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Artykuły w czasopismach na temat "Hypotensive effect of apelin"
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Lee, Dennis K., Victor R. Saldivia, Tuan Nguyen, Regina Cheng, Susan R. George i Brian F. O’Dowd. "Modification of the Terminal Residue of Apelin-13 Antagonizes Its Hypotensive Action". Endocrinology 146, nr 1 (1.01.2005): 231–36. http://dx.doi.org/10.1210/en.2004-0359.
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The apelin peptide is the endogenous ligand for the apelin G protein-coupled receptor. The distribution of the apelin peptides and receptor are widespread in the central nervous system and periphery, with reported roles in the hypothalamic-pituitary-adrenal axis, blood pressure regulation and as one of the most potent positive inotropic substances yet identified. In this report, we show that in native tissues preproapelin exists as a dimer. Dimeric preproapelin was reduced to monomers by dithiothreitol treatment, indicating disulfide linkages. To evaluate the role of the carboxyl-terminal phenylalanine in the hypotensive action of apelin-13, analogs were generated and tested for their role on blood pressure regulation. Injections of apelin-13 and apelin-12 (15 μg/kg) into spontaneously hypertensive rats lowered systolic and diastolic blood pressure to result in decreases of approximately 60% and 15% in mean arterial blood pressure, respectively. Apelin-13(13[d-Phe]) treatment did not differ from apelin-13 in either efficacy or duration of effect, whereas apelin-13(F13A) revealed a loss of function. However, concomitant administration of apelin-13(F13A) (30 μg/kg) blocked hypotensive effects of apelin-13 (15 μg/kg), which revealed that apelin-13(F13A) behaved as an apelin-specific antagonist.
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Fernandez, Kleinberg X., Conrad Fischer, Jennie Vu, Mahmoud Gheblawi, Wang Wang, Samantha Gottschalk, Xavier Iturrioz, Catherine Llorens-Cortés, Gavin Y. Oudit i John C. Vederas. "Metabolically stable apelin-analogues, incorporating cyclohexylalanine and homoarginine, as potent apelin receptor activators". RSC Medicinal Chemistry 12, nr 8 (2021): 1402–13. http://dx.doi.org/10.1039/d1md00120e.
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Besserer-Offroy, Élie, Patrick Bérubé, Jérôme Côté, Alexandre Murza, Jean-Michel Longpré, Robert Dumaine, Olivier Lesur i in. "The hypotensive effect of activated apelin receptor is correlated with β-arrestin recruitment". Pharmacological Research 131 (maj 2018): 7–16. http://dx.doi.org/10.1016/j.phrs.2018.02.032.
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Zhang, Rong, Jingyi Lu, Cheng Hu, Congrong Wang, Weihui Yu, Feng Jiang, Shanshan Tang, Yuqian Bao, Kunsan Xiang i 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.
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Background. Apelin, the endogenous ligand for the APJ receptor, has a potent hypotensive effect via a nitric oxide-dependent mechanism in vivo. The aim of the study was to investigate the association between the common variants of apelin gene (APLN) and hypertension, which was reported recently in a Chinese Han population with and without diabetes.Methods. Three single nucleotide polymorphisms (SNPs) onAPLNwere genotyped in 3156 diabetic patients and 3736 nondiabetic individuals. For non-diabetic subjects, 1779 were enrolled in stage 1 and 1757 were recruited for validation. A meta-analysis combining the two stages was carried out to obtain the overall effect.Results. In diabetic patients, no significant associations of the three SNPs with hypertension were observed. In contrast, we found that rs2235306 was associated with hypertension in non-diabetic males after adjusting for covariates (OR=1.19,P=0.039) while rs2235307 and rs3115759 displayed no evidence of association in both genders. One haplotype, C-C-A, also showed an association with hypertension (OR=1.47,P=0.032) only in men. However, analysis in stage 2 and meta-analysis did not support these findings.Conclusions. We conclude that common variants onAPLNare not associated with the prevalence of hypertension in the Chinese.
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Trojanowicz, Bogusz, Christof Ulrich i Matthias Girndt. "Uremic Apelin and Leucocytic Angiotensin-Converting Enzyme 2 in CKD Patients". Toxins 12, nr 12 (26.11.2020): 742. http://dx.doi.org/10.3390/toxins12120742.
