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Relevant bibliographies by topics / Blood pressure regulation

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Academic literature on the topic 'Blood pressure regulation'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 June 2025

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Journal articles on the topic "Blood pressure regulation"

1

Zhao, Bin. "Biostatistical Analysis on the Regulation of Blood Pressure." Open Access Journal of Cardiology 6, no. 1 (2022): 1–17. http://dx.doi.org/10.23880/oajc-16000170.

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Background: Hypertension is one of the most common diseases in the current era. With the increase in life pressures, the number of people with high blood pressure is constantly increasing. Multiple types of medical drugs are used to treat high blood pressure, but despite their use in treatment, they have many side effects, so with the beginning of the twentieth century, the World Health Organization sought to urge the use of alternative medicine in the treatment of many diseases because of its characteristics that make it superior on medical drugs, the most important of which is that it has no side effects. The purpose of this study was to determine the effectiveness of Fashareen on the regulation of blood pressure. Material and Methods: The study was designed to include hypertensive patients, where 30 participants were taken from OPD of government and private hospitals in Faisalabad according to the inclusion and exclusion criteria of the study. Consent was taken from individuals for an assessment and intervention procedure. A recommended dose of 1 tablet of Fashareen twice a day was given to the patients in 12 hours a part period, and after that, we collected the data again from the patient’s e.g. Blood pressure and heartbeats. Results: Significant change in blood pressure values after the treatment in a group in addition to a significant decrease in heart rate values after the treatment in a group Conclusion: Fashareen is quite effective in controlling blood stress.

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Jones, John Edward, and Pedro A. Jose. "Neonatal blood pressure regulation." Seminars in Perinatology 28, no. 2 (2004): 141–48. http://dx.doi.org/10.1053/j.semperi.2003.11.004.

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Igbe, Ighodaro, and Osaze Edosuyi. "Mitochondrial Function and Blood Pressure Regulation: From Bioenergetics to Pathophysiology." Tropical Journal of Phytochemistry and Pharmaceutical Sciences 1, no. 1 (2022): 2. http://dx.doi.org/10.26538/tjpps/v1i1.2.

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The mitochondrion is the powerhouse of all living cells as it provides the energy needed to maintain obligatory regulatory functions.1 The generation of adenosine triphosphate (ATP) via oxidative phosphorylation underlies the principal role of the mitochondrion in cell survival. Aside this basic contribution to energy generation, the mitochondria has been established to regulate cell death (apoptosis), redox and ion signaling.2 The crosstalk between redox signaling and a myriad of pathological disorders created a nexus between the mitochondrion and the cardiorenal system.3,4 Similarly, the high distribution of mitochondria in organs of the cardiorenal system, meant that these organs such as the kidney, are subject to the effect of mitochondria-induced alterations in redox signaling.5 For instance, mitochondrial dysfunction has been linked to the pathophysiology of kidney disorders.6 Considering the intricate link between the kidneys and blood pressure regulation, mitochondrial dysfunction was suggested to contribute significantly to distortions in renal control of blood pressure. Recently, it was reported that the tricarboxylic acid (TCA) cycle plays a role in the etiology of genetic hypertension.7 This novel iscovery linked the activity of the TCA cycle enzyme, fumarase to a reduction in nitric oxide production and an upregulation in redox signaling in the renal medulla of salt-sensitive rats.7,8 In these animals, an innate mutation in the fumarase enzyme, reduced its activity and increased cellular levels of its substrate, fumarate. Hence, the role of these TCA cycle intermediaries was shifted from being ‘mere’ participants in the generation of energy to endogenous ligands with biochemical targets that alter renal function and by extension, blood pressure. Furthermore, fumarate was shown to reduce blood pressure and modulate the expression of genes that ameliorated hypertension induced renal damage in deoxycorticosterone acetate (DOCA) hypertension, a non-genetic form of hypertension.9 Subsequently, succinate, the upstream product of fumarate was reported to directly stimulate GPR91 receptors to increase blood pressure.10 These actions of fumarate and its intermediaries, exceed the renal system as reports have shown a cardioprotective role via upregulation of nuclear erythroid factor-2 (Nrf2).11 Fumarate is now known to regulate the expression of genes such as hypoxia inducible factor (HIF-1), transforming growth factor (TGF-β), kidney injury molecule (KIM-1) amongst others. What is evident from the foregoing is that the mitochondrion is no longer just an idle energy-generating center. It is now listed as a probable etiology in hypertension, and this has opened new vistas of possibilities as it relates to the pathophysiology of hypertension.8 Is it possible that these intermediaries are involved in the physiological control of blood pressure? Could they also be exerting direct vasoactive effects? Is it likely that they may be modulating the expression of genes that underlie vascular/organ remodeling? And finally, is it possible that mitochondrial dysfunction could partly explain the etiology of idiopathic hypertension? As, far reaching as these insights may be, it is not completely out of place to be optimistic as the foray into these previously uncharted areas of mitochondrial metabolism progress. What is very clear is that there is now a paradigm shift in the function of the mitochondria in blood pressure regulation from that of a bioenergetic center to pathophysiological axis which contributes significantly to the etiology of hypertension.

