Log in

Relevant bibliographies by topics / Cardiovascular receptors / Journal articles

To see the other types of publications on this topic, follow the link: Cardiovascular receptors.

Journal articles on the topic 'Cardiovascular receptors'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Cardiovascular receptors.'

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.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Luft, Friedrich C. "Activating Autoantibodies and Cardiovascular Disease." Physiology 28, no. 4 (July 2013): 254–61. http://dx.doi.org/10.1152/physiol.00014.2013.

Full text

Abstract:

Stimulating antibodies against G-protein-coupled receptors, including the β1- and β2-adrenergic receptors, the α1-adrenergic receptor, and the angiotensin II AT1 receptor, have been described, as well as activating antibodies directed at the platelet-derived growth factor receptor tyrosine kinase. Their existence and actions appear to be established. Lacking are mechanistic studies of receptor activation and translational studies to document receptor-stimulating antibodies as worthwhile therapeutic targets.

APA, Harvard, Vancouver, ISO, and other styles

2

Srejovic, Ivan, Vladimir Jakovljevic, Vladimir Zivkovic, and Dragan Djuric. "Possible Role of N-Methyl-D-Aspartate Receptors in Physiology and Pathophysiology of Cardiovascular System." Serbian Journal of Experimental and Clinical Research 20, no. 1 (March 1, 2019): 3–13. http://dx.doi.org/10.1515/sjecr-2017-0010.

Full text

Abstract:

Abstract N-methyl-D-aspartate (NMDA) receptors belong to ionotropic glutamate receptor family, together with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, kainite receptors and δ-receptors. All of these receptors are tetramers composed of four subunits. NMDA receptors have several unique features in relation to other ionotropic glutamate receptors: requirement for simultaneous action of two coagonists, glutamate and glycine; dual control of receptor activation, ligand-dependent (by glutamate and glycine) and voltage-dependent (Mg2+ block) control; and influx of considerable amounts of Ca2+ following receptor activation. Increasing number of researches deals with physiological and pathophysiological roles of NMDA receptors outside of nerve tissues, especially in the cardiovascular system. NMDA receptors are found in all cell types represented in cardiovascular system, and their overstimulation in pathological conditions, such as hyperhomocysteinemia, is related to a range of cardiovascular disorders. On the other hand we demonstrated that blockade of NMDA receptors depresses heart function. There is a need for the intensive study of NMDA receptor in cardiovascular system as potential theraputical target both in prevention and treatment of cardiovascular disorders.

APA, Harvard, Vancouver, ISO, and other styles

3

KUNAPULI, Satya P., and James L. DANIEL. "P2 receptor subtypes in the cardiovascular system." Biochemical Journal 336, no. 3 (December 15, 1998): 513–23. http://dx.doi.org/10.1042/bj3360513.

Full text

Abstract:

Extracellular nucleotides have been implicated in a number of physiological functions. Nucleotides act on cell-surface receptors known as P2 receptors, of which several subtypes have been cloned. Both ATP and ADP are stored in platelets and are released upon platelet activation. Furthermore, nucleotides are also released from damaged or broken cells. Thus during vascular injury nucleotides play an important role in haemostasis through activation of platelets, modulation of vascular tone, recruitment of neutrophils and monocytes to the site of injury, and facilitation of adhesion of leucocytes to the endothelium. Nucleotides also moderate these functions by generating nitric oxide and prostaglandin I2 through activation of endothelial cells, and by activating different receptor subtypes on vascular smooth muscle cells. In the heart, P2 receptors regulate contractility through modulation of L-type Ca2+ channels, although the molecular mechanisms involved are still under investigation. Classical pharmacological studies have identified several P2 receptor subtypes in the cardiovascular system. Molecular pharmacological studies have clarified the nature of some of these receptors, but have complicated the picture with others. In platelets, the classical P2T receptor has now been resolved into three P2 receptor subtypes: the P2Y1, P2X1 and P2TAC receptors (the last of these, which is coupled to the inhibition of adenylate cyclase, is yet to be cloned). In peripheral blood leucocytes, endothelial cells, vascular smooth muscle cells and cardiomyocytes, the effects of classical P2X, P2Y and P2U receptors have been found to be mediated by more than one P2 receptor subtype. However, the exact functions of these multiple receptor subtypes remain to be understood, as P2-receptor-selective agonists and antagonists are still under development.

APA, Harvard, Vancouver, ISO, and other styles

4

Skaper, Stephen D., Patrizia Debetto, and Pietro Giusti. "P2 Receptors in Neurological and Cardiovascular Disorders." Cardiovascular Psychiatry and Neurology 2009 (June 24, 2009): 1–13. http://dx.doi.org/10.1155/2009/861324.

Full text

Abstract:

P2X receptors are ATP-gated cation channels that mediate fast excitatory transmission in diverse regions of the brain and spinal cord. Several P2X receptor subtypes, including P2, have the unusual property of changing their ion selectivity during prolonged exposure to ATP, which results in a channel pore permeable to molecules as large as 900 daltons. The P2 receptor was originally described in cells of hematopoietic origin, and mediates the influx of and and and ions as well as the release of proinflammatory cytokines. P2 receptors may affect neuronal cell death through their ability to regulate the processing and release of interleukin-1, a key mediator in neurodegeneration, chronic inflammation, and chronic pain. Activation of P2, a key mediator in neurodegeneration, chronic inflammation, and chronic pain. Activation of P2 receptors provides an inflammatory stimulus, and P2 receptor-deficient mice have substantially attenuated inflammatory responses, including models of neuropathic and chronic inflammatory pain. Moreover, P2 receptor activity, by regulating the release of proinflammatory cytokines, may be involved in the pathophysiology of depression. Apoptotic cell death occurs in a number of vascular diseases, including atherosclerosis, restenosis, and hypertension, and may be linked to the release of ATP from endothelial cells, P2 receptor activation, proinflammatory cytokine production, and endothelial cell apoptosis. In this context, the P2 receptor may be viewed as a gateway of communication between the nervous, immune, and cardiovascular systems.

