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Angiotensin II and inflammation: the effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockade.
J Hum Hypertens 2007; 21(1):20-7JH

Abstract

Angiotensin II (Ang II) increases adhesion molecules, cytokines and chemokines and exerts a proinflammatory effect on leucocytes, endothelial cells and vascular smooth muscle cells. Acting via the type 1 receptor, Ang II initiates an inflammatory cascade of reduced nicotinamide-adenine dinucleotide phosphate oxidase, reactive oxygen species (ROS) and nuclear factor-kappaB, which mediates transcription and gene expression and increases adhesion molecules and chemokines. An excess of ROS decreases nitric oxide bioavailability, causes endothelial dysfunction, and promotes atherosclerosis. Moreover, Ang II interrupts the anti-inflammatory effects of insulin. Together, these effects promote a prothrombotic state as well as plaque rupture. Ang II receptor blockers suppress mediators of inflammation, including ROS and C-reactive protein, and they increase expression of inhibitory kappaB (an inhibitor of nuclear factor-kappaB). These anti-inflammatory and antioxidative effects, which are probably due in part to unopposed stimulation of the Ang II type 2 receptor, may be beneficial in acute coronary syndromes and may also contribute to the prevention of type II diabetes mellitus, as insulin resistance is mediated by inflammatory processes.

Authors+Show Affiliations

Division of Endocrinology, Diabetes and Metabolism, State University of New York at Buffalo and Kaleida Health, Buffalo, NY 14209, USA. pdandona@kaleidahealth.orgNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

17096009

Citation

Dandona, P, et al. "Angiotensin II and Inflammation: the Effect of Angiotensin-converting Enzyme Inhibition and Angiotensin II Receptor Blockade." Journal of Human Hypertension, vol. 21, no. 1, 2007, pp. 20-7.
Dandona P, Dhindsa S, Ghanim H, et al. Angiotensin II and inflammation: the effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockade. J Hum Hypertens. 2007;21(1):20-7.
Dandona, P., Dhindsa, S., Ghanim, H., & Chaudhuri, A. (2007). Angiotensin II and inflammation: the effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockade. Journal of Human Hypertension, 21(1), pp. 20-7.
Dandona P, et al. Angiotensin II and Inflammation: the Effect of Angiotensin-converting Enzyme Inhibition and Angiotensin II Receptor Blockade. J Hum Hypertens. 2007;21(1):20-7. PubMed PMID: 17096009.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Angiotensin II and inflammation: the effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockade. AU - Dandona,P, AU - Dhindsa,S, AU - Ghanim,H, AU - Chaudhuri,A, Y1 - 2006/11/09/ PY - 2006/11/11/pubmed PY - 2007/5/26/medline PY - 2006/11/11/entrez SP - 20 EP - 7 JF - Journal of human hypertension JO - J Hum Hypertens VL - 21 IS - 1 N2 - Angiotensin II (Ang II) increases adhesion molecules, cytokines and chemokines and exerts a proinflammatory effect on leucocytes, endothelial cells and vascular smooth muscle cells. Acting via the type 1 receptor, Ang II initiates an inflammatory cascade of reduced nicotinamide-adenine dinucleotide phosphate oxidase, reactive oxygen species (ROS) and nuclear factor-kappaB, which mediates transcription and gene expression and increases adhesion molecules and chemokines. An excess of ROS decreases nitric oxide bioavailability, causes endothelial dysfunction, and promotes atherosclerosis. Moreover, Ang II interrupts the anti-inflammatory effects of insulin. Together, these effects promote a prothrombotic state as well as plaque rupture. Ang II receptor blockers suppress mediators of inflammation, including ROS and C-reactive protein, and they increase expression of inhibitory kappaB (an inhibitor of nuclear factor-kappaB). These anti-inflammatory and antioxidative effects, which are probably due in part to unopposed stimulation of the Ang II type 2 receptor, may be beneficial in acute coronary syndromes and may also contribute to the prevention of type II diabetes mellitus, as insulin resistance is mediated by inflammatory processes. SN - 0950-9240 UR - https://www.unboundmedicine.com/medline/citation/17096009/Angiotensin_II_and_inflammation:_the_effect_of_angiotensin_converting_enzyme_inhibition_and_angiotensin_II_receptor_blockade_ L2 - http://dx.doi.org/10.1038/sj.jhh.1002101 DB - PRIME DP - Unbound Medicine ER -