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Tzeng, Yu-Chieh, and Philip N. Ainslie. "Blood pressure regulation IX: cerebral autoregulation under blood pressure challenges." European Journal of Applied Physiology 114, no. 3 (2013): 545–59. http://dx.doi.org/10.1007/s00421-013-2667-y.

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Lazartigues, Eric D. "Hypothalamic Regulation of Blood Pressure." FASEB Journal 34, S1 (2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.00423.

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Dakshinamurti, K., and S. Dakshinamurti. "Blood pressure regulation and micronutrients." Nutrition Research Reviews 14, no. 1 (2001): 3–44. http://dx.doi.org/10.1079/095442201108729123.

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Luft, F. C., and M. H. Weinberger. "Potassium and blood pressure regulation." American Journal of Clinical Nutrition 45, no. 5 (1987): 1289–94. http://dx.doi.org/10.1093/ajcn/45.5.1289.

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Kienitz, Tina, and Marcus Quinkler. "Testosterone and Blood Pressure Regulation." Kidney and Blood Pressure Research 31, no. 2 (2008): 71–79. http://dx.doi.org/10.1159/000119417.

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9

Ackermann, U. "Regulation of arterial blood pressure." Surgery (Oxford) 22, no. 5 (2004): 120a—120f. http://dx.doi.org/10.1383/surg.22.5.120a.33383.

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Mutig, Kerim, and Sebastian Bachmann. "Hyperkalemia and blood pressure regulation." Nephrology Dialysis Transplantation 34, Supplement_3 (2019): iii26—iii35. http://dx.doi.org/10.1093/ndt/gfz218.

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Abstract Hypertension is common in the general population. Management of hypertensive patients at risk of hyperkalemia is challenging due to potential life-threatening complications such as cardiac arrest. Chronic hyperkalemia is often associated with impaired renal ability to excrete excessive potassium ions (K+). This may refer to chronic kidney disease or certain pharmacological interventions, including broadly used renin–angiotensin–aldosterone system and calcineurin inhibitors. Understanding the intrinsic mechanisms permitting kidney adaptations to hyperkalemia is critical for choosing therapeutic strategies. Valuable insights were obtained from the analysis of familial hyperkalemic hypertension (FHHt) syndrome, which became a classic model for coincidence of high blood pressure and hyperkalemia. FHHt can be caused by mutations in several genes, all of them resulting in excessive activity of with-no-lysine kinases (WNKs) in the distal nephron of the kidney. WNKs have been increasingly recognized as key signalling enzymes in the regulation of renal sodium ions (Na+) and K+ handling, enabling adaptive responses to systemic shifts of potassium homoeostasis consequent to variations in dietary potassium intake or disease. The WNK signalling pathway recruits a complex protein network mediating catalytic and non-catalytic effects of distinct WNK isoforms on relevant Na+- or K+-transporting proteins. In this review article, we summarize recent progress in understanding WNK signalling. An update of available models for renal adaptation to hyperkalemic conditions is presented. Consequences for blood pressure regulation are discussed. Pharmacological targeting of WNKs or their substrates offers promising options to manage hypertension while preventing hyperkalemia.

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Dissertations / Theses on the topic "Blood pressure regulation"

1

Johnson, J. V. "Vasopressin and blood pressure regulation in the rat." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376525.

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Galla, Sarah L. "Studies on the Holobiont and Blood Pressure Regulation." University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco1556099980339015.

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Peirce, Susan Caroline. "Investigating short-term blood pressure regulation : peripheral baroreceptor sensitivity." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/29891.