APA, Harvard, Vancouver, ISO, and other styles

5

Fenouillet, Emmanuel, Giovanna Mottola, Nathalie Kipson, Franck Paganelli, Régis Guieu, and Jean Ruf. "Adenosine Receptor Profiling Reveals an Association between the Presence of Spare Receptors and Cardiovascular Disorders." International Journal of Molecular Sciences 20, no. 23 (November 27, 2019): 5964. http://dx.doi.org/10.3390/ijms20235964.

Full text

Abstract:

Adenosine and its receptors exert a potent control on the cardiovascular system. This review aims to present emerging experimental evidence supporting the existence and implication in cardiovascular disorders of specific adenosinergic pharmacological profiles, conforming to the concept of “receptor reserve”, also known as “spare receptors”. This kind of receptors allow agonists to achieve their maximal effect without occupying all of the relevant cell receptors. In the cardiovascular system, spare adenosine receptors appear to compensate for a low extracellular adenosine level and/or a low adenosine receptor number, such as in coronary artery disease or some kinds of neurocardiogenic syncopes. In both cases, the presence of spare receptors appears to be an attempt to overcome a weak interaction between adenosine and its receptors. The identification of adenosine spare receptors in cardiovascular disorders may be helpful for diagnostic purposes.

APA, Harvard, Vancouver, ISO, and other styles

6

Jeong, Jin Kwon, Julie A. Horwath, Hayk Simonyan, Katherine A. Blackmore, Scott D. Butler, and Colin N. Young. "Subfornical organ insulin receptors tonically modulate cardiovascular and metabolic function." Physiological Genomics 51, no. 8 (August 1, 2019): 333–41. http://dx.doi.org/10.1152/physiolgenomics.00021.2019.

Full text

Abstract:

Insulin acts within the central nervous system through the insulin receptor to influence both metabolic and cardiovascular physiology. While a major focus has been placed on hypothalamic regions, participation of extrahypothalamic insulin receptors in cardiometabolic regulation remains largely unknown. We hypothesized that insulin receptors in the subfornical organ (SFO), a forebrain circumventricular region devoid of a blood-brain barrier, are involved in metabolic and cardiovascular regulation. Immunohistochemistry in mice revealed widespread insulin receptor-positive cells throughout the rostral to caudal extent of the SFO. SFO-targeted adenoviral delivery of Cre-recombinase in insulin receptorlox/lox mice resulted in sufficient ablation of insulin receptors in the SFO. Interestingly, when mice were maintained on a normal chow diet, deletion of SFO insulin receptors resulted in greater weight gain and adiposity, relative to controls, independently of changes in food intake. In line with this, ablation of insulin receptors in the SFO was associated with marked hepatic steatosis and hypertriglyceridemia. Selective removal of SFO insulin receptors also resulted in a lower mean arterial blood pressure, which was primarily due to a reduction in diastolic blood pressure, whereas systolic blood pressure remained unchanged. Cre-mediated targeting of SFO insulin receptors did not influence heart rate. These data demonstrate multidirectional roles for insulin receptor signaling in the SFO, with ablation of SFO insulin receptors resulting in an overall deleterious metabolic state while at the same time maintaining blood pressure at low levels. These novel findings further suggest that alterations in insulin receptor signaling in the SFO could contribute to metabolic syndrome phenotypes.

APA, Harvard, Vancouver, ISO, and other styles

7

Rickard, Amanda J., and Morag J. Young. "Corticosteroid receptors, macrophages and cardiovascular disease." Journal of Molecular Endocrinology 42, no. 6 (January 21, 2009): 449–59. http://dx.doi.org/10.1677/jme-08-0144.

Full text

Abstract:

The mineralocorticoid receptor (MR) and glucocorticoid receptor are ligand-activated transcription factors that have important physiological and pathophysiological actions in a broad range of cell types including monocytes and macrophages. While the glucocorticoids cortisol and corticosterone have well-described anti-inflammatory actions on both recruited and tissue resident macrophages, a role for the mineralocorticoid aldosterone in these cells is largely undefined. Emerging evidence, however, suggests that MR signalling may promote pro-inflammatory effects. This review will discuss the current understanding of the role of corticosteroid receptors in macrophages and their effect on diseases involving inflammation, with a particular focus on cardiovascular disease.

APA, Harvard, Vancouver, ISO, and other styles

8

Strassheim, Derek, Alexander Verin, Robert Batori, Hala Nijmeh, Nana Burns, Anita Kovacs-Kasa, Nagavedi S. Umapathy, et al. "P2Y Purinergic Receptors, Endothelial Dysfunction, and Cardiovascular Diseases." International Journal of Molecular Sciences 21, no. 18 (September 18, 2020): 6855. http://dx.doi.org/10.3390/ijms21186855.

Full text

Abstract:

Purinergic G-protein-coupled receptors are ancient and the most abundant group of G-protein-coupled receptors (GPCRs). The wide distribution of purinergic receptors in the cardiovascular system, together with the expression of multiple receptor subtypes in endothelial cells (ECs) and other vascular cells demonstrates the physiological importance of the purinergic signaling system in the regulation of the cardiovascular system. This review discusses the contribution of purinergic P2Y receptors to endothelial dysfunction (ED) in numerous cardiovascular diseases (CVDs). Endothelial dysfunction can be defined as a shift from a “calm” or non-activated state, characterized by low permeability, anti-thrombotic, and anti-inflammatory properties, to a “activated” state, characterized by vasoconstriction and increased permeability, pro-thrombotic, and pro-inflammatory properties. This state of ED is observed in many diseases, including atherosclerosis, diabetes, hypertension, metabolic syndrome, sepsis, and pulmonary hypertension. Herein, we review the recent advances in P2Y receptor physiology and emphasize some of their unique signaling features in pulmonary endothelial cells.

