Role of prostaglandins in hypertension

Ja, Colina-Chourio; Godoy-Godoy, Nereyda; Avila-Hernández, RM

doi:10.1038/sj.jhh.1000981

Cited by 15 publications

(4 citation statements)

References 25 publications

(40 reference statements)

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“…Prostaglandins (PGs) are important modulators of inflammatory responses. For example, a variety of hormones, cytokines, and growth factors enhance synthesis of PGs, which serve as autacoids, mediating a variety of responses in the cardiovascular system (Colina-Chourio et al, 2000). PG synthesis is a multistep process, controlled by several important rate-limiting enzymes; an important and extensively studied process involves activation of PLA 2 , which catalyzes the release of arachidonic acid (AA) from phospholipids in membranes (Dennis, 1997 andBingham andAusten, 1999).…”

mentioning

confidence: 99%

Angiotensin II Increases Expression of Cyclooxygenase-2: Implications for the Function of Vascular Smooth Muscle Cells

Kerb²,

Shi³

et al. 2002

J Pharmacol Exp Ther

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In vascular smooth muscle, increased expression of cyclooxygenase-2 (COX-2) has emerged as an important mechanism for regulation of prostanoid synthesis influenced by vessel injury, cytokines, and growth factors. We have investigated how COX-2 participates in angiotensin II (ANG II)-mediated cell responses in cultured human vascular smooth muscle cells (VSMCs). ANG II type 1 (AT1) receptors induce increased accumulation of COX-2, both at the mRNA and protein levels. ANG II increased transcription of the COX-2 gene; also, nuclear extracts from stimulated cells had increased NF-B binding to its DNA consensus sequence. ANG II-induced COX-2 expression was markedly blunted by inhibition of mitogen-activated protein kinase. Furthermore, the ANG II-induced increase in COX-2 protein abundance was attenuated by both the peroxisome proliferator-activated receptor ␣ (PPAR␣) activator Wy-14,643 [pyrinixic acid; 4-chloro-6-(2,3-xylidino)-2-pyrimidinyl)thioacetic acid] and the PPAR␥ activator 15d-PGJ2 (15-deoxy-⌬ 12-14 -prostaglandin J2). Not only did ANG II increase COX-2 expression and prostaglandin synthesis, ANG II-stimulated DNA synthesis and cell migration were dependent on COX-2 activity. PPAR␣ and PPAR␥ activators inhibited ANG II-stimulated DNA synthesis and cell migration. These results suggest that ANG II enhances COX-2 expression at the transcription level; also, COX-2 activity plays an important role in mediating ANG IIinduced proliferation and migration of VSMCs, suggesting the possibility of magnification of ANG II effects over time due to the induction of COX-2 expression. These results also demonstrate that both the ␣ and ␥ type of PPAR activators inhibit COX-2 expression induced by angiotensin II in VSMCs which may have therapeutic significance in vascular diseases.Proliferation and migration of VSMCs in arteries plays an important role in the pathophysiology of atherosclerosis, hypertension, and restenosis after angioplasty. A wide variety of growth factors, cytokines, and hormones have been found to activate these responses in blood vessels (Ross, 1999). A prominent growth factor for VSMCs is ANG II. These effects of ANG II are mediated via the ANG II type 1 (AT1) receptor signaling system (Kim and Iwao, 2000). Multiple signal transduction pathways, including activation of phospholipase C, phospholipase A 2 (PLA 2 ), tyrosine protein kinases/ mitogen-activated protein (MAP) kinase, and PI 3-kinase/p70 S6 kinase signaling pathways are involved in mediating AT1 receptor stimulation of cell responses (Schieffer et al., 1996;

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mentioning

confidence: 99%

Angiotensin II Increases Expression of Cyclooxygenase-2: Implications for the Function of Vascular Smooth Muscle Cells

Kerb²,

Shi³

et al. 2002

J Pharmacol Exp Ther

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“…Prostaglandins elicit many effects throughout the body, including constriction and relaxation of smooth muscles and regulation of the immune response. 6,7 Early studies analyzing the effects of prostaglandins in the eye revealed significant irritation and initial IOP elevation. Whereas the prevailing thought in the early 1970s was that prostaglandins elevate IOP, it was not until 1977 when Drs.…”

Section: Identifying Prostaglandins As Ocular Hypotensive Agentsmentioning

confidence: 99%

Effects of Prostaglandin Analogues on Aqueous Humor Outflow Pathways

Winkler

Fautsch

2014

Journal of Ocular Pharmacology and Therapeutics

107

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Elevated intraocular pressure (IOP) is the most prevalent risk factor for glaucoma. All treatments, whether surgical or pharmaceutical, are aimed at lowering IOP. Prostaglandin analogues are a first line therapy for glaucoma due to their ability to reduce IOP, once-daily dosing, efficacy, and minimal side-effect profile. Whereas prostaglandin analogues have been known to alter aqueous humor outflow through the unconventional (uveoscleral) pathway, more recent evidence suggests their action also occurs through the conventional (trabecular) pathway. Understanding how prostaglandin analogues successfully lower IOP is important, as this information may lead to the discovery of new molecular targets for future therapeutic intervention. This review explores the current understanding of prostaglandin analogue biology as it pertains to IOP reduction and improved aqueous humor outflow facility.

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“…The role of prostaglandins (PGs) in blood pressure regulation has been well studied. 3 The imbalances between vasodilator and vasoconstrictor PGs may affect blood pressure. 4 On the partial basis of their ability to inhibit PG production, nonsteroidal anti-inflammatory drugs (NSAIDs) have been postulated to increase blood pressure.…”

Section: H Ypertension Is a Majormentioning

confidence: 99%