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Apelin peptides (APLN) serve as second substrates for angiotensin-converting enzyme 2 (ACE2) and, in contrast to angiotensin II (AngII), exert blood-pressure lowering and vasodilatation effects through binding to G-coupled APLN receptor (APLNR). ACE2-mediated cleavage of the APLN may reduce its vasodilatory effects, but decreased ACE2 may potentiate the hypotensive properties of APLN. The role of APLN in uremia is unclear. We investigated the correlations between serum-APLN, leucocytic APLNR, and ACE2 in 32 healthy controls (NP), 66 HD, and 24 CKD3–5 patients, and the impact of APLN peptides on monocytic behavior and ACE2 expression under uremic conditions in vitro. We observed that serum APLN and leucocytic APLNR or SLCO2B1 were significantly elevated in uremic patients and correlated with decreased ACE2 on uremic leucocytes. APLN-treated THP-1 monocytes revealed significantly increased APLNR and ACE2, and reduced TNFa, IL-6, and MCSF. Uremic toxins induced a dramatic increase of miR-421 followed by significant reduction of ACE2 transcripts, partially counteracted with APLN-13 and -36. APLN-36 triggered the most potent transmigration and reduction of endothelial adhesion. These results suggest that although APLN peptides may partly protect against the decay of monocytic ACE2 transcripts, uremic milieu is the most dominant modulator of local ACE2, and likely to contribute to the progression of atherosclerosis.
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Пальцын, А. А., i Н. Б. Свиридкина. "Apelin". Nauchno-prakticheskii zhurnal «Patogenez», nr 2 (28.06.2021): 83–90. http://dx.doi.org/10.25557/2310-0435.2021.02.83-90.
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Апелин - слово, появившееся в 1998 году. Так, по аббревиатуре рецептора APJ, авторы назвали, найденный ими лиганд этого рецептора. Существует в нескольких изоформах, от 13 до 77 аминокислотных остатков. Наиболее активна самая короткая форма: апелин-13. Образуется жировой и мышечной тканью - адипокин и миокин. В экспериментах на мышах обнаружено много положительных эффектов действия апелина, в том числе торможение развития старости. В нарастающем потоке клинических результатов есть сообщения о благоприятном действии апелина при нарушениях энергетического обмена, сердечно-сосудистой патологии, гипоксических состояниях, саркопении, ожирении, диабете. Apelin is a word that emerged in 1998. This is how the authors named the APJ receptor ligand they discovered, by the abbreviation of this receptor. Apelin exists in several isoforms ranging in size from 13 to 77 amino acid residues. The shortest form, apelin-13, is the most active one. Apelin is produced by adipose and muscle tissue as an adipokine and a myokine. Experiments on mice have shown multiple beneficial effects of apelin, including slowing the ageing process. In the growing stream of clinical results, there are reports of the beneficial effect of apelin in disorders of energy metabolism, cardiovascular diseases, hypoxic conditions, sarcopenia, obesity, and diabetes mellitus.
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SUZUKI, KEIKO. "Studies on estimation of hypotensive effect by hypotensive drugs." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 21, nr 1 (1990): 143–44. http://dx.doi.org/10.3999/jscpt.21.143.
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Abdul-Ghani, A. S., R. Amin i M. S. Suleiman. "Hypotensive Effect ofCrataegus oxyacantha". International Journal of Crude Drug Research 25, nr 4 (styczeń 1987): 216–20. http://dx.doi.org/10.3109/13880208709055196.
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Villar, A., M. J. Sanz i M. Paya. "Hypotensive Effect ofPistacia lentiscusL". International Journal of Crude Drug Research 25, nr 1 (styczeń 1987): 1–3. http://dx.doi.org/10.3109/13880208709060902.
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PRIETO, Juan Carlos, Mónica QUEVEDO, Hugo F. MIRANDA i Gianni PINARDI. "Hypotensive effect of dopamine". Acta Cardiologica 60, nr 3 (1.06.2005): 253–57. http://dx.doi.org/10.2143/ac.60.3.2005004.
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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.