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Autonomically-mediated baroreflex control of heart rate has been extensively studied (cardiac BRS, cBRS), but peripheral control of blood pressure is less well known. Total peripheral resistance (TPR) was derived from pulse contour stroke volume (SVPC) using non-invasive blood pressure (Finapres). The beat-to-beat variability of Finapres SVPC was evaluated in cardiac catheterisation patients against aortic blood pressure SVPC. Correlations were generally good (mean R = 0.75), but regression slopes tended to be less than unity and several aortic recordings were significantly affected by the dynamic response of the measurement system. Finapres SVPC was also compared to Doppler stroke distance (SD) in healthy volunteers. Both measures followed respiratory movements well, although SVPC had higher coherence with respiration. Discrepancies between the results were considered to be mainly due to errors in the Doppler method. Coherence thresholds for spectral cBRS were determined as a function of the number of subrecords available for ensemble averaging and the effect of ventricular ectopics on cBRS estimates was investigated. Pulse contour TPR data was then used to determine peripheral BRS (pBRS) in healthy controls and neurocardiogenic syncope patients (NCS) using methods adapted from cardiac BRS analysis. Diastolic pressure produced greater pBRS estimates than systolic pressure and pBRS was generally higher in patients and fainters than in controls and non-fainters. Tilt did not have a consistent effect on pBRS and it was not linearly related to age or resting blood pressure, although it may be increased in hypertension and the elderly. pBRS was able to discriminate between the subject groups when cBRS methods showed no difference.

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Ashraf, Usman Mohammad. "Novel Regulators of Kidney Homeostasis and Blood Pressure Regulation." University of Toledo Health Science Campus / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=mco1596206028212986.

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Correia, Anabela G. 1975. "The renal medullary circulation and blood pressure control." Monash University, Dept. of Physiology, 2001. http://arrow.monash.edu.au/hdl/1959.1/8480.

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Lopez, Kyle Eric, and Kyle Eric Lopez. "Uncovering Signal Transduction in Blood Pressure Regulation by Nitric Oxide." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625045.

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Nitric Oxide (NO) is an important signaling molecule in blood pressure regulation. The NO receptor, soluble guanylate cyclase (sGC), produces the secondary messenger cGMP in response to NO binding. Because of its role in blood pressure regulation, sGC is increasingly targeted for drug discovery and several new drugs treating hypertensive individuals are sGC stimulators. Unfortunately, stimulator development is limited by our understanding of NO and simulator induced conformational changes. In the present study, we used lanthanide resonance energy transfer (LRET) to measure distances between sGC domains in truncated M. sexta sGC constructs and assessed the magnitude of distance changes induced by ligand binding. Our strategy was to place a lanthanide binding domain at various locations in the protein and measure changes in lanthanide luminescence in the presence of the quenching domain, His6 with coordinated copper or nickel ion, which quenches luminescence in a distance dependent manner. Terbium luminescence decayed bi-exponentially in the absence of quencher, and displayed a slow phase with a rate constant of ~2.3 ms. Quencher presence altered the time constant for the slow phase, but not the fast phase. Distances obtained from fitting these data indicate sGC is a compact molecule with the coiled-coil ~23 Å from the a H-NOX N-terminal end. However, we must further develop our system to ensure the decays measured reflect the distance between donor and acceptor. In the future, distances will be measured after ligand or stimulators are bound to determine the change in distance, which will give insight into the conformational dynamics of sGC.

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Huang, Chunhua. "Impact of dietary salt intake during growth on cardiovascular homeostasis and neural control of the kidney : role of brain angiotensin II (Ang II)." Thesis, University of Birmingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368519.

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Rees, Daryl David. "The role of nitric oxide in the cardiovascular system." Thesis, Open University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293301.

