Review: Intrarenal angiotensin II levels in normal and hypertensive states

Navar, L. Gabriel; Mitchell, Kenneth D.; Harrison‐Bernard, Lisa M.; Kobori, Hiroyuki; Nishiyama, Akira

doi:10.1177/14703203010020013001

Cited by 58 publications

(42 citation statements)

References 92 publications

(147 reference statements)

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“…Apart from age, individual susceptibility, genetic factors, implication of multiple biological pathogenic factors, and the lag time between proteinuria appearance and treatment initiation, this insufficient response may be explained by incomplete blockade of the RAS, 51 especially if intrarenal RAS is regulated independently of circulating RAS. 52 The huge amount of renin synthesized and released locally, the limited amount of renal endothelial ACE, 53 the compartmentalization of Ang II in interstitial and tubular fluids, 54 the intrarenal consumption of angiotensinogen, 52 and the uptake of Ang II by the renal AT1Rs 55 influences the intrarenal levels of Ang I and Ang II, which differ from their plasma levels. By increasing and prolonging intrarenal Ang II neutralization, specific renal benefits are expected from the combined blockade in renal tissue under pathological circumstances, but adverse renal effects may also be expected as a consequence of renal hypoperfusion and vasodilatation under certain circumstances.…”

Section: Azizi and Ménard Combined Blockade Of Renin-angiotensin Systemmentioning

confidence: 99%

Combined Blockade of the Renin-Angiotensin System With Angiotensin-Converting Enzyme Inhibitors and Angiotensin II Type 1 Receptor Antagonists

2004

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Section: Azizi and Ménard Combined Blockade Of Renin-angiotensin Systemmentioning

confidence: 99%

Combined Blockade of the Renin-Angiotensin System With Angiotensin-Converting Enzyme Inhibitors and Angiotensin II Type 1 Receptor Antagonists

2004

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“…Studies in isolated proximal tubular cells showed that Ang II stimulates Na + /H + exchanger via AT1 receptors [66]. Although some AT2 receptors have been confirmed on proximal tubules [20], most functional studies suggest that the major effects of Ang II on proximal tubules are via AT1 receptors [67]. Recent studies have also indicted that Ang II contributes to the regulation of distal tubular sodium reabsorption rate [68].…”

Section: Tubular Function Of Ras Angiotensin IImentioning

confidence: 99%

Renal Renin-Angiotensin System

Ichihara

Kobori

Nishiyama

et al. 2004

Contributions to Nephrology

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The cardinal role of the intrarenal renin-angiotensin system (RAS) in the control of sodium excretion and the pathophysiology of hypertension continues to receive increased attention. In addition to its very powerful vasoconstrictor action, angiotensin (Ang) II exerts important actions on tubular transport function and several recent studies have emphasized the potential importance of actions of angiotensin peptides on receptors localized to the luminal membranes of both proximal and distal nephron segments. Furthermore, a strong case is being developed supporting the importance of local mechanisms regulating the activity of the RAS. This is due to the fact that all components of the RAS are strongly expressed in the kidneys.

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“…[31][32][33] Sustained elevations in circulating Ang II lead to progressive accumulation of intrarenal Ang II levels even though there is marked suppression of renin formation and release. 34,35 Increased Ang II levels occur in renin-depleted kidneys of 2K1C Goldblatt hypertensive …”

mentioning

confidence: 99%

Regulation of Intrarenal Angiotensin II in Hypertension

et al. 2002

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Abstract-Intrarenal angiotensin II (Ang II) is regulated by several complex processes involving formation from both systemically delivered and intrarenally formed substrate, as well as receptor-mediated internalization. There is substantial compartmentalization of intrarenal Ang II, with levels in the renal interstitial fluid and in proximal tubule fluid being much greater than can be explained from the circulating levels. In Ang II-dependent hypertension, elevated intrarenal Ang II levels occur even when intrarenal renin expression and content are suppressed. Studies in Ang II-infused rats have demonstrated that augmentation of intrarenal Ang II is due, in part, to uptake of circulating Ang II via an Ang II type 1 (AT 1 ) receptor mechanism and also to sustained endogenous production of Ang II. Some of the internalized Ang II accumulates in the light and heavy endosomes and is therefore potentially available for intracellular actions. The enhanced intrarenal Ang II also exerts a positive feedback action to augment intrarenal levels of angiotensinogen (AGT) mRNA and protein, which contribute further to the increased intrarenal Ang II in hypertensive states. In addition, renal AT 1 receptor protein and mRNA levels are maintained, allowing increased Ang II levels to elicit progressive effects. The increased intrarenal Ang II activity and AGT production are associated with increased urinary AGT excretion rates. The urinary AGT excretion rates show a clear relationship to kidney Ang II content, suggesting that urinary AGT may serve as an index of Ang II-dependent hypertension. Collectively, the data support a powerful role for intrarenal Ang II in the pathogenesis of hypertension. Key Words: renin-angiotensin system Ⅲ angiotensinogen Ⅲ receptors, angiotensin Ⅲ hypertension, experimental I t is an honor and a privilege to be selected to present the Arthur C. Corcoran Memorial Lecture and I greatly appreciate this recognition that has been given to our research group. We all realize, however, that this year is very different for our country. The terrorist attacks have burned the date of September 11, 2001, indelibly in our minds. In the light of these tragic events, it has been difficult to move forward with the ordinary business of our lives. Compared with the sacrifices of the victims and their families, our activities have seemed irrelevant. Aside from moral and financial support, there is little that we personally can do. As scientists, however, we are comforted by the conviction that what we do collectively provides significant long-term benefits to the health and well-being of our citizens. Thus, going about our business and minimizing the disruptions is the most positive response that we can make. In doing so, however, we keep in mind that others less fortunate lost their lives or their loved ones while they were going about the ordinary business of their lives.As a renal physiologist, receiving this Corcoran Award is particularly meaningful because Dr. Corcoran performed so many interesting studies related to ...

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Review: Intrarenal angiotensin II levels in normal and hypertensive states

Cited by 58 publications

References 92 publications

Combined Blockade of the Renin-Angiotensin System With Angiotensin-Converting Enzyme Inhibitors and Angiotensin II Type 1 Receptor Antagonists

Combined Blockade of the Renin-Angiotensin System With Angiotensin-Converting Enzyme Inhibitors and Angiotensin II Type 1 Receptor Antagonists

Renal Renin-Angiotensin System

Regulation of Intrarenal Angiotensin II in Hypertension

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