Diameter Changes of Retinal Arterioles During Acute Hypoxia<i>In Vivo</i>are Modified by the Inhibition of Nitric Oxide and Prostaglandin Synthesis

Petersen, Line; Bek, Toke

doi:10.3109/02713683.2014.954676

Cited by 22 publications

(25 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The observed vasoconstriction secondary to isometric exercise at baseline was comparable to previous observations in normal persons [10,22], confirming that pressure autoregulation is preserved in diabetic patients without retinopathy [23], and is in accordance with the GF around 1 as calculated from the resting diameters. The reduced vasoconstriction during hypoxia was in accordance with results from a study in normal persons [11], but may depend on the degree of hypoxia since a similar response was neither found in a study with a verified lower degree of hypoxia [10] nor in a study where a lower oxygen saturation was intended but in which a <2% contraction of retinal arterioles was achieved, and the accompanying changes in the arterial blood pressure were not monitored [3].…”

Section: Discussionsupporting

confidence: 89%

“…The significant constriction of retinal arterioles during inhibition of NO synthesis also confirms previous studies in normal persons [19,20], but the lack of effect of NO synthesis inhibition on hypoxia-induced vasodilatation is in contrast to a previous finding on normal persons [10]. The finding may be a consequence of generalized changes in NO metabolism in diabetes mellitus [21] rather than primary changes in the retinal vascular response pattern.…”

Section: Discussionsupporting

confidence: 87%

“…The observed dilatation of arterioles of approximately 4% during hypoxia is in accordance with the dilatation observed in normal persons [10,16,17], and confirms that hypoxia-induced dilatation of retinal vessels is unaffected by diabetes mellitus [18]. The significant constriction of retinal arterioles during inhibition of NO synthesis also confirms previous studies in normal persons [19,20], but the lack of effect of NO synthesis inhibition on hypoxia-induced vasodilatation is in contrast to a previous finding on normal persons [10].…”

Section: Discussionsupporting

confidence: 81%

“…This notion is supported by the fact that the concentration of COX products in the vitreous is abnormal in diabetic animals [5] and in diabetic patients with proliferative retinopathy [6,7], and by the finding that diabetic patientshave abnormal endogenous NO synthesis, probably related to endothelial dysfunction [8,9]. It has previously been shown that interventions on the synthesis of NO and COX products interfere with diameter regulation of retinal arterioles during hypoxia in normal persons [10,11], but it remains unknown how these interventions may affect hypoxia-induced vasodilatation in diabetic patients, and especially whether the changes occur before the development of diabetic retinopathy to suggest a role in the early stages of the pathophysiology of the disease.…”

Section: Introductionmentioning

confidence: 98%

See 3 more Smart Citations

Preserved Pressure Autoregulation but Disturbed Cyclo-Oxygenase and Nitric Oxide Effects on Retinal Arterioles during Acute Hypoxia in Diabetic Patients without Retinopathy

Petersen

Bek²

2016

Ophthalmologica

Self Cite

View full text Add to dashboard Cite

Background: Acute hypoxia induces retinal vasodilatation, which depends on cyclooxygenase (COX) products and nitric oxide (NO) in vitro. However, it is unknown whether these mechanisms are active in diabetic patients and may contribute to the development of diabetic retinopathy. Methods: The Dynamic Vessel Analyzer was used to study the diameter regulation in retinal vessels during hypoxia in type 1 diabetic patients without retinopathy. The influence of NO and COX synthesis inhibition on the diameter of larger retinal vessels was studied during hypoxia, during isometric exercise and during flicker stimulation. Results: Increased arterial blood pressure during L-NMMA infusion and isometric exercise were paralleled by constriction of the retinal arterioles suggesting normal pressure autoregulation. Hypoxia significantly reduced the diameter responses during isometric exercise and during flicker stimulation as compared to normal persons. Conclusion: The findings support that changes in metabolic autoregulation develop before changes in pressure autoregulation in diabetic patients.