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Nitric oxide is generated by the vascular endothelium from L-arginine by a constitutive, Ca2+-dependent, NO synthase. Analogues of L-arginine were characterised as inhibitors of NO synthase to investigate the biological significance of the L-arginine-NO pathway in the vessel wall and its role in the cardiovascular system. These inhibitors attenuate the endothelium-dependent vasorelaxation and hypotension induced by various agents, produce an increase in vascular tone and an increase in blood pressure. This suggests that NO is involved in endothelium-dependent relaxation and its continuous release maintains a vasodilator tone and plays a fundamental role in the regulation of blood flow and blood pressure. The removal of the NO-dependent vasodilator tone, results in an `upregulation' of its intracellular receptor, the soluble guanylate cyclase and an increased sensitivity to those vasodilators which act by stimulating this enzyme. This phenomenon of `supersensitivity' to nitrovasodilators may be an important component of their therapeutic action in certain cardiovasulcar disorders. Vascular tissue also expresses an inducible, Ca2+-independent, NO-synthase after activation by lipopolysaccharide (LPS) which results in the generation of large quantities of NO, predominantly from the smooth muscle layer, with a consequent loss of vascular tone and a hyporeactivity to the vasoconstrictor action of phenylephrine. Induction of NO synthase in the vasculature may therefore be responsible for the hypotension and hyporesponsiveness to pressor agents characteristic of endotoxin shock. The glucocorticoid, dexamethasone inhibits the expression of this enzyme but not its activity, which may explain why steroids are more effective at preventing rather than treating this condition. These results suggest that in the cardiovascular system, NO can be considered to have both a protective and a pathological role. The release of small amounts of NO from the constitutive, Ca2+-dependent NO synthase, acts as an adaptive mechanism whereby the vascular endothelium responds to changes in its environment and regulates blood flow and blood pressure to maintain organ perfusion. In contrast, following the induction of the Ca2+-independent NO synthase, after immunological stimulation, NO is released in large quantities from vascular tissue, which may result in pathological vasodilation and tissue damage.

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Muzs, Karolin. "The influence of short chain fatty acids on blood pressure regulation." Thesis, University of Aberdeen, 2017. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=236055.

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Hypertension is a widespread condition which may cause cardiovascular events when left untreated. If high blood pressure (BP) is noticed at all, it is mostly only sub-optimally controlled making nutritional interventions a cost-effective and safe preventive measure and an alternative to medical treatment. Previous studies have shown that increased fibre consumption reduces BP which was particularly effective in hypertensive subjects. Fibres are indigestible and hence are available for fermentation by the colonic microbiota which produces the short chain fatty acids (SCFAs) acetate, propionate and butyrate. Intriguingly, recent studies carried out in mice showed that SCFAs can reduce BP. Therefore, we hypothesised that gut microbiota-derived SCFAs can (1) reduce BP in middle-aged male volunteers and (2) influence the protein expression of BP regulatory systems in a cellular model. As the development of a cellular angiotensin II-induced hypertension model was unsuccessful, the effects of SCFAs on a molecular level were assessed in unstimulated human aortic endothelial cells (HAECs). The expression of proteins involved in the BP regulating renin angiotensin system (RAS) was assessed by western blotting. Additionally, a human supplementation trial is being carried out looking at the acute consumption of a low (0.16 g) and high (2.35 g) propionate dose on BP and other cardiovascular markers in middle-aged male volunteers. In vitro work showed that SCFAs did not affect RAS expression in HAECs. However, acute propionate supplementation influenced BP and its regulation. Preliminary data show, that while a high propionate dose led to increases in plasma propionate by on average 4 µM and acetate levels with concurrent increases in BP, arterial stiffness and plasma renin concentration, a low propionate dose resulted in plasma propionate increases of about 0.5 µM with simultaneous reductions in systolic BP. Taken together, these results suggest that SCFAs play a regulatory role in the homoeostasis of BP.

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Rahsid, Imad Hatim. "Role of C1-adrenergic neurones in the regulation of vasopressin and pressor response." Thesis, University of Nottingham, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294526.

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Books on the topic "Blood pressure regulation"

1

Berbari, Adel E., and Giuseppe Mancia, eds. Disorders of Blood Pressure Regulation. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-59918-2.

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W, Harding Joseph, ed. Angiotensin and blood pressure regulation. Academic Press, 1988.

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(Firm), Infinite Ideas, ed. Blood pressure: Relief and remedies to ease hypertension. Infinite Ideas, 2012.

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Yakovlevitch, Marko. Causes of resistant hypertension in patients referred to a tertiary care clinic. s.n.], 1990.

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-L, Elghozi J., and Chalmers J. P, eds. Cardiovascular and renal control of blood pressure. Blackwell Scientific Publications, 1992.