APA, Harvard, Vancouver, ISO, and other styles

9

Brown, Lindsay, and Conrad Sernia. "ANGIOTENSIN RECEPTORS IN CARDIOVASCULAR DISEASES." Clinical and Experimental Pharmacology and Physiology 21, no. 10 (October 1994): 811–18. http://dx.doi.org/10.1111/j.1440-1681.1994.tb02450.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Baysal, Kemal, and Douglas W. Losordo. "OESTROGEN RECEPTORS AND CARDIOVASCULAR DISEASE." Clinical and Experimental Pharmacology and Physiology 23, no. 6-7 (July 1996): 537–48. http://dx.doi.org/10.1111/j.1440-1681.1996.tb02775.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

McShane, Lucy, Ira Tabas, Greg Lemke, Mariola Kurowska-Stolarska, and Pasquale Maffia. "TAM receptors in cardiovascular disease." Cardiovascular Research 115, no. 8 (April 13, 2019): 1286–95. http://dx.doi.org/10.1093/cvr/cvz100.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Maack, Thomas. "Cardiovascular receptors as drug targets." Molecular Medicine Today 3, no. 3 (March 1997): 101–2. http://dx.doi.org/10.1016/s1357-4310(97)01007-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Villalón, Carlos M., Peter de Vries, and Pramod R. Saxena. "Serotonin receptors as cardiovascular targets." Drug Discovery Today 2, no. 7 (July 1997): 294–300. http://dx.doi.org/10.1016/s1359-6446(97)01055-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Osborne, Nick, and Didier Y. R. Stainier. "Lipid Receptors in Cardiovascular Development." Annual Review of Physiology 65, no. 1 (March 2003): 23–43. http://dx.doi.org/10.1146/annurev.physiol.65.092101.142235.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

WANG, WenJing, ZiJian LI, KaiHang GUAN, and ErDan DONG. "Adrenergic receptors and cardiovascular diseases." SCIENTIA SINICA Vitae 50, no. 8 (June 19, 2020): 791–801. http://dx.doi.org/10.1360/ssv-2020-0090.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Funder, John W. "Mineralocorticoid Receptors and Cardiovascular Damage." Hypertension 47, no. 4 (April 2006): 634–35. http://dx.doi.org/10.1161/01.hyp.0000203732.03784.3b.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

BOUSQUET, PASCAL, HUGUES GRENEY, FATIMA BENNAI, JOSIANE FELDMAN, JEANNE STUTZMANN, ALAIN BELCOURT, and MONIQUE DONTENWILL. "Imidazoline Receptors and Cardiovascular Regulations." Annals of the New York Academy of Sciences 763, no. 1 The Imidazoli (July 1995): 526–30. http://dx.doi.org/10.1111/j.1749-6632.1995.tb32446.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Liang, Bruce T. "Adenosine receptors and cardiovascular function." Trends in Cardiovascular Medicine 2, no. 3 (May 1992): 100–108. http://dx.doi.org/10.1016/1050-1738(92)90014-j.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Guieu, Régis, Michele Brignole, Jean Claude Deharo, Pierre Deharo, Giovanna Mottola, Antonella Groppelli, Franck Paganelli, and Jean Ruf. "Adenosine Receptor Reserve and Long-Term Potentiation: Unconventional Adaptive Mechanisms in Cardiovascular Diseases?" International Journal of Molecular Sciences 22, no. 14 (July 15, 2021): 7584. http://dx.doi.org/10.3390/ijms22147584.

Full text

Abstract:

While the concept of a receptor reserve (spare receptors) is old, their presence on human cells as an adaptive mechanism in cardiovascular disease is a new suggestion. The presence of spare receptors is suspected when the activation of a weak fraction of receptors leads to maximal biological effects, in other words, when the half-maximal effective concentration (EC50) for a biological effect (cAMP production, for example) is lower than the affinity (KD) of the ligand for a receptor. Adenosine is an ATP derivative that strongly impacts the cardiovascular system via its four membrane receptors, named A1R, A2AR, A2BR, and A3R, with the A1R being more particularly involved in heart rhythm, while the A2AR controls vasodilation. After a general description of the tools necessary to explore the presence of spare receptors, this review focuses on the consequences of the presence of spare adenosine receptors in cardiovascular physiopathology. Finally, the role of the adenosinergic system in the long-term potentiation and its possible consequences on the physiopathology are also mentioned.

APA, Harvard, Vancouver, ISO, and other styles

20

Saternos, Hannah C., Daniyah A. Almarghalani, Hayley M. Gibson, Mahmood A. Meqdad, Raymond B. Antypas, Ajay Lingireddy, and Wissam A. AbouAlaiwi. "Distribution and function of the muscarinic receptor subtypes in the cardiovascular system." Physiological Genomics 50, no. 1 (January 1, 2018): 1–9. http://dx.doi.org/10.1152/physiolgenomics.00062.2017.

Full text

Abstract:

Muscarinic acetylcholine receptors belong to the G protein-coupled receptor superfamily and are widely known to mediate numerous functions within the central and peripheral nervous system. Thus, they have become attractive therapeutic targets for various disorders. It has long been known that the parasympathetic system, governed by acetylcholine, plays an essential role in regulating cardiovascular function. Unfortunately, due to the lack of pharmacologic selectivity for any one muscarinic receptor, there was a minimal understanding of their distribution and function within this region. However, in recent years, advancements in research have led to the generation of knockout animal models, better antibodies, and more selective ligands enabling a more thorough understanding of the unique role muscarinic receptors play in the cardiovascular system. These advances have shown muscarinic receptor 2 is no longer the only functional subtype found within the heart and muscarinic receptors 1 and 3 mediate both dilation and constriction in the vasculature. Although muscarinic receptors 4 and 5 are still not well characterized in the cardiovascular system, the recent generation of knockout animal models will hopefully generate a better understanding of their function. This mini review aims to summarize recent findings and advances of muscarinic involvement in the cardiovascular system.

APA, Harvard, Vancouver, ISO, and other styles

21

Paris, Andrea, Melanie Philipp, Peter H. Tonner, Markus Steinfath, Martin Lohse, Jens Scholz, and Lutz Hein. "Activation of α2B-Adrenoceptors Mediates the Cardiovascular Effects of Etomidate." Anesthesiology 99, no. 4 (October 1, 2003): 889–95. http://dx.doi.org/10.1097/00000542-200310000-00022.

