Regulation of Renal Medullary Circulation by the Renin–angiotensin System in Genetically Hypertensive Rats

Liu, Kiao Ling

doi:10.1111/j.1440-1681.2009.05153.x

Cited by 17 publications

(9 citation statements)

References 60 publications

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“…The Nox2 gene, located on the X chromosome, is inducible and is highly regulated by Ang II and stretch and is upregulated in experimental hypertension. [84][85][86] Nox4 is found in vascular cells, fibroblasts and osteoclasts and is abundantly expressed in the kidney. 87,88 In vascular smooth muscle cells, Nox4 and p22phox co-localize with vinculin in focal adhesions and has been implicated in cell migration, proliferation, tube formation, angiogenesis and cell differentiation.…”

Section: Vascular Generation Of Rosmentioning

confidence: 99%

Reactive oxygen species and vascular biology: implications in human hypertension

2010

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Increased vascular production of reactive oxygen species (ROS; termed oxidative stress) has been implicated in various chronic diseases, including hypertension. Oxidative stress is both a cause and a consequence of hypertension. Although oxidative injury may not be the sole etiology, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors. Oxidative stress is a multisystem phenomenon in hypertension and involves the heart, kidneys, nervous system, vessels and possibly the immune system. Compelling experimental and clinical evidence indicates the importance of the vasculature in the pathophysiology of hypertension and as such much emphasis has been placed on the (patho)biology of ROS in the vascular system. A major source for cardiovascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4. Nox-derived ROS is important in regulating endothelial function and vascular tone. Oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in vascular remodeling in hypertension. Despite a plethora of data implicating oxidative stress as a causative factor in experimental hypertension, findings in human hypertension are less conclusive. This review highlights the importance of ROS in vascular biology and focuses on the potential role of oxidative stress in human hypertension.

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Section: Vascular Generation Of Rosmentioning

confidence: 99%

Reactive oxygen species and vascular biology: implications in human hypertension

2010

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“…IN THE KIDNEY, BLOOD FLOW in the cortex and medulla is regulated independently (2,7,22). Only a small fraction (ϳ10%) of total renal blood flow enters the renal medulla.…”

mentioning

confidence: 99%

Renal cortical and medullary blood flow responses to altered NO availability in humans

Damkjær

Vafaee

Möller

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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The objective of this study was to quantify regional renal blood flow in humans. In nine young volunteers on a controlled diet, the lower abdomen was CT-scanned, and regional renal blood flow was determined by positron emission tomography (PET) scanning using H(2)(15)O as tracer. Measurements were performed at baseline, during constant intravenous infusion of nitric oxide (NO) donor glyceryl nitrate and after intravenous injection of NO synthase inhibitor N(ω)-monomethyl-L-arginine (L-NMMA). Using the CT image, the kidney pole areas were delineated as volumes of interest (VOI). In the data analysis, tissue layers with a thickness of one voxel were eliminated stepwise from the external surface of the VOI (voxel peeling), and the blood flow subsequently was determined in each new, reduced VOI. Blood flow in the shrinking VOIs decreased as the number of cycles of voxel peeling increased. After 4-5 cycles, blood flow was not reduced further by additional voxel peeling. This volume-insensitive flow was measured to be 2.30 ± 0.17 ml·g tissue(-1)·min(-1) during the control period; it increased during infusion of glyceryl nitrate to 2.97 ± 0.18 ml·g tissue(-1)·min(-1) (P < 0.05) and decreased after L-NMMA injection to 1.57 ± 0.17 ml·g tissue(-1)·min(-1) (P < 0.05). Cortical blood flow was 4.67 ± 0.31 ml·g tissue(-1)·min(-1) during control, unchanged by glyceryl nitrate, and decreased after L-NMMA [3.48 ± 0.23 ml·(g·min)(-1), P < 0.05]. PET/CT scanning allows identification of a renal medullary region in which the measured blood flow is 1) low, 2) independent of reduction in the VOI, and 3) reactive to changes in systemic NO supply. The technique seems to provide indices of renal medullary blood flow in humans.

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“…95 In SHR and Lyon genetically hypertensive rats, the vasoconstrictor component was more pronounced, and/or the vasodilator component was attenuated after stimulation with Ang II. 95,96 ANGIOTENSIN III Ang III is generated from Ang II by the enzyme aminopeptidase A (Figure 3), 97 or from Ang I, which can be converted directly to Ang III by ACE. 98 Like Ang II, Ang III displays similar affinity for AT 1 and AT 2 receptors (Figure 2), 99 but it is more sensitive to aminopeptidase N. 100 Ang III reduces RBF after systemic administration.…”

Section: Angiotensin II At 1 and At 2 Receptorsmentioning

confidence: 99%

Blood pressure and renal hemodynamic effects of angiotensin fragments

Yang

Smolders

Dupont³

2011

Hypertens Res

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Regulation of Renal Medullary Circulation by the Renin–angiotensin System in Genetically Hypertensive Rats

Cited by 17 publications

References 60 publications

Reactive oxygen species and vascular biology: implications in human hypertension

Reactive oxygen species and vascular biology: implications in human hypertension

Renal cortical and medullary blood flow responses to altered NO availability in humans

Blood pressure and renal hemodynamic effects of angiotensin fragments

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