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Ivanova, L. N. doktor medit͡s︡inskikh nauk., Shterentalʹ I. Sh та Novosibirskiĭ institut bioorganicheskoĭ khimii (Akademii͡a︡ nauk SSSR), ред. Perifericheskie mekhanizmy reguli͡a︡t͡s︡ii arterialʹnogo davlenii͡a︡: Rolʹ sosudistoĭ reaktivnosti i tkanevogo obmena natrii͡a︡. "Nauka," Sibirskoe otd-nie, 1988.

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International Symposium on Resistance Arteries (2nd 1988 Stowe, Vt.). Second International Symposium on Resistance Arteries, January 12-15, 1988. Perinatology Press, 1988.

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Arfi, Robert A. Systolic blood pressure: Influences, associations, and management. Nova Science Publishers, 2012.

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Cechella, Achutti Aloysio, ed. Controle da hipertensão arterial: Uma proposta de integração ensino-serviço. Ministério da Saúde, 1993.

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1952-, Portaluppi Francesco, Smolensky Michael H, and New York Academy of Sciences., eds. Time-dependent structure and control of arterial blood pressure. New York Academy of Sciences, 1996.

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Book chapters on the topic "Blood pressure regulation"

1

Kobzik, Alexander, and Michael R. Pinsky. "Arterial Blood Pressure Regulation." In Hemodynamic Monitoring. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69269-2_5.

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Anile, C., A. Rinaldi, A. Mangiola, et al. "Biomechanical Regulation of Cerebral Blood Flow." In Intracranial Pressure VIII. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77789-9_56.

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Girndt, J. "Magnesium and Blood Pressure Regulation." In Salt and Hypertension. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73917-0_21.

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Kalil, R. S., and L. G. Hunsicker. "Kidney and Blood Pressure Regulation." In Contributions to Nephrology. KARGER, 2004. http://dx.doi.org/10.1159/000078717.

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Kam, Peter, Ian Power, Michael J. Cousins, and Philip J. Siddal. "Regulation of Arterial Blood Pressure." In Principles of Physiology for the Anaesthetist. CRC Press, 2020. http://dx.doi.org/10.1201/9780429288210-31.

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Mannelli, Massimo, Gian Paolo Rossi, Paul-Emmanuel Vanderriele, and Gabriele Parenti. "The Endocrine Regulation of Blood Pressure." In Endocrinology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-44675-2_23.

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Cassis, Lisa A., and Sara B. Police. "Adipose Tissue and Blood Pressure Regulation." In Adipose Tissue in Health and Disease. Wiley-VCH Verlag GmbH & Co. KGaA, 2010. http://dx.doi.org/10.1002/9783527629527.ch13.

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Mannelli, Massimo, Gian Paolo Rossi, Paul-Emmanuel Vanderriele, and Gabriele Parenti. "The Endocrine Regulation of Blood Pressure." In Endocrinology. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27318-1_23-1.

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Rocchini, Albert P. "Childhood Obesity and Blood Pressure Regulation." In Pediatric Hypertension. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-824-9_17.

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Rocchini, Albert P. "Childhood Obesity and Blood Pressure Regulation." In Pediatric Hypertension. Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-797-0_18.

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Conference papers on the topic "Blood pressure regulation"

1

Abouali, Abolfazl, and Hamed Mojallali. "Blood Pressure Regulation Using a FOPID Controller Based on a Hybrid-Evolutionary Optimization Algorithm." In 2025 Fifth National and the First International Conference on Applied Research in Electrical Engineering (AREE). IEEE, 2025. https://doi.org/10.1109/aree63378.2025.10880286.

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Sandu, Ciprian, Dumitru Popescu, and Catalin Dimon. "Blood Pressure Regulation -- Robust Control." In 2015 20th International Conference on Control Systems and Computer Science (CSCS). IEEE, 2015. http://dx.doi.org/10.1109/cscs.2015.33.

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Sandu, Ciprian, Dumitru Popescu, and Catalin Dimon. "Polynomial RST Control for Blood Pressure Regulation." In 2015 20th International Conference on Control Systems and Computer Science (CSCS). IEEE, 2015. http://dx.doi.org/10.1109/cscs.2015.103.

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Hegyi, Gina, and Gary Drzewiecki. "Nonlinear dynamic model of baroreceptor blood pressure regulation." In 2014 40th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2014. http://dx.doi.org/10.1109/nebec.2014.6972813.