Full text

Abstract:

Background The intravenous anesthetic etomidate exhibits structural similarities to specific alpha2-adrenoceptor agonists of the type such as dexmedetomidine. The current study was performed to elucidate the possible interaction of etomidate with alpha2-adrenoceptors in mice lacking individual alpha2-adrenoceptor subtypes (alpha2-KO). Methods Sedative and cardiovascular responses to etomidate and the alpha2-agonist, dexmedetomidine, were determined in mice deficient in alpha2-receptor subtypes. Inhibition of binding of the alpha2-receptor antagonist [3H]RX821002 to recombinant alpha2-receptors by etomidate was tested in human embryonic kidney (HEK293) cells in vitro. Results In vivo, loss and recovery of the righting reflex required similar times after intraperitoneal injection of etomidate in wild-type and in alpha2A-receptor-deficient mice, indicating that the hypnotic effect of etomidate in mice does not require the alpha2A-receptor subtype. Intravenous injection of etomidate resulted in a transient increase (duration 2.4 +/- 0.2 min) in arterial blood pressure in wild-type mice (17 +/- 3 mmHg). Etomidate did not affect blood pressure in alpha2B-KO or alpha2AB-KO mice. In membranes from HEK293 cells transfected with alpha2-receptors, etomidate inhibited binding of the alpha2-antagonist, [3H]RX821002, with higher potency from alpha2B- and alpha2C-receptors than from alpha2A-receptors (Ki alpha2A 208 microm, alpha2B 26 microm, alpha2C 56 microm). In alpha2B-receptor-expressing HEK293 cells, etomidate rapidly increased phosphorylation of the extracellular signal-related kinases ERK1/2. Conclusions These results indicate that etomidate acts as an agonist at alpha2-adrenoceptors, which appears in vivo primarily as an alpha2B-receptor-mediated increase in blood pressure. This effect of etomidate may contribute to the cardiovascular stability of patients after induction of anesthesia with etomidate.

APA, Harvard, Vancouver, ISO, and other styles

22

Leger, Andrew J., Lidija Covic, and Athan Kuliopulos. "Protease-Activated Receptors in Cardiovascular Diseases." Circulation 114, no. 10 (September 5, 2006): 1070–77. http://dx.doi.org/10.1161/circulationaha.105.574830.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Gencer, Selin, Emiel van der Vorst, Maria Aslani, Christian Weber, Yvonne Döring, and Johan Duchene. "Atypical Chemokine Receptors in Cardiovascular Disease." Thrombosis and Haemostasis 119, no. 04 (February 4, 2019): 534–41. http://dx.doi.org/10.1055/s-0038-1676988.

Full text

Abstract:

AbstractInflammation has been well recognized as one of the main drivers of atherosclerosis development and therefore cardiovascular diseases (CVDs). It has been shown that several chemokines, small 8 to 12 kDa cytokines with chemotactic properties, play a crucial role in the pathophysiology of atherosclerosis. Chemokines classically mediate their effects by binding to G-protein-coupled receptors called chemokine receptors. In addition, chemokines can also bind to atypical chemokine receptors (ACKRs). ACKRs fail to induce G-protein-dependent signalling pathways and thus subsequent cellular response, but instead are able to internalize, scavenge or transport chemokines. In this review, we will give an overview of the current knowledge about the involvement of ACKR1–4 in CVDs and especially in atherosclerosis development. In the recent years, several studies have highlighted the importance of ACKRs in CVDs, although there are still several controversies and unexplored aspects that have to be further elucidated. A better understanding of the precise role of these atypical receptors may pave the way towards novel and improved therapeutic strategies.

APA, Harvard, Vancouver, ISO, and other styles

24

Ludbrook, J. "Cardiovascular reflexes from cardiac sensory receptors." Australian and New Zealand Journal of Medicine 20, no. 4 (August 1990): 597–606. http://dx.doi.org/10.1111/j.1445-5994.1990.tb01325.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Gomez Sanchez, Elise P. "Central Mineralocorticoid Receptors and Cardiovascular Disease." Neuroendocrinology 90, no. 3 (2009): 245–50. http://dx.doi.org/10.1159/000227807.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

? "I1 receptors, cardiovascular function, and metabolism." American Journal of Hypertension 14, no. 11 (November 2001): A264. http://dx.doi.org/10.1016/s0895-7061(01)02057-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Williams, David Y. "CARDIOVASCULAR FUNCTION OF PERIPHERAL DOPAMINE RECEPTORS." Chest 98, no. 4 (October 1990): 21. http://dx.doi.org/10.1016/s0012-3692(16)34431-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

DEKLEIJN, D., and G. PASTERKAMP. "Toll-like receptors in cardiovascular diseases." Cardiovascular Research 60, no. 1 (October 15, 2003): 58–67. http://dx.doi.org/10.1016/s0008-6363(03)00348-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

BOUSQUET, P. "I1 receptors, cardiovascular function, and metabolism." American Journal of Hypertension 14, no. 11 (November 2001): S317—S321. http://dx.doi.org/10.1016/s0895-7061(01)02238-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Mary, David A. S. G. "Cardiovascular Receptors and the Coronary Circulation." Clinical Science 77, no. 1 (July 1, 1989): 1–5. http://dx.doi.org/10.1042/cs0770001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Kebabian, John. "Cardiovascular function of peripheral dopamine receptors." Trends in Pharmacological Sciences 11, no. 10 (October 1990): 430. http://dx.doi.org/10.1016/0165-6147(90)90152-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Domenico, Regoli. "Kinin receptors in the cardiovascular system." Regulatory Peptides 64, no. 1-3 (July 1996): 160. http://dx.doi.org/10.1016/0167-0115(96)88040-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Perrot-Applanat, Martine. "Estrogen receptors in the cardiovascular system." Steroids 61, no. 4 (April 1996): 212–15. http://dx.doi.org/10.1016/0039-128x(96)00016-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Olsson, Ray A. "Adenosine receptors in the cardiovascular system." Drug Development Research 39, no. 3-4 (November 1996): 301–7. http://dx.doi.org/10.1002/(sici)1098-2299(199611/12)39:3/4<301::aid-ddr9>3.0.co;2-v.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Ralevic, Vera. "P2X receptors in the cardiovascular system." Wiley Interdisciplinary Reviews: Membrane Transport and Signaling 1, no. 5 (August 6, 2012): 663–74. http://dx.doi.org/10.1002/wmts.58.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Aryan, Laila, David Younessi, Michael Zargari, Somanshu Banerjee, Jacqueline Agopian, Shadie Rahman, Reza Borna, Gregoire Ruffenach, Soban Umar, and Mansoureh Eghbali. "The Role of Estrogen Receptors in Cardiovascular Disease." International Journal of Molecular Sciences 21, no. 12 (June 17, 2020): 4314. http://dx.doi.org/10.3390/ijms21124314.

