Regulatory Mechanisms in the Retinal and Choroidal Circulation

Delaey, Christophe; Voorde, Johan Van de

doi:10.1159/000055622

Cited by 378 publications

(290 citation statements)

References 52 publications

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“…Since the decrease in systemic blood pressure caused by RAS inhibition did not alter RBF in NDM rats it is unlikely that this small change in blood pressure contributed to the normalization of RBF in captopril-or candesartantreated DM rats. Previous work has shown that RBF is mainly controlled by autoregulatory mechanisms and local factors [29]. These results suggest that RAS inhibition blocked a diabetes-induced abnormality in the retinal vasculature, which thereby preserved retinal haemodynamics.…”

Section: Discussionsupporting

confidence: 57%

Angiotensin AT 1 receptor antagonism normalizes retinal blood flow and acetylcholine-induced vasodiliation in normotensive diabetic rats

et al. 2004

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Aims/hypothesis. The renin angiotensin system is emerging as a potential therapeutic target for diabetic retinopathy. This study examines the effects of angiotensin-converting-enzyme inhibition by captopril and angiotensin AT 1 receptor antagonism using candesartan-cilexetil on retinal blood flow and acetylcholinestimulated vasodilatation in normotensive diabetic rats. Methods. Non-diabetic or streptozotocin-induced diabetic rats were treated for 2 weeks with captopril (100 mg/kg/day) or candesartan cilexetil (2 mg/kg/day). Retinal haemodynamics were measured using video fluorescein angiography. Effects of exogenous acetylcholine on retinal haemodynamics were examined following intravitreal injection. Total retinal diacylglycerol was labelled using diacylglycerol kinase, separated by thin-layer chromatography, and quantified using autoradiography. Results. Diabetic rats had prolonged retinal mean circulation time and decreased retinal blood flow compared with non-diabetic rats. Treatment of diabetic rats with either captopril or candesartan blocked the development of these blood flow abnormalities. Intraviteral injection of acetylcholine (10 −5 mol/l) in non-diabetic rats increased retinal blood flow by 53.9±22.0% relative to baseline whereas this response to acetylcholine was blunted in diabetic rats (4.4±19.6%, p<0.001). Candesartan treatment of diabetic rats restored the acetylcholine-stimulated retinal blood flow response to 60.0±18.7% compared with a 56.2+20.1% response in candesartan-treated non-diabetic rats. Total retinal diacylglycerol levels were increased in diabetic rats (3.75±0.98 nmol/mg, p<0.05) compared with non-diabetic rats (2.13±0.25 nmol/mg) and candesartan-treatment of diabetic rats normalized diacylglycerol levels (2.10±0.25 nmol/mg, p<0.05). Conclusion/interpretation. This report provides evidence that angiotensin-converting enzyme inhibition and AT 1 receptor antagonism ameliorates retinal haemodynamic dysfunctions in normotensive diabetic rats. [Diabetologia (2004) 47:113-123]

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Section: Discussionsupporting

confidence: 57%

Angiotensin AT 1 receptor antagonism normalizes retinal blood flow and acetylcholine-induced vasodiliation in normotensive diabetic rats

et al. 2004

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“…In contrast, the choroidal circulation (that is, the ophthalmic artery) is mainly controlled by sympathetic innervation and is not autoregulated. 24 Thus, the results of the ocular blood flow velocity in the cited study and in our study were influenced by different regulatory mechanisms. Nevertheless, the time-related observations of blood pressure changes and subsequent local alterations in healthy men could be reproduced by our observations in men with normal bBP, who have achieved the SI peak after the blood pressure peak.…”

Section: Discussionmentioning

confidence: 50%

Cold stimulation induces different responses of ophthalmic artery blood flow velocity depending on baseline blood pressure and gender

2009

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Earlier, we have introduced the spectral index (SI), which was derived from the harmonic content of the blood flow velocity envelope of the ophthalmic artery. SI changed in dependency on the baseline blood pressure (bBP). We now examined SI during sympathetic activation by cold stimulation for 300 s in dependency on bBP to investigate the response to sympathetic neural activity in arterial hypertension. Ten men and 12 women with normal bBP (age, 60.5 ± 4.6 years and 61.9 ± 7.2 years) and age-adjusted men and women with increased bBP underwent the cold pressor test, including a periodical measurement of blood pressure and blood flow velocity in the ophthalmic artery, the latter by pulsed Doppler sonography. From this, the course of the SI was calculated. During cold stimulation men with increased bBP achieved their SI peak and their systolic blood pressure peak earlier than those with normal bBP (P ¼ 0.002 and P ¼ 0.035, respectively) and their SI slope was steeper than in normotensive men (P ¼ 0.002). Multiple testing showed that the difference of SI decrease between men with normal and increased bBP occurs on average 60 s after the beginning of cold stimulation (P ¼ 0.018). These differences were not found between female blood pressure groups, but the results in women may be influenced by antihypertensive treatment of some of the hypertensive women. In conclusion, the SI is useful to evaluate the response to sympathetic activation in hypertensive men but a larger study population should confirm the study results in women.

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“…It was equally prominent at all retinal poles and eccentricities, comprising~7-8 % of the total length of horizontally running blood vessels. As retinal vasculature lacks autonomic control, and shows an efficient local regulation [47,48], the function of vascular cells may be modulated by neurons in this region. Pericytes are the contractile cells of the vasculature [15], and are more dense in retinal blood vessels than anywhere in the brain [49].…”

Section: Neuronal Control Of Blood Flow: a Role For Cholinergic Regulmentioning

confidence: 99%

Leveraging Optogenetic-Based Neurovascular Circuit Characterization for Repair

2016

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Optogenetic techniques are a powerful tool for determining the role of individual functional components within complex neural circuits. By genetically targeting specific cell types, neural mechanisms can be actively manipulated to gain a better understanding of their origin and function, both in health and disease. The potential of optogenetics is not limited to answering biological questions, as it is also a promising therapeutic approach for neurological diseases. An important prerequisite for this approach is to have an identified target with a uniquely defined role within a given neural circuit. Here, we examine the retinal neurovascular unit, a circuit that incorporates neurons and vascular cells to control blood flow in the retina. We highlight the role of a specific cell type, the cholinergic amacrine cell, in modulating vascular cells, and demonstrate how this can be targeted and controlled with optogenetics. A better understanding of these mechanisms will not only extend our understanding of neurovascular interactions in the brain, but ultimately may also provide new targets to treat vision loss in a variety of retinal diseases.

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Regulatory Mechanisms in the Retinal and Choroidal Circulation

Cited by 378 publications

References 52 publications

Angiotensin AT 1 receptor antagonism normalizes retinal blood flow and acetylcholine-induced vasodiliation in normotensive diabetic rats

Angiotensin AT 1 receptor antagonism normalizes retinal blood flow and acetylcholine-induced vasodiliation in normotensive diabetic rats

Cold stimulation induces different responses of ophthalmic artery blood flow velocity depending on baseline blood pressure and gender

Leveraging Optogenetic-Based Neurovascular Circuit Characterization for Repair

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