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Sekaj, Ivan, Josef Zicha, Michal Behuliak, Peter Balis, and Iveta Bernatova. "Modelling of the blood pressure regulation in rats." In 2012 5th International Conference on Biomedical Engineering and Informatics (BMEI). IEEE, 2012. http://dx.doi.org/10.1109/bmei.2012.6513136.

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Lan, L., and K. Y. Zhu. "Design and implementation of blood pressure regulation systems." In the 1st international convention. ACM Press, 2007. http://dx.doi.org/10.1145/1328491.1328547.

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Enbiya, S., A. Hossain, and F. Mahieddine. "Neuro-PID adaptive control scheme for blood pressure regulation." In 5th International Conference on Software, Knowledge Information, Industrial Management and Applications (SKIMA 2011). IEEE, 2011. http://dx.doi.org/10.1109/skima.2011.6163199.

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Feng, Jin, Qu Bo, and Zhu Kuanyi. "Implementation of Drug Delivery system for blood pressure regulation." In 2006 9th International Conference on Control, Automation, Robotics and Vision. IEEE, 2006. http://dx.doi.org/10.1109/icarcv.2006.345210.

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Zhu, K. Y., H. Zheng, and J. Lavanya. "Adaptive PI Regulation of Blood Pressure of Hypertension patients." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1615738.

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O’Clock, George D., Bruce H. KenKnight, and Elena G. Tolkacheva. "Vagus Nerve Stimulation for Blood Pressure and Heart Rate Regulation." In 2018 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/dmd2018-6847.

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For more than 27 years, implanted vagus nerve stimulation (VNS) devices, with electric current outputs in the 1 to 3.5 mA range, have been developed for many health care applications, including epilepsy and heart disease [1]. Mechanical compression approaches for VNS were administered under surgical conditions, using forceps, in the 1800’s [2]. Outcomes such as Electrocardiogram (ECG) data, blood pressure (BP), and heart rate (HR) were evaluated. Also, non-invasive (NI) mechanical compression of the vagus nerve for various nervous system disorders using hand, thumb, finger and belt pressure was popular in the 1800’s [3]. Cyberonics (now LivaNova) received the first FDA clearance for a surgically implanted electrical VNS device to treat refractory epilepsy in 1997.

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Reports on the topic "Blood pressure regulation"

1

กาญจนทัต, อภิชาติ. โปรตีนไฮโดรไลเสตจากเมล็ดผลไม้ไทยเพื่อการบำบัดโรค : รายงานวิจัยฉบับสมบูรณ์ (ปีที่ 1). จุฬาลงกรณ์มหาวิทยาลัย, 2014. https://doi.org/10.58837/chula.res.2014.89.

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Blood pressure regulation is partially dependent on the renin-angiotensin system; renin acts on angiotensinogen to release angiotensin-I, which is further converted into the angiotensin II by the angiotensin I-converting enzyme (ACE). ACE plays a key physiological role in the regulation of blood pressure by virtue of two different reactions that it catalyzes: conversion of the inactive angiotensin I to the powerful vasoconstrictor angiotensin II, and inactivation of the vasodilator bradykinin. Crude extract and ammonium sulphate cut protein extracts, and their pepsin-pancreatin hydrolysates, from the seeds of 4 Thai fruits (i) Carica papaya L.; (papaya; unripen and ripen form), (ii) Nephelium lappaceum L. (rambutan) (iii) Dimocarpus longan Lour. subsp. (longan), and (iv) Litchi chinensis Sonn. (lychee) were screened for their in vitro angiotensin I- converting enzyme inhibitory (ACEI) activity. The protein hydrolysate of lychee seeds shows the highest potential of ACE inhibitory activity at IC50 value 0.22±0.010 mg protein/ml. The protein hydrolysate of unripen papaya seeds, longan seeds, and lychee seeds show uncompetitive and non-competitive inhibition with Ki values at 6.02, 2.82, and 5.62 mg protein/ml, with optimum pH in range of 6-8. After partial purification with ultrafiltration technique, UF-3 (below 5 kDa) of longan seeds show the highest inhibitory activity with IC50 values at 0.43±0.011 mg protein/ml. This fraction was subjected to RP-HPLC and five peaks were separated, and subjected to LC/MS/MS for amino acids sequences analysis. The P1-F1, P3-F1, and P3-F4 show the most inhibitory activity.

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