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L'apéline est un neuropeptide vasoactif qui joue un rôle crucial dans le maintien de l'équilibre hydrique et des fonctions cardiovasculaires. Des études réalisées au laboratoire sur les effets de l'apéline-17 (K17F) et du fragment d'apéline K16P, correspondant à K17F delétée de la phénylalanine (Phe) à son extrémité C-terminale, ont montré que la présence de cette Phe est nécessaire pour que l'apéline puisse d'une part, induire l'internalisation du récepteur de l'apéline, et d'autre part, provoquer une baisse de la pression artérielle. Par la suite, nous avons identifié dans les cellules CHO, exprimant de façon stable le récepteur murin de l'apéline que l'internalisation du récepteur de l'apéline induite par K17F avait pour conséquence d'induire l'activation d'une seconde voie de signalisation indépendante de la protéine Gi et dépendante de la beta-arrestine, correspondant à la voie des MAP kinases (Mitogen Activator Protein Kinase), qui pourrait être impliquée dans l'effet hypotenseur de l'apéline. Mes travaux ont ensuite consisté à caractériser dans un modèle physiologique, les artérioles afférentes juxtamédullaires de rein de rat (AAJM), si la voie de signalisation médiée par la beta-arrestine était impliquée dans l'effet vasodilatateur de K17F. Sachant que l'AngII induit une vasoconstriction en augmentant la mobilisation de calcium intracellulaire ([Ca2+]i), nous avons montré en mesurant les variations de diamètre artériolaire et de [Ca2+]i, que lorsque la voie Gi est bloquée par la toxine de pertussis (PTX), l'effet vasorelaxant induit par K17F n'est pas modifié. Ces données suggèrent que l'effet vasorelaxant de K17F sur les AAJM précontractées par l'AngII est protéine Gi-indépendant. En présence de PTX et de différents inhibiteurs d'internalisation, l'effet vasorelaxant induit par K17F sur les AAJM pré-contractées par l'AngII est aboli. De plus, en présence de PTX et de ces inhibiteurs, lorsque l'on applique K17F sur la phase plateau de la réponse calcique induite par l'AngII, aucune diminution significative de la mobilisation du [Ca2+]i est observée. Ceci est en accord avec notre hypothèse, à savoir que l'effet vasorelaxant de K17F est protéine Gi-indépendant et beta-arrestine-dépendant. L'ApélineR constitue une cible thérapeutique potentielle dans le traitement de l'insuffisance cardiaque et des rétentions hydriques. Sachant que la demi-vie de l'apéline dans la circulation sanguine est de l'ordre de la minute, un autre volet de mon travail de thèse a été de développer des analogues de K17F métaboliquement stables par deux stratégies différentes. Premièrement, nous avons substitué chacun des résidus de l'apéline par son énantiomère de la série D ou par un acide aminé synthétique. Deuxièmement, nous avons ajouté une chaîne fluoroalkyle à l'extrémité N-terminale de K17F. Ces deux stratégies nous ont permis d'obtenir plusieurs composés dont les plus actifs sont le P92 et le LIT01-196 qui conservent des propriétés pharmacologiques identiques à celles de K17F et qui présentent une demi-vie plasmatique largement supérieure à celle du peptide endogène. Ces deux analogues se sont révélés actifs in vivo avec une capacité à diminuer la pression artérielle et à réduire la sécrétion de vasopressine dans le sang conduisant à une augmentation de la diurèse aqueuseApeline 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
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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/.
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A selective a2-adrenergic agonist, lofexidine, significantly reduced intraocular pressure (lOP) in intact ocular normotensive NZW rabbits, producing a differential dose-dependent decrease in IOP in'the ipsilateral and contralateral eye. Contralateral IOP reduction was most observable at low doses. Unilateral superior cervical ganglionectomy and extraocular muscle excision studies were undertaken to elucidate the factors influencing differential IOP reduction by lofexidine. Similar significant contralateral decreases in IOP were noted when the agent was applied to either the intact or operated eye. Biochemical studies demonstrated that lofexidine inhibited isoproterenol-stimulated adenylcyclase in isolated iris-ciliary body preparations. Yohimbine, an α2-adrenergic antagonist, blocked this inhibitory response. Hence, these observations suggested that lofexidine's site of IOP reduction was probably at the cellular level.
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Bonsu, 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.
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Thesis (MScSportSc)--Stellenbosch University, 2013.ENGLISH 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.
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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.