Full text

Abstract:

Cardiovascular Diseases (CVDs) are the leading cause of death globally. More than 17 million people die worldwide from CVD per year. There is considerable evidence suggesting that estrogen modulates cardiovascular physiology and function in both health and disease, and that it could potentially serve as a cardioprotective agent. The effects of estrogen on cardiovascular function are mediated by nuclear and membrane estrogen receptors (ERs), including estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), and G-protein-coupled ER (GPR30 or GPER). Receptor binding in turn confers pleiotropic effects through both genomic and non-genomic signaling to maintain cardiovascular homeostasis. Each ER has been implicated in multiple pre-clinical cardiovascular disease models. This review will discuss current reports on the underlying molecular mechanisms of the ERs in regulating vascular pathology, with a special emphasis on hypertension, pulmonary hypertension, and atherosclerosis, as well as in regulating cardiac pathology, with a particular emphasis on ischemia/reperfusion injury, heart failure with reduced ejection fraction, and heart failure with preserved ejection fraction.

APA, Harvard, Vancouver, ISO, and other styles

37

HONORÉ, Jean-Claude, Caroline PROTEAU, and Pedro D'ORLÉANS-JUSTE. "Endothelin B receptors located on the endothelium provide cardiovascular protection in the hamster." Clinical Science 103, s2002 (September 1, 2002): 280S—283S. http://dx.doi.org/10.1042/cs103s280s.

Full text

Abstract:

Endothelins (ETs) act through two receptors, namely ETA and ETB. In the cardiovascular system, the activation of both receptors leads to vasoconstriction. However, ETB receptors also mediate endothelium-dependent vasodilatation and clearance of plasma ET-1. With regard to these latter properties, we wanted to assess the contribution of ETB receptors and the effects of selective and mixed ET receptor blockade on vascular tone in control Syrian Golden hamsters and in Bio 14.6 cardiomyopathic hamsters after bolus injection of ET-1 and IRL-1620, a selective ETB agonist. In 12-week-old anaesthetized control hamsters, ET-1 (0.5nmol/kg) induced a sustained pressor response which was only partly reduced by the selective ETA receptor antagonist BQ-123, suggesting a contribution of ETB receptor activation to the vasoconstrictive effects of ET-1. This was confirmed by injection of the selective ETB receptor agonist IRL-1620 (1 nmol/kg). However, the pressor response to this agonist was always preceded by a transient vasodilatation, indicating activation of endothelium-located ETB receptors. When the selective ETB receptor antagonist BQ-788 was administered, the hypotensive phase following IRL-1620 injection was abolished. Interestingly, BQ-788 or a mixture of BQ-788 and BQ-123 significantly potentiated the pressor responses to ET-1. In 12-week-old Bio 14.6 cardiomyopathic hamsters, ET-1 and IRL-1620 induced haemodynamic responses similar to those observed in control hamsters, although the IRL-1620-induced pressor increase was lower. No difference in cardiac prepro ET-1 mRNA expression was observed between the two strains of hamsters. In conclusion, we suggest that endothelium-located ETB receptors are involved in the physiological antagonism of ET-dependent protracted pressor effects, and thus may play a protective role in both normal hamsters and those with cardiomyopathy.

APA, Harvard, Vancouver, ISO, and other styles

38

Stephen, Sam L., Katie Freestone, Sarah Dunn, Michael W. Twigg, Shervanthi Homer-Vanniasinkam, John H. Walker, Stephen B. Wheatcroft, and Sreenivasan Ponnambalam. "Scavenger Receptors and Their Potential as Therapeutic Targets in the Treatment of Cardiovascular Disease." International Journal of Hypertension 2010 (2010): 1–21. http://dx.doi.org/10.4061/2010/646929.

Full text

Abstract:

Scavenger receptors act as membrane-bound and soluble proteins that bind to macromolecular complexes and pathogens. This diverse supergroup of proteins mediates binding to modified lipoprotein particles which regulate the initiation and progression of atherosclerotic plaques. In vascular tissues, scavenger receptors are implicated in regulating intracellular signaling, lipid accumulation, foam cell development, and cellular apoptosis or necrosis linked to the pathophysiology of atherosclerosis. One approach is using gene therapy to modulate scavenger receptor function in atherosclerosis. Ectopic expression of membrane-bound scavenger receptors using viral vectors can modify lipid profiles and reduce the incidence of atherosclerosis. Alternatively, expression of soluble scavenger receptors can also block plaque initiation and progression. Inhibition of scavenger receptor expression using a combined gene therapy and RNA interference strategy also holds promise for long-term therapy. Here we review our current understanding of the gene delivery by viral vectors to cells and tissues in gene therapy strategies and its application to the modulation of scavenger receptor function in atherosclerosis.

APA, Harvard, Vancouver, ISO, and other styles

39

Corinaldesi, Giorgio. "Platelet Activation in Cardiovascular Disease." Blood 118, no. 21 (November 18, 2011): 5242. http://dx.doi.org/10.1182/blood.v118.21.5242.5242.

