Relevant bibliographies by topics / Blood pressure regulation

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Blood pressure regulation'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Blood pressure regulation.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Blood pressure regulation"

1

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 (September 4, 2022): 2. http://dx.doi.org/10.26538/tjpps/v1i1.2.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
2

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Luft, F. C., and M. H. Weinberger. "Potassium and blood pressure regulation." American Journal of Clinical Nutrition 45, no. 5 (May 1, 1987): 1289–94. http://dx.doi.org/10.1093/ajcn/45.5.1289.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Mutig, Kerim, and Sebastian Bachmann. "Hyperkalemia and blood pressure regulation." Nephrology Dialysis Transplantation 34, Supplement_3 (December 1, 2019): iii26—iii35. http://dx.doi.org/10.1093/ndt/gfz218.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
9

Chao, Julie, and Lee Chao. "Kallistatin in Blood Pressure Regulation." Trends in Cardiovascular Medicine 7, no. 8 (November 1997): 307–11. http://dx.doi.org/10.1016/s1050-1738(97)00089-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Watts, Stephanie W., Shaun F. Morrison, Robert Patrick Davis, and Susan M. Barman. "Serotonin and Blood Pressure Regulation." Pharmacological Reviews 64, no. 2 (March 8, 2012): 359–88. http://dx.doi.org/10.1124/pr.111.004697.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Blood pressure regulation"

1

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

M, Magro Albert, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Central and peripheral mechanisms of cardiovascular regulation. New York: Plenum Press, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Orthostatic disorders of the circulation: Mechanisms, manifestations, and treatment. New York: Plenum Medical Book Co., 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

1932-, Trouth C. Ovid, ed. Ventral brainstem mechanisms and control of respiration and blood pressure. New York: M. Dekker, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Workshop on Cation Transport and Nartriurietic Factors (1985 Cambridge, Mass.). Workshop on Cation Transport and Natriuretic Factors: Cambridge, Massachusetts May 13-14, 1985. Edited by Dzau Victor J, Horan Michael J, Canessa Mitzy, and American Heart Association. [Dallas, Tex.]: American Heart Association, 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Human cardiovascular control. New York: Oxford University Press, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

J, Mulvany M., ed. Resistance arteries: Structure and function : proceedings of the third International Symposium on Resistance Arteries, Rebild, Skörping, Denmark, 21-25 May 1991. Amsterdam: Excerpta Medica, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Blood pressure regulation"

1

Kobzik, Alexander, and Michael R. Pinsky. "Arterial Blood Pressure Regulation." In Hemodynamic Monitoring, 39–48. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69269-2_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Anile, C., A. Rinaldi, A. Mangiola, P. Amante, P. Palma, G. Maira, F. Della Corte, R. Calimici, and A. Ferraresi. "Biomechanical Regulation of Cerebral Blood Flow." In Intracranial Pressure VIII, 265–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77789-9_56.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Girndt, J. "Magnesium and Blood Pressure Regulation." In Salt and Hypertension, 235–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73917-0_21.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Kalil, R. S., and L. G. Hunsicker. "Kidney and Blood Pressure Regulation." In Contributions to Nephrology, 131–44. Basel: KARGER, 2004. http://dx.doi.org/10.1159/000078717.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Kam, Peter, Ian Power, Michael J. Cousins, and Philip J. Siddal. "Regulation of Arterial Blood Pressure." In Principles of Physiology for the Anaesthetist, 189–94. Fourth edition. | Boca Raton : CRC Press, Taylor & Francis Group, 2020.: CRC Press, 2020. http://dx.doi.org/10.1201/9780429288210-31.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Mannelli, Massimo, Gian Paolo Rossi, Paul-Emmanuel Vanderriele, and Gabriele Parenti. "The Endocrine Regulation of Blood Pressure." In Endocrinology, 611–25. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-44675-2_23.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Cassis, Lisa A., and Sara B. Police. "Adipose Tissue and Blood Pressure Regulation." In Adipose Tissue in Health and Disease, 245–63. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2010. http://dx.doi.org/10.1002/9783527629527.ch13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Mannelli, Massimo, Gian Paolo Rossi, Paul-Emmanuel Vanderriele, and Gabriele Parenti. "The Endocrine Regulation of Blood Pressure." In Endocrinology, 1–15. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27318-1_23-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Rocchini, Albert P. "Childhood Obesity and Blood Pressure Regulation." In Pediatric Hypertension, 301–28. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-824-9_17.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Rocchini, Albert P. "Childhood Obesity and Blood Pressure Regulation." In Pediatric Hypertension, 307–34. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-797-0_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Blood pressure regulation"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
10

Garg, Sunidhi, and Swati Sondhi. "Design of Fuzzy PID Controller for Mean Arterial Blood Pressure Regulation." In Modelling, Simulation and Identification / 854: Intelligent Systems and Control. Calgary,AB,Canada: ACTAPRESS, 2017. http://dx.doi.org/10.2316/p.2017.854-004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Blood pressure regulation' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography