathetic nervous system that potentially increases in efficacy with physical training. The general objective of this thesis was to further tease apart those factors that contribute to post exercise reductions in IOP and to elucidate possible mechanisms. Study 1, a meta-analysis, was conducted to quantify the relative contributions of intensity and duration to the effect of exercise on IOP and the degree to which these variables affect sedentary and normally active populations. A pattern of results emerged such that those persons who are Sedentary experience a greater drop in IOP after aerobic exercise than those who are physically fit (ES = -4.198 mm Hg and -2.340 mm Hg, respectively). A lack of pre-exercise control over covariates such as fluid ingestion was also observed. Hyperosmolarity (a side effect of dehydration) is one of the proposed mechanisms driving the hypotensive effect of exercise. Study 2 compared reductions in IOP in both a hypo-hydrated (water restricted) and hyper-hydrated condition before, during and after an ergocycle ride of 90 minutes. After an initial decrease in both conditions, IOP returned to baseline in the Hypo-hydrated condition despite a significant loss of bodyweight and increased in the Hyper-hydrated condition as a result of the hydration protocol. Given the high level of physical fitness among our participants in Study 2, Study 3 was designed to further elucidate the relationship between physical conditioning and IOP. Using correlational analyses we observed the relationship between a test of VO2max and an average of IOP measurements made over the course of eight weeks. A significant relationship existed only for those participants in the upper range of the fitness continuum. Conclusion. The results of the current study suggest that the hypotensive effect of exercise on IOP is likely a homeostatic response to dysregulation of the aqueous humor caused by the initiation of exercise and pre-exercise fluid intake protocols.
Livres sur le sujet "Hypotensive effect of apelin"
1933-, Aoki K., International Symposium on Mechanism and Treatment in Essential Hypertension (1st : 1985 : Nagoya-shi, Japan) et International Symposium on Rats with Spontaneous Hypertension and Related Studies (5th : 1985 : Kyoto, Japan), dir. Essential hypertension : Calcium mechanisms and treatment. Tokyo : Springer-Verlag, 1986.
Trouver le texte intégralJ, Bailey C., dir. Metformin : The gold standard. Chichester, UK : John Wiley & Sons, 2007.
Trouver le texte intégralMoore, R. Leigh Hill. Hypotensive effect of isometric exercise on resting blood pressure in high normotensive subjects. 1986.
Trouver le texte intégralChapitres de livres sur le sujet "Hypotensive effect of apelin"
Prichard, B. N. C., et F. Bompart. « Hypotensive Effect of β-Adrenoceptor Blockers ». Dans New Aspects in Hypertension Adrenoceptors, 166–91. Berlin, Heidelberg : Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71418-4_16.
Texte intégralPodos, S. M., et C. B. Camras. « The Ocular Hypotensive Effect of Topically Applied Prostaglandins in Primates ». Dans Glaucoma Update IV, 198–205. Berlin, Heidelberg : Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76084-6_30.
Texte intégralBönner, Gerd, et Ulrike Schunk. « Hypotensive Effect of Bradykinin in Normotensives and Patients with Renovascular Hypertension ». Dans Kinins IV, 321–27. Boston, MA : Springer US, 1986. http://dx.doi.org/10.1007/978-1-4757-0154-8_40.
Texte intégralHärtl, A., E. Kirchner et H. Hoffmann. « Characterization of the Hypotensive Side Effect of Macrolide Antibiotics in Animals ». Dans Archives of Toxicology, 140–43. Berlin, Heidelberg : Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-74936-0_28.
Texte intégralBatlle, Daniel C., Wu-Chang Yang, Alisa Von Riotte et Salim K. Mujais. « Dissociation between the Hypotensive Effect of Thiazides and Plasma Divalent Cations ». Dans Phosphate and Mineral Homeostasis, 433–41. Boston, MA : Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5206-8_54.
Texte intégralSen, Abirlal, et Geeta Baruah. « Effect of HYPERTENSION on ECG Parameters ». Dans Cardiorespiratory Fitness - New Topics [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.104613.
Texte intégral« The effect of hypotensive agents on regional cerebral blood flow and intracranial pressure in baboons with space occupying lesions ». Dans Timing of Aneurysm Surgery, 385–90. De Gruyter, 1985. http://dx.doi.org/10.1515/9783110858853-051.
Texte intégralColreavy, Frances. « Hypotension ». Dans Oxford Textbook of Advanced Critical Care Echocardiography, sous la direction de Anthony McLean, Stephen Huang et Andrew Hilton, 265–74. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198749288.003.0018.
