Selective inhibition of angiotensin II-mediated vasoconstriction by lipoxygenase blockade

Stern, Naftali; Golub, Michael S.; Nozawa, Kenichi; Berger, Morris E.; Knoll, Esther; Yanagawa, Norimoto; Natarajan, Rama; Nadler, Jerry L.; Tuck, Michael L.

doi:10.1152/ajpheart.1989.257.2.h434

Cited by 51 publications

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“…These findings, combined with the previous observation that inhibition of the 12-LO pathway attenuates the afferent arteriolar response to angiotensin II, provide convincing evidence that 12(S)-HETE is importantly involved in the renal vascular actions of angiotensin II. There are a number of studies that provide corroborating evidence for the view that 12(S)-HETE is a mediator for the vascular intracellular actions of angiotensin II (3,8,(18)(19)(20)(21). The involvement of 12(S)-HETE in the renal vasoconstrictor response to angiotensin II has been demonstrated in several studies (11,21,26).…”

Section: Discussionmentioning

confidence: 83%

“…In contrast, LO inhibition attenuated the renal arcuate artery vasoconstrictor response to norepinephrine and KCl but had no effect on the vascular response to ET-1 (27). Attenuation of the vasoconstrictor response to angiotensin II but not norepinephrine has also been demonstrated for the aorta and large arteries of the skeletal muscle and pulmonary vasculatures (19)(20)(21)(28)(29)(30). 12(S)-HETE also directly potentiates angiotensin II-mediated contraction of hamster aorta and SHR aorta (3,31).…”

Section: Discussionmentioning

confidence: 93%

“…The 12-LO pathway or 12(S)-HETE levels are elevated in a diabetic pig model, ischemic preconditioned rat hearts, the spontaneously hypertensive rat (SHR), and patients with essential hypertension (1-3, 17). The increased 12(S)-HETE levels in hypertension and diabetes appear to play a key role in mediating the smooth muscle cell hypertrophy, and atherosclerotic and vascular constrictor actions of angiotensin II (3,8,(18)(19)(20)(21). In the kidney, 12(S)-HETE decreases renal blood flow, constricts renal vessels, and is involved in the afferent arteriolar response to angiotensin II (5,9,11).…”

Section: Discussionmentioning

confidence: 99%

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12-Hydroxyeicosatetraenoic acid participates in angiotensin II afferent arteriolar vasoconstriction by activating L-type calcium channels

Yiu

Zhao

Inscho

et al. 2003

Journal of Lipid Research

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The arachidonate lipoxygenase (LO) product, 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE), has been implicated as a key contributor to the pathogenesis of atherosclerosis, hypertension, and diabetic nephropathy (1-4). 12-LO expression has been detected in renal vascular and glomerular cells, and these cells have the capacity to produce 12(S)-HETE (5-8). In addition to its involvement in glomerular inflammation and vascular smooth muscle cell growth, 12(S)-HETE is a renal vasoconstrictor (5,(8)(9)(10). 12(S)-HETE decreases renal blood flow and glomerular filtration independent of cyclooxygenase (COX) activity (9). Additionally, the action of angiotensin II on the renal vasculature involves participation of the LO pathway. A previous study by our laboratory demonstrated that the afferent arteriolar constriction to angiotensin II is attenuated in the presence of 12-LO inhibition (11). In contrast, norepinephrine-mediated renal microvascular vasoconstriction was unaffected by 12-LO inhibition (11). One aim of the current study was to determine renal microvascular production of COX metabolites and 12(S)-HETE in response to angiotensin II and norepinephrine.Although the importance of 12(S)-HETE in renal and cardiovascular disease is now established, the mechanism by which 12(S)-HETE constricts the preglomerular vasculature remains to be identified. It is known that 12(S)-HETE causes depolarization of the vascular smooth muscle cell membrane and may act through activation of protein kinase C to constrict blood vessels (9). Depolarization of vascular smooth muscle should activate L-type calcium channels. Therefore, a second aim of the present study was to determine the contribution of L-type calcium channel activation to the 12(S)-HETE mediated renal vasoconstriction. METHODS Renal microvessel 12(S)-HETE and COX metabolite productionMale Sprague-Dawley rats were anesthetized with sodium pentobarbital (40 mg/kg body weight ip), and the abdominal cavity was

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

12-Hydroxyeicosatetraenoic acid participates in angiotensin II afferent arteriolar vasoconstriction by activating L-type calcium channels

