Exaggerated renal thromboxane and prostaglandin release by angiotensin II in suprarenal aortic coarctation hypertension

Miller, Mark J.S.; McNeill, Helen; Westlin, William; Carroll, Mairéad A.; McGiff, John C.

doi:10.1016/1043-6618(89)90239-9

Cited by 4 publications

(2 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Perfusion of isolated rabbit kidneys 7 days after suprarenal aortic constriction revealed these to be exquisitely sensitive to the vascular effects of Ang II as compared with a sham group. 31 In addition, Ang II caused the release of great quantities of PGEj, PGF^ 6-keto-PGF lm and thromboxane (TXB2) into the venous effluent. In sham kidneys Ang II did not cause release of TxBj, indicating a particular enhancement of this vasoconstrictor eicosanoid by arterial constriction.…”

Section: Various Phases Of Goldblatt Hypertension Phase I or Renin-anmentioning

confidence: 99%

Pathophysiology of renovascular hypertension.

1991

View full text Add to dashboard Cite

Renovascular hypertension has its experimental counterpart in the two-kidney, one clip model (Goldblatt hypertension). From the study of this model, a general pathophysiological scheme has evolved suggesting that temporal stages in the development and maintenance of hypertension are regulated by complicated hormonal and neural interrelations. The central roles played by the renin-angiotensin system and the renal nerves is discussed as they relate to other hormones. In addition, the possible contribution of converting enzyme inhibitors to understanding the pathophysiology of this condition is discussed. (Hypertension 1991

show abstract

Section: Various Phases Of Goldblatt Hypertension Phase I or Renin-anmentioning

confidence: 99%

Pathophysiology of renovascular hypertension.

1991

View full text Add to dashboard Cite

show abstract

“…It is possible that the increased availability of EPA or DHA or both may lead to an enhanced formation of resolvins, protectins and maresins that could have reversed the development of AAA. Yet, the other possibility that needs to be considered is the action of angiotensin-II on the formation of proinflammatory prostaglandins (PGs), thromboxanes (TXs) and leukotrienes (LTs) from AA, [7][8][9][10] an n-6 PUFA. It is likely that the supplementation of EPA and DHA displaced AA from the cell membrane phospholipid pool that can lead to an increased formation of LXA4 (see figure 3) and decreased formation of pro-inflammatory PGs, TXs and LTs (from AA).…”

Section: Pufas and Their Metabolites Angiotensin-ii Aa And Aaamentioning

confidence: 99%

Is aortic aneurysm preventable?

Das¹

2017

Journal of Translational Internal Medicine

View full text Add to dashboard Cite

Abdominal aortic aneurysm (AAA) is a chronic inflammatory condition, triggered by the local accumulation of macrophages, oxidative stress and damage to the aortic wall. Pro-inflammatory eicosanoids seem to play a significant role in AAA. The pro-inflammatory events seen in AAA could be due to a deficiency of anti-inflammatory eicosanoids such as lipoxin A4 (LXA4), resolvins, protectins and maresins as a result of reduced tissue concentrations of their precursors: arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Thus, an imbalance between pro- and anti-inflammatory eicosanoids may underlie AAA. Angiotensin-II (Ang-II), a pro-inflammatory molecule, seems to have a role in AAA. I propose that AAA is due to the local (abdominal aortic wall) deficiency of AA and other PUFAs and their anti-inflammatory metabolites especially LXA4. The beneficial action of EPA and DHA reported in the animal experimental models of AAA induced by Ang-II infusion can be attributed to their (EPA and DHA) ability to enhance the formation of not only resolvins, protectins and maresins but also LXA4. It is likely that abdominal aortic tissue (endothelial cells, smooth muscle cells and other cells) may be deficient in AA, EPA and DHA, and have defective activity of 5-, 12-, and 15-lipoxygenases and cyclooxygenase, especially COX-2 resulting in decreased formation of LXA4, resolvins, protectins and maresins. Thus, methods designed to enhance the formation of LXA4 and other anti-inflammatory eicosanoids may form a new approach to prevent and manage AAA.

show abstract

Cyclooxygenase‐2 and macula densa control of renin secretion

Schnermann

2001

Nephrology Dialysis Transplantation

View full text Add to dashboard Cite

Exaggerated renal thromboxane and prostaglandin release by angiotensin II in suprarenal aortic coarctation hypertension

Cited by 4 publications

References 21 publications

Pathophysiology of renovascular hypertension.

Pathophysiology of renovascular hypertension.

Is aortic aneurysm preventable?

Cyclooxygenase‐2 and macula densa control of renin secretion

Contact Info

Product

Resources

About