Texte intégralCarolina Cardoso-Teixeira, Ana, Klausen Oliveira-Abreu, Levy Gabriel de Freitas Brito, Andrelina Noronha Coelho-de-Souza et José Henrique Leal-Cardoso. « Effects of Terpenes and Terpenoids of Natural Occurrence in Essential Oils on Vascular Smooth Muscle and on Systemic Blood Pressure : Pharmacological Studies and Perspective of Therapeutic Use ». Dans Terpenes and Terpenoids [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.94194.
Texte intégralSood-Mendiratta, Shalini. « Medical Management for Glaucoma ». Dans Glaucoma. Oxford University Press, 2012. http://dx.doi.org/10.1093/oso/9780199757084.003.0015.
Texte intégralActes de conférences sur le sujet "Hypotensive effect of apelin"
Kechyn, Svyatoslav, Gareth Barnes, Akaphot Thongmee et Luke Sebastian Howard. « Effect of apelin on cardiopulmonary performance during endurance exercise ». Dans Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2241.
Texte intégralÖzkan, Naziye. « The Effect of Apelin on Podocytes in Doxorubicin Induced Nephrotic Syndrome ». Dans 15th International Congress of Histochemistry and Cytochemistry. Istanbul : LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-230.
Texte intégralTristantini, Dewi, et Kelly Amelinda. « Hypotensive effect of aqueous extract of jamu antiatherosclerosis in male rats ». Dans 2ND BIOMEDICAL ENGINEERING’S RECENT PROGRESS IN BIOMATERIALS, DRUGS DEVELOPMENT, AND MEDICAL DEVICES : Proceedings of the International Symposium of Biomedical Engineering (ISBE) 2017. Author(s), 2018. http://dx.doi.org/10.1063/1.5023959.
Texte intégralBaum, Olga I., Emil N. Sobol, Andrei V. Bolshunov, Olga Khomchik et George I. Zheltov. « Laser-induced hypotensive effect in treatment of the resistant open-angle glaucoma ». Dans Optical Interactions with Tissue and Cells XXXII, sous la direction de Bennett L. Ibey et Norbert Linz. SPIE, 2021. http://dx.doi.org/10.1117/12.2588455.
Texte intégralYan-qin Yu, Zhi-guo Ye et Qiang Xia. « The Role of Opioid in the Mechanism of the Hypotensive Effect by Simulating Acupuncture on Rat Hindlimb ». Dans 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1615579.
Texte intégralBuczko, W., M. Pietraszek, E. Chabielska et B. Malinowska. « THE INFLUENCE OF SOME HYPOTENSIVE DRUGS ON THE SEROTONERGIC MECHANISMS IN RATS PLATELETS ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643440.
Texte intégralToscano, José Jean de Oliveira, Kettury Maria da Silva Barros, Amaro Wellington da Silva, Naira Sabrina Ferreira da Costa, Vicente de Paulo Silva Moreira, Carlos Alencar Souza Alves Júnior et Diego Augusto dos Santos Silva. « CHANGES IN BLOOD PRESSURE IN BREAST CANCER SURVIVORS UNDER A PHYSICAL EXERCISE PROGRAM ». Dans Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2080.
Texte intégralSaldeen, K., R. Moalli et T. Saldeen. « EFFECT OF A FIBRIN-DERIVED PEPTIDE ON PULMONARY ANGIOTENSIN CONVERTING ENZYME (ACE) ACTIVITY AND ON PRESSURE RESPONSES TO BRADYKININ (BK) ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644331.
Texte intégralRapports d'organisations sur le sujet "Hypotensive effect of apelin"
Schreiber, Martin A. The Effect of Hypotensive Resuscitation and Fluid Type on Mortality, Bleeding, Coagulation and Dysfunctional Inflammation in a Swine Grade V Liver Injury Model. Fort Belvoir, VA : Defense Technical Information Center, janvier 2008. http://dx.doi.org/10.21236/ada490734.
Texte intégralSchreiber, Martin. The Effect of Hypotensive Resuscitation and Fluid Type on Mortality, Bleeding, Coagulation, & ; Dysfunctional Inflammation in a Swine Grade V Liver Injury Model. Fort Belvoir, VA : Defense Technical Information Center, janvier 2006. http://dx.doi.org/10.21236/ada446801.
Texte intégralSchreiber, Martin A. The Effect Of Hypotensive Resuscitation And Fluid Type On Mortality, Bleeding,Coagulation And Dysfunctional Inflammation In A Swine Grade V Liver Injury Model. Fort Belvoir, VA : Defense Technical Information Center, janvier 2012. http://dx.doi.org/10.21236/ada559947.
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