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Aims: To investigate the human production of the vasodilating, inotropic peptide apelin in heart failure (HF) and the effect of cardiac resynchronisation therapy (CRT) on left ventricular remodelling (LVR), venous apelin, serum cytokines and their soluble receptors in humans. Methods: Plasma apelin and B-type natriuretic peptide (BNP) were measured in coronary sinus (CS), Aorta (Ao) and renal vein (RV) of patients with HF and healthy controls. In a population of patients who were eligible for CRT clinical parameters apelin, soluble ST2 (sST2), and an array of cytokines: Interferon (IFN)-γ, Interleukin (IL) -1b, IL-1ra, IL-6, Tumour necrosis factor (TNF)-α, soluble TNF receptor (sTNFR)1, sTNFR2, IL-4 and IL-10 were measured at baseline, 6 and 12 months. LVR was assessed by radionuclide ventriculography. Results: Apelin was higher in CS compared to Ao in controls and this was not maintained in patients with HF. After 12 months of CRT clinical parameters and left ventricular ejection fraction (LVEF) improved. Apelin was unchanged in the whole group, but was decreased in those that failed to remodel at 6 months and LVEF was increased significantly more in individuals whose apelin rose early. sST2 was unchanged at 12 months, but changes correlated with change in BNP and negatively with changes in LVEF. In individuals where sST2 decreased, LVEF was significantly increased. IFN-γ, IL-10 and IL-6 were reduced following 12 months of CRT. In those that remodelled favourably IL-10 was reduced whereas in those who failed to remodel IFN-γ was reduced. Conclusions: Apelin is produced in the heart and myocardial apelin is reduced in HF. Early changes in apelin are associated with LVR post CRT. A reduction in sST2 post CRT is associated with favourable LVR and a fall in BNP. Following CRT there is a relative shift away from a TH2 towards a TH1 pattern of cytokines.
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Bernardes, 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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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.
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Der-Shiang, Tsai, i 蔡德祥. "Hypotensive Effect of Scutellaria baicalensis Georgi (huangqin) on Spontaneously Hypertensive Rats". Thesis, 2000. http://ndltd.ncl.edu.tw/handle/40653214872639846238.
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碩士國防醫學院
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.
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Su, Yu-ting, i 蘇渝庭. "Modulation of central hypotensive effect of resveratrol in fructose-fed rats". Thesis, 2012. http://ndltd.ncl.edu.tw/handle/77931604424697904965.
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碩士國立中山大學
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.
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Sarvaiya, Sushil R. "Studies on hypertension with special references to hypotensive effect of ocimum sanctum". Thesis, 1986. http://hdl.handle.net/2009/5067.
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Hung, Chih-Peng, i 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.
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碩士中國醫藥學院
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
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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.
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Suite à une centaine de publications sur la réduction de la PIO post-exercice, il est connu que parmi un grand nombre de programme d'exercices de différentes durées et intensités, les effets hypotenseurs de l'exercice sur la PIO sont atténués chez les sujets en bonne condition physique. Le mécanisme proposé est l'augmentation potentielle de l'efficacité du système parasympathique avec l'activité physique. Le principal objectif de cette thèse est d'identifier les facteurs contribuants à la réduction de la PIO post-exercice et d'élucider les différents mécanismes possibles.
L'étude 1, une méta-analyse, a été menée afin de quantifier les contributions relatives de l'intensité et de la durée de l'effet de l'exercice sur la PIO et la mesure dans laquelle ces variables affectent les sujets sédentaires et normalement actifs. La tendance ressortant des résultats est que la diminution de la PIO suite à de l'exercice aérobie est plus élevée chez les sujets sédentaires que les sujets en bonne condition physique. (ES = -4.198 mm Hg et -2.340 mm Hg, respectivement). L'absence d'un contrôle des liquides ingérés avant l'activité physique est à souligné dans cette étude.
L'hyperosmolarité (un effet secondaire de la déshydratation) est l'un des mécanismes proposés influant l'effet hypotenseur de l'exercice. L'étude 2 comparait la réduction de la PIO dans deux conditions, soit hypohydraté et hyperhydraté, avant, pendant et après un effort de 90 minutes sur un ergocycle. Après une diminution initiale pour les deux conditions, la PIO revient aux valeurs de départ pour la condition hypohydratée malgré une perte de poids significative et elle augmente pour la condition hyperhydratée (résultat du protocole d'hydratation).
Étant donné le niveau élevé de participants en bonne condition physique dans l'étude 2, la troisième étude a été conçue afin de etude la relation entre la PIO et la condition physique. À l'aide d'analyses corrélationnelles il a été possible d'observer la relation entre le test de vo2max et la moyenne des mesures de PIO prises sur un intervalle de huit semaines. Une relation significative n'existait que pour les participants se situant dans la portion supérieure du continuum de la condition physique.
Conclusion: Les résultats de la présente étude suggèrent que l'effet hypotenseur de l'exercice sur la PIO est probablement une réponse homéostatique à la dérégulation de l'humeur aqueuse causée par l'initiation de l'exercice et le protocole d'ingestion de fluides pré-exercice.After 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.
Książki na temat "Hypotensive effect of apelin"
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1933-, Aoki K., International Symposium on Mechanism and Treatment in Essential Hypertension (1st : 1985 : Nagoya-shi, Japan) i International Symposium on Rats with Spontaneous Hypertension and Related Studies (5th : 1985 : Kyoto, Japan), red. Essential hypertension: Calcium mechanisms and treatment. Tokyo: Springer-Verlag, 1986.
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J, Bailey C., red. Metformin: The gold standard. Chichester, UK: John Wiley & Sons, 2007.
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Moore, R. Leigh Hill. Hypotensive effect of isometric exercise on resting blood pressure in high normotensive subjects. 1986.
Znajdź pełny tekst źródłaCzęści książek na temat "Hypotensive effect of apelin"
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Prichard, B. N. C., i F. Bompart. "Hypotensive Effect of β-Adrenoceptor Blockers". W 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.
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Podos, S. M., i C. B. Camras. "The Ocular Hypotensive Effect of Topically Applied Prostaglandins in Primates". W Glaucoma Update IV, 198–205. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76084-6_30.
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Bönner, Gerd, i Ulrike Schunk. "Hypotensive Effect of Bradykinin in Normotensives and Patients with Renovascular Hypertension". W Kinins IV, 321–27. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4757-0154-8_40.
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Härtl, A., E. Kirchner i H. Hoffmann. "Characterization of the Hypotensive Side Effect of Macrolide Antibiotics in Animals". W Archives of Toxicology, 140–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-74936-0_28.
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Batlle, Daniel C., Wu-Chang Yang, Alisa Von Riotte i Salim K. Mujais. "Dissociation between the Hypotensive Effect of Thiazides and Plasma Divalent Cations". W Phosphate and Mineral Homeostasis, 433–41. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5206-8_54.
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Sen, Abirlal, i Geeta Baruah. "Effect of HYPERTENSION on ECG Parameters". W Cardiorespiratory Fitness - New Topics [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.104613.
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Introduction: Across the world the prevalence of hypertension and other cardiovascular diseases are increasing at an alarming rate. These diseases also affect the young age and medical students are no exception. In this study, ECG variables like R-R interval, QRS Axis of the medical students along with their Blood pressure were recorded and the relationship between ECG variables and Blood pressure was studied. Materials and methods: The study was done in Dept. of Physiology, Jorhat Medical College. Sample size was calculated as 160 using EpiTools Software. Recording of Electrocardiogram and Blood pressure of 160 students were done. P values were calculated by Anova test in case of > two variables. Tukey HSD test was used for Post hoc analysis. Scatter diagrams were used to see relationship between study variables. P value <0.05 was considered as significant. Results: Comparison of ECG Variables between hypotensive, normotensive and hypertensive students showed that R-R Interval decreased significantly from 21.37 ± 4.24 in hypotensives to 19.74 ± 3.39 in normotensives and 18.27 ± 4.07 in hypertensive students. QRS Axis decreased from 75.35 ± 10.99 degrees in hypotensives to 54.80 ± 34.94 degrees in normotensives and 50.43 ± 25.59 degrees in hypertensive students. Conclusion: Changing of life style that includes reduced consumption of fat rich diets, fast foods, red meat and salt, performing regular physical exercises, and regular health check up in the form of Blood pressure and Electrocardiogram recording could be beneficial for the students to identify and take preventive measures against any cardiovascular ailments..
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"The effect of hypotensive agents on regional cerebral blood flow and intracranial pressure in baboons with space occupying lesions". W Timing of Aneurysm Surgery, 385–90. De Gruyter, 1985. http://dx.doi.org/10.1515/9783110858853-051.
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Colreavy, Frances. "Hypotension". W Oxford Textbook of Advanced Critical Care Echocardiography, redaktorzy Anthony McLean, Stephen Huang i Andrew Hilton, 265–74. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198749288.003.0018.
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In critically ill patients it is imperative to resolve and treat the cause of haemodynamic shock as quickly as possible in order to save lives and minimize end-organ damage. Intensive Care doctors trained to perform echocardiography can rapidly diagnose and effect management changes in hypotensive patients. A goal-directed approach is required seeking to urgently identify and differentiate distinct clinical syndromes that may occur in this setting. Such an approach utilizes the primary transthoracic echocardiographic subcostal, parasternal, and apical windows and identifies the key issues that can be addressed in the available views. Key to the success of goal-directed echocardiography is the integration of clinical and echocardiographic data in each individual patient. Keeping an open mind regarding the coexistence of more than one cause of hypotension and the need for more comprehensive echocardiography testing is important. Specific situations such as papillary muscle rupture, localized tamponade following cardiac surgery and prosthetic valve malfunction are more reliably diagnosed using the transoesophageal approach. Some diagnoses, such as aortic dissection, acute mitral or aortic regurgitation and acute cardiomyopathy require a multidisciplinary approach and immediate consultation with Cardiology and cardiothoracic services will be required. The simultaneous interpretation of echocardiographic images and the institution of active management are what distinguish critical care echocardiography.
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Carolina Cardoso-Teixeira, Ana, Klausen Oliveira-Abreu, Levy Gabriel de Freitas Brito, Andrelina Noronha Coelho-de-Souza i 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". W Terpenes and Terpenoids [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.94194.
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Terpenes are a class of chemical compounds with carbon and hydrogen atoms in their structure. They can be classified into several classes according to the quantity of isoprene units present in its structure. Terpenes can have their structure modified by the addition of various chemical radicals. When these molecules are modified by the addition of atoms other than carbon and hydrogen, they become terpenoids. Terpenes and terpenoids come from the secondary metabolism of several plants. They can be found in the leaves, fruits, stem, flowers, and roots. The concentration of terpenes and terpenoids in these organs can vary according to several factors such as the season, collection method, and time of the day. Several biological activities and physiological actions are attributed to terpenes and terpenoids. Studies in the literature demonstrate that these molecules have antioxidant, anticarcinogenic, anti-inflammatory, antinociceptive, antispasmodic, and antidiabetogenic activities. Additionally, repellent and gastroprotective activity is reported. Among the most prominent activities of monoterpenes and monoterpenoids are those on the cardiovascular system. Reports on literature reveal the potential effect of monoterpenes and monoterpenoids on systemic blood pressure. Studies show that these substances have a hypotensive and bradycardic effect. In addition, the inotropic activity, both positive and negative, of these compounds has been reported. Studies also have shown that some monoterpenes and monoterpenoids also have a vasorelaxing activity on several vascular beds. These effects are attributed, in many cases to the blocking of ion channels, such as voltage-gated calcium channels. It can also be observed that monoterpenes and monoterpenoids can have their effects modulated by the action of the vascular endothelium. In addition, it has been shown that the molecular structure and the presence of chemical groups influence the potency and efficacy of these compounds on vascular beds. Here, the effect of several monoterpenes and monoterpenoids on systemic blood pressure and vascular smooth muscle will be reported.
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Sood-Mendiratta, Shalini. "Medical Management for Glaucoma". W Glaucoma. Oxford University Press, 2012. http://dx.doi.org/10.1093/oso/9780199757084.003.0015.