Full text

Abstract:

Abstract 5242 Platelets play a pivotal role in the pathogenesis of coronary artery disease (CAD). Among a number of platelet integrin receptors ITGA2B and ITGB3 appear to be fundamental mediators of platelet aggregation as they interact with fibrinogen, VWF, fibronectin, vitronectin, and thrombospondin; for these major properties these two receptors are risk-determining factors for increased platelet thrombogenicity, enhancement of leukocytes trafficking and activation by CD11a/CD18 (LFA-1) and CD11b/CD18 (MAC-1), thus leading to CAD. Receptor clustering promote cell adhesion by increasing the number of ligand receptor bonds GPIb-IX-VWF, fibrinogen /alfaIIb-beta 3 which promote platelet aggregation; this is showed by various parameters including increased platelet-monocyte aggregates, P-selectin (CD62P), CD42b, CD63, and EMMPRIN (CD147). The link between platelet activation, leukocyte recruitment, endothelial dysfunction, progression of atherosclerosis plaque and CAD has been demonstrated through the involvement of inflammatory cytokines that play a central role in the development of atherosclerotic plaques with MCP-1, CCL-2, Rantes, IL-8, and CD40L. In this study, we investigated a total of 38 subjects (mean age of 62 +/− 6 years) with confirmed CAD (unstable angina: 18 patients; ST elevation myocardial infarction: 20 patients) on coronary angiography and 32 controls. They were examined for CD62P, CD63, CD42b, and CD147 expression, troponin level, creatine-kinase-MB level (indicator of myocardial injury), C-reactive protein, and IL-6 (being both indicators of systemic inflammation). Patients with CAD had significantly higher markers of platelet activation (p<0.001) which were constituted by the expression of GP receptors (CD62P/PSGL-1, CD162, CD61/63, CD147). This activity closely correlates with a significant increase of acute phase reactant in cases than in controls (p<0.0001), and mostly, it confirmed that these associations may be largely responsible of cardiovascular events. Disclosures: No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

40

Liu, Samuel, Preston J. Anderson, Sudarshan Rajagopal, Robert J. Lefkowitz, and Howard A. Rockman. "G Protein-Coupled Receptors: A Century of Research and Discovery." Circulation Research 135, no. 1 (June 21, 2024): 174–97. http://dx.doi.org/10.1161/circresaha.124.323067.

Full text

Abstract:

GPCRs (G protein-coupled receptors), also known as 7 transmembrane domain receptors, are the largest receptor family in the human genome, with ≈800 members. GPCRs regulate nearly every aspect of human physiology and disease, thus serving as important drug targets in cardiovascular disease. Sharing a conserved structure comprised of 7 transmembrane α-helices, GPCRs couple to heterotrimeric G-proteins, GPCR kinases, and β-arrestins, promoting downstream signaling through second messengers and other intracellular signaling pathways. GPCR drug development has led to important cardiovascular therapies, such as antagonists of β-adrenergic and angiotensin II receptors for heart failure and hypertension, and agonists of the glucagon-like peptide-1 receptor for reducing adverse cardiovascular events and other emerging indications. There continues to be a major interest in GPCR drug development in cardiovascular and cardiometabolic disease, driven by advances in GPCR mechanistic studies and structure-based drug design. This review recounts the rich history of GPCR research, including the current state of clinically used GPCR drugs, and highlights newly discovered aspects of GPCR biology and promising directions for future investigation. As additional mechanisms for regulating GPCR signaling are uncovered, new strategies for targeting these ubiquitous receptors hold tremendous promise for the field of cardiovascular medicine.

APA, Harvard, Vancouver, ISO, and other styles

41

Sadykova, D. I., R. R. Nigmatullina, and G. N. Aflyatumova. "The role of serotonergic system in cardiovascular diseases development in children." Kazan medical journal 96, no. 4 (August 15, 2015): 665–69. http://dx.doi.org/10.17750/kmj2015-665.

Full text

Abstract:

The role of the serotonin system as a link in the pathogenesis of atherosclerosis and arterial hypertension is widely discussed during the recent decades. Serotonin and histamine are part of humoral system of physiological processes regulators and modulators which under pathological conditions are transformed into factors contributing to the disease development. The membrane serotonin transporter has been identified on neurons, platelets, myocardium and smooth muscle cells. The higher is the activity of membrane transporter, the higher is the platelet serotonin concentration, its release into the blood plasma increases thus implementing its negative effects on platelets and wall of the vessels. 5-HT1A, 5-HT2 and 5-HT3 receptor subtypes play a key role in the central mechanisms of regulation of cardiovascular activities while peripheral effects of serotonin on the vascular system are mediated by 5-HT1, 5-HT2, 5-HT3, 5-HT4 and 5-HT7 receptor subtypes. Activation of 5-HT1A receptors causes inhibition of central sympathetic influences and further bradycardia, while 5-HT2 receptors activation - arousal of the sympathetic division, blood pressure elevation, and tachycardia. With the development of anaerobic processes serotonin via 5-HT2 receptors triggers apoptosis of cardiomyocytes leading to the development and progression of heart failure. Participation of 5HT2B receptors in the regulation of heart development during embryogenesis was shown on the mutant mice: cardiomyopathy with ventricular mass loss due to reduction of cardiomyocytes number and size was revealed. The involvement of 5-HT4 receptors in the development of sinus tachycardia and atrial fibrillation; in turn, the use of 5-HT4 receptor antagonists proved to be effective in the treatment of this kind of arrhythmias. Therefore, the study of the serotonergic system role in the development of cardiovascular diseases will allow to open new links in the pathogenesis of arterial hypertension in childhood.

APA, Harvard, Vancouver, ISO, and other styles

42

Durik, Matej, Bruno Sevá Pessôa, and Anton J. M. Roks. "The renin–angiotensin system, bone marrow and progenitor cells." Clinical Science 123, no. 4 (April 24, 2012): 205–23. http://dx.doi.org/10.1042/cs20110660.

Full text

Abstract:

Modulation of the RAS (renin–angiotensin system), in particular of the function of the hormones AngII (angiotensin II) and Ang-(1–7) [angiotensin-(1–7)], is an important target for pharmacotherapy in the cardiovascular system. In the classical view, such modulation affects cardiovascular cells to decrease hypertrophy, fibrosis and endothelial dysfunction, and improves diuresis. In this view, excessive stimulation of AT1 receptors (AngII type 1 receptors) fulfils a detrimental role, as it promotes cardiovascular pathogenesis, and this is opposed by stimulation of the AT2 receptor (angiotensin II type 2 receptor) and the Ang-(1–7) receptor encoded by the Mas proto-oncogene. In recent years, this view has been broadened with the observation that the RAS regulates bone marrow stromal cells and stem cells, thus involving haematopoiesis and tissue regeneration by progenitor cells. This change of paradigm has enlarged the field of perspectives for therapeutic application of existing as well as newly developed medicines that alter angiotensin signalling, which now stretches beyond cardiovascular therapy. In the present article, we review the role of AngII and Ang-(1–7) and their respective receptors in haematopoietic and mesenchymal stem cells, and discuss possible pharmacotherapeutical implications.