Yiu

Zhao

Inscho

et al. 2003

Journal of Lipid Research

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“…Increased formation of LO products such as 12(S)-HETE by the biological agents involved in cardiovascular dysfunction has been reported in VSMCs, endothelial cells, and monocytes (6,(13)(14)(15)22). 12(S)-HETE has direct effects like chemotaxis (23); changes in vascular tone (24); and production of vascular endothelial growth factor, a potent angiogenic agent (25). It can also induce monocyte binding to endothelial cells (22) and can mediate AngII-induced changes in neuronal K ϩ currents (26).…”

mentioning

confidence: 99%

The Oxidized Lipid and Lipoxygenase Product 12(S)-Hydroxyeicosatetraenoic Acid Induces Hypertrophy and Fibronectin Transcription in Vascular Smooth Muscle Cells via p38 MAPK and cAMP Response Element-binding Protein Activation

Reddy¹,

Thimmalapura²,

Lanting³

et al. 2002

Journal of Biological Chemistry

124

137

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Growth factor-and cytokine-induced vascular smooth muscle cell proliferation, migration, hypertrophy, and matrix production have been shown to play important roles in the development of vascular disorders such as atherosclerosis, hypertension, and restenosis. Growth factors such as angiotensin II (AngII) 1 and platelet-derived growth factor (PDGF) activate intracellular phospholipases, leading to the formation of arachidonic acid, which can be further metabolized by cyclooxygenases, cytochrome P-450 oxygenases, and lipoxygenases (1). Lipoxygenase (LO) action leads to the formation of oxidized lipids such as 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE). LOs and their products of arachidonic acid and linoleic acid metabolism have been shown to mediate growth factor effects in vascular smooth muscle cells (VSMCs) as well as responses to vascular injury. Lipoxygenases are classified as 5-, 8-, 12-, and 15-lipoxygenases based on their ability to insert molecular oxygen at the corresponding carbon atom of arachidonic acid. Three major isoforms of 12-LO have been cloned. They are platelet-type 12-LO, leukocyte-type 12-LO, and epidermis-type 12-LO. These proteins are products of distinct genes and vary in tissue distribution (2, 3).Leukocyte 12-LO has been cloned from porcine and mouse leukocytes (4, 5). The presence of leukocyte-type 12-LO (also termed 12/15-LO) has also been demonstrated in various cell types and tissues, including VSMCs, adrenal cells, rat brain, and kidney (6 -11). Studies from this and other laboratories (12-21) have implicated the leukocyte-type 12-LO pathway in the pathogenesis of atherosclerosis and restenosis. 12-LO expression was demonstrated in atherosclerotic lesions (12). In vascular and mononuclear cells, growth factors and cytokines as well as high glucose stimulate both the activity and expression of 12-LO (6, 13-15). Furthermore, expression of 12-LO protein and mRNA is markedly increased in neointima of balloon-injured rat carotid arteries, and pretreatment with LO inhibitors reduces the rate of neointimal thickening in this model (16,17). We have demonstrated that treatment with a chimeric DNA-RNA hammerhead ribozyme targeted to cleave rat leukocyte-type 12-LO mRNA significantly reduces neointimal thickening in balloon-injured rat arteries (18). We have

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“…30 Inhibition of lipoxygenase has been reported to attenuate AII-induced vasoconstriction in rat aorta. 31 …”

Section: Phospholipase C (Plc) and Protein Kinase C (Pkc)mentioning

confidence: 99%

Molecular and cellular mechanisms of action of angiotensin II (AT1) receptors in vascular smooth muscle

Hughes

1998

J Hum Hypertens

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Selective inhibition of angiotensin II-mediated vasoconstriction by lipoxygenase blockade

Cited by 51 publications

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12-Hydroxyeicosatetraenoic acid participates in angiotensin II afferent arteriolar vasoconstriction by activating L-type calcium channels

12-Hydroxyeicosatetraenoic acid participates in angiotensin II afferent arteriolar vasoconstriction by activating L-type calcium channels

The Oxidized Lipid and Lipoxygenase Product 12(S)-Hydroxyeicosatetraenoic Acid Induces Hypertrophy and Fibronectin Transcription in Vascular Smooth Muscle Cells via p38 MAPK and cAMP Response Element-binding Protein Activation

Molecular and cellular mechanisms of action of angiotensin II (AT1) receptors in vascular smooth muscle

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