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When evaluating patients for glaucoma or ocular hypertension, the question remains whether or not the patient should be treated, and when treatment should be initiated. Treatment decisions are usually guided by risk factor assessment, and these include race, age, family history, medical history, IOP, central corneal thickness, and clinical examination, including optic nerve appearance and ancillary diagnostic testing. The information is compiled in each individual to determine the risk of significant visual loss in the patient’s lifetime. Numerous studies have demonstrated that lowering IOP slows progression of this disease. Most common current medical therapies are therefore ocular hypotensive medications. The armamentarium of medications has expanded over the past two decades in terms of number and classes. Future potential therapies may include those that provide neuroprotection, but the main focus of this chapter will be on medications most frequently used to treat glaucoma. The goal of therapy is to slow progression of disease with the fewest side effects and medications and the lowest doses and cost of therapy. Consideration of these issues maximizes compliance and effectiveness of therapy in long-term disease control. An effective medication lowers the IOP 20% to 30% from baseline. Figure 10.1 lists the most common classes of medications with mechanism of action and common side effects; sample bottles of medications are also shown. We will discuss each class of medications and offer clinical pearls. • Direct-acting: pilocarpine HCl, pilocarpine gel •Indirect-acting: echothiophate iodide, eserine sulfate ointment, demecarium bromide, isofluorophate •Affect the parasympathetic or cholinergic system through direct- or indirect-acting Agents •In addition to effects on ciliary muscle, parasympathomimetics stimulate muscarinic receptors of the iris sphincter to cause miosis. This may improve outflow facility in eyes with angle-closure glaucomas by relieving pupillary block or by changing the anatomy of the peripheral iris in the angle. •Miosis may cause dimness of vision, contraction of visual fields, and pinhole effect. •Patients may develop brow ache due to ciliary muscle spasm.
Streszczenia konferencji na temat "Hypotensive effect of apelin"
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Kechyn, Svyatoslav, Gareth Barnes, Akaphot Thongmee i Luke Sebastian Howard. "Effect of apelin on cardiopulmonary performance during endurance exercise". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2241.
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Özkan, Naziye. "The Effect of Apelin on Podocytes in Doxorubicin Induced Nephrotic Syndrome". W 15th International Congress of Histochemistry and Cytochemistry. Istanbul: LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-230.
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Tristantini, Dewi, i Kelly Amelinda. "Hypotensive effect of aqueous extract of jamu antiatherosclerosis in male rats". W 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.
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Baum, Olga I., Emil N. Sobol, Andrei V. Bolshunov, Olga Khomchik i George I. Zheltov. "Laser-induced hypotensive effect in treatment of the resistant open-angle glaucoma". W Optical Interactions with Tissue and Cells XXXII, redaktorzy Bennett L. Ibey i Norbert Linz. SPIE, 2021. http://dx.doi.org/10.1117/12.2588455.
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Yan-qin Yu, Zhi-guo Ye i Qiang Xia. "The Role of Opioid in the Mechanism of the Hypotensive Effect by Simulating Acupuncture on Rat Hindlimb". W 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1615579.
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Buczko, W., M. Pietraszek, E. Chabielska i B. Malinowska. "THE INFLUENCE OF SOME HYPOTENSIVE DRUGS ON THE SEROTONERGIC MECHANISMS IN RATS PLATELETS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643440.
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Serotonin (5HT) is a vasoactive amine that has been reported to be involved in a number of forms of circulatory failure. The 5HT content and metabolism in platelets is changed in hypertension and in peripheral arteriolar diseases. The present study concerns the effect of verapamil (VER), propranolol (PRO) and cap-topril (CAP) - drugs having different hypotensive mechanisms of action, on serotonergic mechanisms in rat blood platelets. In vitro, VER produced noncompetitive inhibition of 14C-5HT uptake (IC50=8.2μM), PRO inhibited the uptake in a competitive fashion (Km =0.9μM), whereas CAP was ineffective. Only PRO released (24%) radioactive 5HT from incubated platelets. Inhibition of amine uptake was also obtained when plateletswere prepared from-irats pretreated with VER (10 mg.kg−1 ), PRO (5 mg.kg−1) or CAP (10 mg.kg−1 ). Moreover, the concentration of endogenous 5HT in blood platelets was reduced after VER and PRO administration. Platelets aggregation induced by ADP was inhibited by VER and CAP. They also diminished the potentiating effect of 5HT on ADP-induced platelet aggregation. It can be concluded that these effects may be a secondary mechanism of action in vivo. Thus “serotonergic component” of studied drugs should be taken under consideration at least in therapy of hypertension.Supported by CPBR, no 11.6
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Toscano, 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 i Diego Augusto dos Santos Silva. "CHANGES IN BLOOD PRESSURE IN BREAST CANCER SURVIVORS UNDER A PHYSICAL EXERCISE PROGRAM". W Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2080.