APA, Harvard, Vancouver, ISO, and other styles

43

Bkaily, Ghassan, Levon Avedanian, Johny Al-Khoury, Chantale Provost, Moni Nader, Pedro D'Orléans-Juste, and Danielle Jacques. "Nuclear membrane receptors for ET-1 in cardiovascular function." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 2 (February 2011): R251—R263. http://dx.doi.org/10.1152/ajpregu.00736.2009.

Full text

Abstract:

Plasma membrane endothelin type A (ETA) receptors are internalized and recycled to the plasma membrane, whereas endothelin type B (ETB) receptors undergo degradation and subsequent nuclear translocation. Recent studies show that G protein-coupled receptors (GPCRs) and ion transporters are also present and functional at the nuclear membranes of many cell types. Similarly to other GPCRs, ETA and ETB are present at both the plasma and nuclear membranes of several cardiovascular cell types, including human cardiac, vascular smooth muscle, endocardial endothelial, and vascular endothelial cells. The distribution and density of ETARs in the cytosol (including the cell membrane) and the nucleus (including the nuclear membranes) differ between these cell types. However, the localization and density of ET-1 and ETB receptors are similar in these cell types. The extracellular ET-1-induced increase in cytosolic ([Ca]c) and nuclear ([Ca]n) free Ca2+ is associated with an increase of cytosolic and nuclear reactive oxygen species. The extracellular ET-1-induced increase of [Ca]c and [Ca]n as well as intracellular ET-1-induced increase of [Ca]n are cell-type dependent. The type of ET-1 receptor mediating the extracellular ET-1-induced increase of [Ca]c and [Ca]n depends on the cell type. However, the cytosolic ET-1-induced increase of [Ca]n does not depend on cell type. In conclusion, nuclear membranes' ET-1 receptors may play an important role in overall ET-1 action. These nuclear membrane ET-1 receptors could be targets for a new generation of antagonists.

APA, Harvard, Vancouver, ISO, and other styles

44

Pasanisi, Fabrizio, Lesley Sloan, and Peter C. Rubin. "Cardiovascular Properties of Metkephamid, a δ Opioid Receptor Agonist, in Man." Clinical Science 68, no. 2 (February 1, 1985): 209–13. http://dx.doi.org/10.1042/cs0680209.

Full text

Abstract:

1. Opioid receptors exist in at least three forms: μ, δ and κ. Agonists at μ receptors produce orthostatic hypotension in man by a mechanism involving a reduction in baroreflex sensitivity. We describe here the cardiovascular properties of metkephamid, a relatively selective δ opioid receptor agonist. 2. Blood pressure, heart rate and plasma noradrenaline concentration were measured over a 7 h period in eight normal young male volunteers in the supine position and after 70° 5 min head-up tilt, after receiving metkephamid (50 mg intramuscularly) or placebo. 3. Metkephamid increased heart rate in the supine position with no change in blood pressure or plasma noradrenaline concentration. This was accompanied by symptoms consistent with an anti-muscarinic anticholinergic effect. 4. Head-up tilt resulted in substantial hypotension after metkephamid with an attenuated change in heart rate and no increase in noradrenaline concentration. 5. We conclude that δ as well as μ opioid receptor agonists can produce orthostatic hypotension with attenuation of heart rate response. Metkephamid possesses anticholinergic properties not seen with μ receptor agonists, suggesting a possible role of δ opioid receptors in cholinergic activity.

APA, Harvard, Vancouver, ISO, and other styles

45

CHO, Hyeseon, Kathleen HARRISON, Owen SCHWARTZ, and John H. KEHRL. "The aorta and heart differentially express RGS (regulators of G-protein signalling) proteins that selectively regulate sphingosine 1-phosphate, angiotensin II and endothelin-1 signalling." Biochemical Journal 371, no. 3 (May 1, 2003): 973–80. http://dx.doi.org/10.1042/bj20021769.

Full text

Abstract:

Normal cardiovascular development and physiology depend in part upon signalling through G-protein-coupled receptors (GPCRs), such as the angiotensin II type 1 (AT1) receptor, sphingosine 1-phosphate (S1P) receptors and endothelin-1 (ET-1) receptor. Since regulator of G-protein signalling (RGS) proteins function as GTPase-activating proteins for the Gα subunit of heterotrimeric G-proteins, these proteins undoubtedly have functional roles in the cardiovascular system. In the present paper, we show that human aorta and heart differentially express RGS1, RGS2, RGS3S (short-form), RGS3L (long-form), PDZ-RGS3 (PDZ domain-containing) and RGS4. The aorta prominently expresses mRNAs for all these RGS proteins except PDZ-RGS3. Various stimuli that are critical for both cardiovascular development and function regulate dynamically the mRNA levels of several of these RGS proteins in primary human aortic smooth muscle cells. Both RGS1 and RGS3 inhibit signalling through the S1P1 (formerly known as EDG-1), S1P2 (formerly known as EDG-5) and S1P3 (formerly known as EDG-3) receptors, whereas RGS2 and RGS4 selectively attenuate S1P2-and S1P3-receptor signalling respectively. All of the tested RGS proteins inhibit AT1-receptor signalling, whereas only RGS3 and, to a lesser extent, RGS4 inhibit ETA-receptor signalling. The conspicuous expression of RGS proteins in the cardiovascular system and their selective effects on relevant GPCR-signalling pathways provide additional evidence that they have functional roles in cardiovascular development and physiology.

APA, Harvard, Vancouver, ISO, and other styles

46

Nguyen, Albert, Nathalie Thorin-Trescases, and Eric Thorin. "Working under pressure: coronary arteries and the endothelin system." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 5 (May 2010): R1188—R1194. http://dx.doi.org/10.1152/ajpregu.00653.2009.

