Control of renin secretion from adrenal gland in transgenic Ren-2 and normal rats

Rong, Pei; Wilkinson-Berka, Jennifer L.; Skinner, Sandford L.

doi:10.1016/s0303-7207(00)00406-8

Cited by 17 publications

(6 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Plethora researchers highlighted the significance of the local RAS in various extrarenal tissues, including the adrenal glands, 10 thymus, 11 and ocular tissues. 12 The presence and functional role of the RAS components, including prorenin, renin, ACE, angiotensinogen, Ang-II, (pro)renin receptor ((P)RR), and AT 1 R in the eye have been established in the several species ( Table 1 ).…”

Section: Introductionmentioning

confidence: 99%

Therapeutic targets of renin-angiotensin system in ocular disorders

Choudhary

Kapoor

Singh

et al. 2017

Journal of Current Ophthalmology

139

134

View full text Add to dashboard Cite

PurposeTo review current literature on the renin-angiotensin system (RAS)-mediated pathogenic mechanisms and therapeutic targets in ocular diseases.MethodsA comprehensive literature survey was performed on PubMed, Scopus, and Google Scholar databases published from 1977 to 2016. The search terms were a RAS, angiotensin, angiotensin receptor, prorenin, pro (renin) receptor, angiotensin converting enzyme inhibitor, angiotensin receptor blocker associated with ocular disorders like cataract, glaucoma, diabetic retinopathy (DR), macular degeneration, and uveitis. Articles were reviewed on the basis of the association between ocular disorders and RAS and relevant articles were discussed.ResultsThe literature revealed that the individual RAS components including renin, angiotensins, angiotensin converting enzymes, and RAS receptors have been expressed in the specific ocular tissues like retina, choroid, and ciliary body. The activation of both circulatory and local RAS potentiate the various inflammatory and angiogenic signaling molecules, including vascular endothelial growth factor (VEGF), extracellular signal-regulated kinase, and advanced glycation end products (AGE) in the ocular tissues and leads to several blinding disorders like DR, glaucoma, and macular degeneration. The classical and newer RAS inhibitors have illustrated protective effects on blinding disorders, including DR, glaucoma, macular degeneration, uveitis, and cataract.ConclusionsThe RAS components are present in the extrarenal tissues including ocular tissue and have an imperative role in the ocular pathophysiology. The clinical studies are needed to show the role of therapeutic modalities targeting RAS in the treatment of different ocular disorders.

show abstract

Section: Introductionmentioning

confidence: 99%

Therapeutic targets of renin-angiotensin system in ocular disorders

Choudhary

Kapoor

Singh

et al. 2017

Journal of Current Ophthalmology

139

134

View full text Add to dashboard Cite

show abstract

“…However, in the past two decades, several laboratories 32-36 have provided evidence of an expanded concept of the classic RAS to include independent Ang II-generating systems in the brain, 37 heart, 38 kidney, 39,40 and adrenal glands. 41,42 In the context of the neural retina, the localization of Ang II in neurons in many brain regions [43][44][45][46] and in glial cells of the brain 47 and the neuromodulatory actions of Ang II on central nervous system neurons is of interest. 48,49 The complexity of the RAS was further expanded in 2000 by the discovery of ACE2, 50 a "homologue" of ACE capable of producing Ang peptides such as angiotensin (Ang)-(1-7) Current research demonstrates that Ang-(1-7) may be the endogenous antagonist of the pathologic actions of Ang II.…”

mentioning

confidence: 99%

Angiotensin II and Its Receptor Subtypes in the Human Retina

Senanayake

Drazba

Shadrach

et al. 2007

Invest. Ophthalmol. Vis. Sci.

214

156

View full text Add to dashboard Cite

PURPOSE.To quantify and evaluate the distribution of angiotensin II (Ang II) and its receptors in the human retina. METHODS. Donor eyes were obtained within 12 hours postmortem and classified as hypertensive or normotensive and diabetic or nondiabetic, based on the donors' medical histories. Ang II in retina and vitreous was quantified by RIA. Ang II receptors were characterized and quantified by competitive membrane-binding assays. Ang II, its heptapeptide metabolite Ang-(1-7), and AT1 and AT2 receptors were localized by immunohistochemistry and confocal imaging. RESULTS. Levels of Ang II in the retina were significantly higher than in vitreous (P Ͻ 0.05). Ang II in the diabetic retina had a higher median compared with that in the nondiabetic retina. Ang II and Ang-(1-7) colocalized in retinal Müller cells. The retina had the highest levels of Ang II receptors that were significantly higher than the optic nerve, retinal pigment epithelium-choroid complex, and ciliary body-iris complex (P Ͻ 0.05). AT1 receptors were more abundant than AT2 receptors in the retina. Immunoreactivity for AT1 was detected in Müller cells and on blood vessels. AT2 receptors were localized throughout the Müller cells and nuclei of ganglion cells and neurons in the inner nuclear layer. CONCLUSIONS. In the human retina, identification of Ang II and its bioactive metabolite Ang-(1-7) in Müller cells suggests that these glial cells are able to produce and process Ang II. Ang receptors were localized in the blood vessels and neural cells. Local Ang II signaling may thus allow for autoregulation of neurovascular activity. Such an autonomous system could modulate the onset and severity of retinovascular disease. (Invest Ophthalmol Vis Sci. 2007;48:3301-3311) DOI:10.1167/iovs.06-1024 D iabetic retinopathy is one of the major complications of diabetes mellitus and the leading cause of visual loss and blindness in the adult population of the United States. It has been viewed as a disorder of the retinal vasculature 1,2 ; however, evidence from numerous reports indicate that neural function of the retina is compromised before the vascular lesions are clinically diagnosed. At the cellular level, diabetes alters the structure and function of most cell types.3-9 Many factors have been implicated in the pathogenesis of diabetic retinopathy. Clinical and experimental studies have shown that the renin-angiotensin system (RAS) plays a pivotal role in the progression of the disease, presumably through local changes in blood flow and production of vascular endothelial growth factor (VEGF 10 -22 ). Furthermore, Ang II may act as an inflammatory agent by enhancing vascular permeability through prostaglandins and VEGF 23 and contribute to the recruitment of inflammatory cells by inducing chemokines and adhesion molecules. 23,24 Although an independent RAS has not been established in the retina, many reports support the concept of a paracrine RAS in this organ. [25][26][27][28] In the classic pathway, Ang II is produced by the sequential processing of plasma...

show abstract

“…The classical view of the renin-angiotensin system (RAS) as a systemic regulator of blood pressure has been extended, and a substantial number of studies have highlighted the importance of local RAS in a variety of extra-renal tissues, including adrenal glands [132], thymus [133] and recently in the eye [134,135]. In the eye, Ang II, and Ang II type 1 and type 2 receptors (AT1R, AT2R) have been found in the retina, particularly in the retinal pigment epithelium (RPE) [59,60,[136][137][138][139].…”

Section: Hypertension and Age-related Macular Degenerationmentioning

confidence: 99%

Cigarette Smoking and Hypertension Two Risk Factors for Age- Related Macular Degeneration

Marin‐Castaño¹

2013

View full text Add to dashboard Cite

Control of renin secretion from adrenal gland in transgenic Ren-2 and normal rats

Cited by 17 publications

References 39 publications

Therapeutic targets of renin-angiotensin system in ocular disorders

Therapeutic targets of renin-angiotensin system in ocular disorders

Angiotensin II and Its Receptor Subtypes in the Human Retina

Cigarette Smoking and Hypertension Two Risk Factors for Age- Related Macular Degeneration

Contact Info

Product

Resources

About