Increased renal vascular reactivity to ANG II after unilateral nephrectomy in the rat involves 20-HETE

Joly, Emma; Seqqat, Rachid; Flamion, Bruno; Caron, Nathalie; Michel, Alain; Imig, John D.; Kramp, R.

doi:10.1152/ajpregu.00401.2005

Cited by 25 publications

(23 citation statements)

References 40 publications

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“…MAP responses to ANG II were blunted in the uni-x animals, in contrast to studies in some models of reduced nephron endowment that have shown an increased sensitivity to ANG II (20,37). Aside from methodological considerations, such as species differences and anesthetized vs. conscious measurements, it is also possible that since basal ANG II levels are lower in uni-x animals, infusion of graded ANG II doses would not have increased the circulating levels of ANG II in uni-x animals compared with sham.…”

Section: Discussioncontrasting

confidence: 94%

Fetal uninephrectomy in male sheep alters the systemic and renal responses to angiotensin II infusion and AT1R blockade

Singh

Moritz

Wintour

et al. 2011

American Journal of Physiology-Renal Physiology

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Fetal uninephrectomy (uni-x) at 100 days of gestation results in compensatory nephrogenesis in the remaining kidney, resulting in a 30% reduction in total nephron number in male sheep. Recently, we showed that uni-x males at 6 mo of age have elevated arterial pressure, reduced renal blood flow (RBF), glomerular filtration rate (GFR), and low plasma renin levels (Singh R, Denton K, Bertram J, Jefferies A, Head G, Lombardo P, Schneider-Kolsky M, Moritz K. J Hypertens 27: 386-396, 2009; Singh R, Denton K, Jefferies A, Bertram J, Moritz K. Clin Sci (Lond) 118: 669-680, 2010). We hypothesized this was due to upregulation of the intrarenal renin-angiotensin system (RAS). In this study, renal responses to ANG II infusion and ANG II type 1 receptor (AT1R) blockade were examined in the same 6-mo-old male sheep. Uni-x animals had reduced levels of renal tissue and plasma renin and ANG II. Renal gene expression of renin, and gene and protein levels of AT1R and AT2R, were significantly lower in uni-x animals. In response to graded ANG II infusion, sham animals had the expected decrease in conscious RBF and GFR. Interestingly, the response was biphasic in uni-x sheep, with GFR initially decreasing, but then increasing at higher ANG II doses (34 ± 7%; P(group × treatment) < 0.001), due to a paradoxical decrease in renal vascular resistance (P(group × treatment) < 0.001). In response to AT1R blockade, while GFR and RBF responded similarly between groups, there was a marked increase in sodium excretion in uni-x compared with sham sheep (209 ± 35 vs. 25 ± 12%; P < 0.001). In conclusion, in 6-mo-old male sheep born with a single kidney, these studies demonstrate that this is a low-renin form of hypertension, in which responses to ANG II are perturbed and the intrarenal RAS is downregulated.

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Section: Discussioncontrasting

confidence: 94%

Fetal uninephrectomy in male sheep alters the systemic and renal responses to angiotensin II infusion and AT1R blockade

Singh

Moritz

Wintour

et al. 2011

American Journal of Physiology-Renal Physiology

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“…20-HETE not only induces vasoconstriction but also reduces vascular relaxation. For example, 20-HETE attenuates the relaxing response to acetylcholine in renal interlobar arteries pre-constricted with phenylephrine [66–68]. These vascular effects depend on the complex relationship between RAS and 20-HETE as concurrent pretreatment of vessels with 20-HETE and an ACE inhibitor (Lisinopril) or AT1R blocker (Losartan) attenuate 20-HETE’s effects [54].…”

Section: Vascular Reactivity Endothelial Dysfunction and Endothelialmentioning

confidence: 99%

Vascular actions of 20-HETE

Hoopes

García

Edin

et al. 2015

Prostaglandins & Other Lipid Mediators

115

101

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20-hydroxyeicosatetraenoic acid (20-HETE) is a metabolite of arachidonic acid that exhibits a myriad of biological effects in the vascular system. This review discusses the current knowledge related to the effects of 20-HETE on vascular reactivity, activation, and remodeling, as well as its role in vascular inflammation and angiogenesis. The information explaining how 20-HETE and the renin-angiotensin system interact to promote hypertension, vasoconstriction, and vascular dysfunction is summarized in this article. 20-HETE enhances vascular inflammation and injury in models of diabetes, ischemia/reperfusion, and cerebrovascular oxidative stress. Recent studies also established a role for 20-HETE in normal and pathological angiogenesis conditions. This review will also discuss the molecular mechanisms through which 20-HETE induces these vascular actions. Potential additional studies are suggested to address shortcomings in the current knowledge of 20-HETE in the vascular system.

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“…180 20-HETE has been shown to mediate responses to Ang II. Hence, increased production of 20-HETE in the peripheral vasculature contributes to the acute vasoconstrictor response to Ang II, 181 whereas acute 182 and chronic 183 inhibition of 20-HETE synthesis attenuates the renal pressor response to Ang II and the development of Ang II–dependent hypertension, respectively. In cultured aortic vascular smooth muscle cells, 20-HETE mediates Ang II–induced mitogenic effects.…”

Section: -Hete and The Renin–angiotensin Systemmentioning

confidence: 99%

20-HETE and Blood Pressure Regulation

Wu¹,

Gupta

García

et al. 2014

Cardiology in Review

126

148

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20-Hydroxy-5, 8, 11, 14-eicosatetraenoic acid (20-HETE) is a cytochrome P450 (CYP)–derived omega-hydroxylation metabolite of arachidonic acid. 20-HETE has been shown to play a complex role in blood pressure regulation. In the kidney tubules, 20-HETE inhibits sodium reabsorption and promotes natriuresis, thus, contributing to antihypertensive mechanisms. In contrast, in the microvasculature, 20-HETE has been shown to play a pressor role by sensitizing smooth muscle cells to constrictor stimuli and increasing myogenic tone, and by acting on the endothelium to further promote endothelial dysfunction and endothelial activation. In addition, 20-HETE induces endothelial angiotensin-converting enzyme, thus, setting forth a potential feed forward prohypertensive mechanism by stimulating the renin–angiotensin–aldosterone system. With the advancement of gene sequencing technology, numerous polymorphisms in the regulatory coding and noncoding regions of 20-HETE–producing enzymes, CYP4A11 and CYP4F2, have been associated with hypertension. This in-depth review article discusses the biosynthesis and function of 20-HETE in the cardiovascular system, the pharmacological agents that affect 20-HETE action, and polymorphisms of CYP enzymes that produce 20-HETE and are associated with systemic hypertension in humans.

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Increased renal vascular reactivity to ANG II after unilateral nephrectomy in the rat involves 20-HETE

Cited by 25 publications

References 40 publications

Fetal uninephrectomy in male sheep alters the systemic and renal responses to angiotensin II infusion and AT1R blockade

Fetal uninephrectomy in male sheep alters the systemic and renal responses to angiotensin II infusion and AT1R blockade

Vascular actions of 20-HETE

20-HETE and Blood Pressure Regulation

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