Full text

Abstract:

Endogenous endothelin-1-dependent (ET-1) tone in coronary arteries depends on the balance between ETA and ETB receptor-mediated effects and on parameters such as receptor distribution and endothelial integrity. Numerous studies highlight the striking functional interactions that exist between nitric oxide (NO) and ET-1 in the regulation of vascular tone. Many of the cardiovascular complications associated with cardiovascular risk factors and aging are initially attributable, at least in part, to endothelial dysfunction characterized by a dysregulation between NO and ET-1. The contribution of the imbalance between smooth muscle ETA/B and endothelial ETB receptors to this process is poorly understood. An increased contribution of ET-1 that is associated with a proportional decrease in that of NO accompanies the development of coronary endothelial dysfunction, coronary vasospasm, and atherosclerosis. These data form the basis for the rationale of testing therapeutic approaches counteracting ET-1-induced cardiovascular dysfunction. It remains to be determined whether the beneficial role of endothelial ETB receptors declines with age and risk factors for cardiovascular diseases, revealing smooth muscle ETB receptors with proconstricting and proinflammatory activities.

APA, Harvard, Vancouver, ISO, and other styles

47

West, M., and W. Huang. "Spinal cord excitatory amino acids and cardiovascular autonomic responses." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 3 (September 1, 1994): H865—H873. http://dx.doi.org/10.1152/ajpheart.1994.267.3.h865.

Full text

Abstract:

The excitatory amino acid subtype receptor agonists, N-methyl-D-aspartate (NMDA) and (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA, a non-NMDA agonist), produce specific dose-related heart rate and vasoconstrictor responses when given by injection into the upper thoracic or lumbar intrathecal space of the conscious rabbit. The responses are inhibited by prior intrathecal injection of the specific excitatory amino acid subtype receptor antagonist, 2-amino-5-phosphonovaleric acid (AP-5) or 6,7-dinitroquinoxaline-2,3-dione (DNQX), respectively. Baroreceptor heart rate reflex function is inhibited by AP-5 and by DNQX applied to the upper thoracic spinal cord. In contrast baroreflex vasoconstrictor function is blocked by AP-5 but not by DNQX given in the lumbar intrathecal space. The experiments support previous evidence that spinal excitatory amino acids are important as neurotransmitters at the level of the sympathetic preganglionic neuron and as such exert tonic and reflex control of autonomic cardiovascular function. It is concluded that 1) intrathecal activation of NMDA and non-NMDA subtype receptors has similar but independent effects on heart rate and on blood pressure and 2) NMDA receptors alone participate in mediation of baroreflex vasoconstrictor function, whereas both sets of receptors determine reflex sympathetic heart rate effects.

APA, Harvard, Vancouver, ISO, and other styles

48

Wang, Lu, Jinxuan Wang, Jianxiong Xu, Weixi Qin, Yuming Wang, Shisui Luo, and Guixue Wang. "The Role and Molecular Mechanism of P2Y12 Receptors in the Pathogenesis of Atherosclerotic Cardiovascular Diseases." Applied Sciences 11, no. 19 (September 29, 2021): 9078. http://dx.doi.org/10.3390/app11199078.

Full text

Abstract:

The P2Y receptor family is a class of G protein-coupled receptors activated primarily by adenosine triphosphate (ATP), adenosine diphosphate (ADP), uridine triphosphate (UTP) and uridine diphosphate (UDP). The P2Y12 receptor is expressed on platelets which mediates platelet aggregation and morphological changes. At the same time, during the process of vascular remodeling and atherosclerosis, ADP can also promote the migration and proliferation of vascular smooth muscle and endothelial cells through P2Y12 receptor activating. Furthermore, P2Y12 is involved in many signal transductions processes, such as intimal hyperplasia, monocyte infiltration and so on, which play an important role in immune inflammation and brain injury. In order to solve the diseases induced by P2Y12 receptor, inhibitors such as ticagrelor, clopidogrel were widely used for cardiovascular diseases. However, there were some problems, such as limited antithrombotic effect, remain unsolved. This article summarizes the role and molecular mechanism of P2Y12 receptors in the pathogenesis of cardiovascular-related diseases, providing in-depth expounding on the molecular mechanism of P2Y12 receptor inhibitors and contributing to the treatment of diseases based on P2Y12 receptors.

APA, Harvard, Vancouver, ISO, and other styles

49

Schiffrin, Ernesto L. "Peroxisome proliferator-activated receptors and cardiovascular remodeling." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 3 (March 2005): H1037—H1043. http://dx.doi.org/10.1152/ajpheart.00677.2004.

Full text

Abstract:

Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that heterodimerize with the retinoid X receptor and then modulate the function of many target genes. Three PPARs are known: α, β/δ, and γ. The better known are PPAR-α and PPAR-γ, which may be activated by different synthetic agonists, although the endogenous ligands are unknown. PPAR-α is involved in fatty acid oxidation and expressed in the liver, kidney, and skeletal muscle, whereas PPAR-γ is involved in fat cell differentiation, lipid storage, and insulin sensitivity. However, both have been shown to be present in variable amounts in cardiovascular tissues, including endothelium, smooth muscle cells, macrophages, and the heart. The activators of PPAR-α (fibrates) and PPAR-γ (thiazolidinediones or glitazones) antagonized the actions of angiotensin II in vivo and in vitro and exerted cardiovascular antioxidant and anti-inflammatory effects. PPAR activators lowered blood pressure, induced favorable effects on the heart, and corrected vascular structure and endothelial dysfunction in several rodent models of hypertension. Activators of PPARs may become therapeutic agents useful in the prevention of cardiovascular disease beyond their effects on carbohydrate and lipid metabolism. Some side effects, such as weight gain, as well as documented aggravation of advanced heart failure through fluid retention by glitazones, may, however, limit their therapeutic application in prevention of cardiovascular disease.

APA, Harvard, Vancouver, ISO, and other styles

50

BAL, Nur Banu, Mecit Orhan ULUDAĞ, and Emine DEMİREL YILMAZ. "Liver X Receptors in the Cardiovascular System." Turkiye Klinikleri Journal of Medical Sciences 39, no. 4 (2019): 430–43. http://dx.doi.org/10.5336/medsci.2019-70199.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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!