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Objective: The main aim of this study was to verify chronic and acute alterations in the systolic blood pressure (SBP) and diastolic blood pressure (DBP) in breast cancer survivors undergoing a physical exercise program. Methodology: In a reference hospital for cancer treatment in the city of Maceió, Alagoas, Brazil, a total of 24 female breast cancer survivors, 56.8 (±7.7) years old, underwent a physical exercise program. Their blood pressure was supervised through digital blood pressure monitors for the wrist, before and after the exercise sessions. To make comparisons in each session — pre- and post-exercise — the paired sample t-test analysis was applied. For the chronic effect analyses, the analysis of variance for repeated measures (ANOVA RM) was used to identify the possible differences in SBP and DBP variables, pre-exercise, throughout the 15 training sessions. A significance level of 5% was considered. Results: Except for the fourth and sixth sessions, it was established that the SBP levels decreased in all sessions after they were completed (p≤0.05). For DBP, there was a significant decrease only after the first three exercise sessions. Regarding chronic effects, there was a mean reduction in SBP values at rest, throughout the sessions, with a hypotensive effect above 70% from the seventh session on (p≤0.05). Regarding DBP, differences in the DBP values at rest were enhanced from the tenth session onward, with a hypotensive effect above 94%. By comparing the beginning of the program with the last session, a difference in SBP and DBP, of -9.0 and -5.5 mmHg, respectively (p<0.01), was identified. Conclusion: Those survivors who joined the physical exercise program showed a chronic and acute decrease in both SBP and DBP levels.
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Saldeen, K., R. Moalli i T. Saldeen. "EFFECT OF A FIBRIN-DERIVED PEPTIDE ON PULMONARY ANGIOTENSIN CONVERTING ENZYME (ACE) ACTIVITY AND ON PRESSURE RESPONSES TO BRADYKININ (BK)". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644331.
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Decreased ACE activity is a common finding in patients with adult respiratory distress syndrome (ARDS) and in animal models of lung injury. The nature of this effect is unknown. Fibrin, also a common finding in lung injury, is degraded to small peptides by proteolytic enzymes. Peptide 6A, corresponding to amino acid residues 43-47 of the BB-chain of fibrin (cgen), is produced by plasmin degradation of fibrin and has been shown to inhibit ACE in vitro. The purpose of the present investigation was to study whether peptide 6A inhibits pulmonary ACE in vivo and, if so, determine its effect of hemodynamic changes induced by bradykinin (BK) in the rabbit. We investigated the effect of peptide 6A an the hydrolysis of a synthetic ACE substrate, benzoyl-phe-ala-pro (BPAP) in anesthetized rabbits and in isolated lungs. Peptide 6A caused a reversible, dose-dependent inhibition of BPAP hydrolysis. The ID 50 for peptide 6A inhibition of ACE hydrolysis of BPAP was approximately 1 micrcmole.In both isolated rabbit lupgp and in the intact animal, BK injection elicited a dose dependent increase in pulmonary arterial pressure. In intact animals, this was accompanied by a dose dependent decrease in systemic arterial pressure.In both preparations, responses to BK were potentiated by addition of 1 micromole of peptide 6A. In isolated lungs, co-injection of peptide 6A significantly increased the pulmonary artery pressure response to every dose of BK except the highest (1 mg). In the anesthetized rabbit, 1 micromole of peptide 6A significantly (p<0.05) increased the pulmonary hypertensive response to 100 and 200 nanograms of BK and significantly (p<0.05) decreased the systemic hypotensive response following 100 , 200 , 300 and 400 nanograms of BK. The amount of BK needed to increase pulmonary arterial pressure was 1000-fold greater in the isolated lungs than in the intact animals. Peptides of this type might contribute to decreased ACE activity in patients with ARDS and may potentiate BK induced pulmonary hypertension and systemic hypotension in these patients.
Raporty organizacyjne na temat "Hypotensive effect of apelin"
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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, styczeń 2008. http://dx.doi.org/10.21236/ada490734.
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Schreiber, 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, styczeń 2006. http://dx.doi.org/10.21236/ada446801.
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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, styczeń 2012. http://dx.doi.org/10.21236/ada559947.
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