show abstract

Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 87%

Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 98%

See 2 more Smart Citations

Preserved Pressure Autoregulation but Disturbed Cyclo-Oxygenase and Nitric Oxide Effects on Retinal Arterioles during Acute Hypoxia in Diabetic Patients without Retinopathy

Petersen

Bek²

2016

Ophthalmologica

Self Cite

View full text Add to dashboard Cite

show abstract

“…1C). To assess this possibility, we monitored the vasomotor response to hypoxia, which triggers a compensatory vasodilation in normal retinas (14). The response to hypoxia was of interest because K ATP channels are activated in hypoxic retinal vessels (12) and play a role in vasodilation (15).…”

Section: Electrogenic Basis For Neovesselmentioning

confidence: 99%

Bioelectric impact of pathological angiogenesis on vascular function

Puro

Kohmoto

Fujita

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Pathological angiogenesis, as seen in many inflammatory, immune, malignant, and ischemic disorders, remains an immense health burden despite new molecular therapies. It is likely that further therapeutic progress requires a better understanding of neovascular pathophysiology. Surprisingly, even though transmembrane voltage is well known to regulate vascular function, no previous bioelectric analysis of pathological angiogenesis has been reported. Using the perforated-patch technique to measure vascular voltages in human retinal neovascular specimens and rodent models of retinal neovascularization, we discovered that pathological neovessels generate extraordinarily high voltage. Electrophysiological experiments demonstrated that voltage from aberrantly located preretinal neovascular complexes is transmitted into the intraretinal vascular network. With extensive neovascularization, this voltage input is substantial and boosts the membrane potential of intraretinal blood vessels to a suprahyperpolarized level. Coincident with this suprahyperpolarization, the vasomotor response to hypoxia is fundamentally altered. Instead of the compensatory dilation observed in the normal retina, arterioles constrict in response to an oxygen deficiency. This anomalous vasoconstriction, which would potentiate hypoxia, raises the possibility that the bioelectric impact of neovascularization on vascular function is a previously unappreciated pathophysiological mechanism to sustain hypoxia-driven angiogenesis.neovascularization | proliferative retinopathy | retinopathy of prematurity | proliferative diabetic retinopathy | retina T he abnormal growth of blood vessels is a key pathophysiological feature of numerous disorders, including tumorigenesis, arthritis, endometriosis, and retinopathies. Despite substantial progress from studies of patients and animal models, abnormal neovascularization remains a common threat to health and wellbeing. To help address this challenge, we devised a unique experimental approach to better understand neovascular pathophysiology. Because almost nothing is known about the electrogenic profile of neovascular complexes and how these complexes functionally interact with their parent vessels, we focused on the bioelectric features of neovascularization. These gaps in knowledge are surprising, considering that it is well established that the transmembrane voltage of vascular cells (1), as well as electrotonic cell-cell interactions within a vascular network (2-4), play vital roles in regulating blood flow.In this electrophysiological analysis of pathological angiogenesis, we focused on abnormal vasoproliferation in rodent and human retinas. For multiple reasons, the retina is an ideal tissue for this undertaking. First is its clinical importance. Retinal vasoproliferation is the major cause of blindness in prematurely born infants (retinopathy of prematurity) and persons with diabetes (proliferative diabetic retinopathy) and sickle cell disease (sickle cell retinopathy). The hallmark of these disorders is abno...

show abstract

Lack of effect of nitroglycerin on the diameter response of larger retinal arterioles in normal persons during hypoxia

Kaya

Petersen

Bek

2015

Graefes Arch Clin Exp Ophthalmol

View full text Add to dashboard Cite

show abstract

Diameter Changes of Retinal Arterioles During Acute HypoxiaIn Vivoare Modified by the Inhibition of Nitric Oxide and Prostaglandin Synthesis

Cited by 22 publications

References 25 publications

Preserved Pressure Autoregulation but Disturbed Cyclo-Oxygenase and Nitric Oxide Effects on Retinal Arterioles during Acute Hypoxia in Diabetic Patients without Retinopathy

Preserved Pressure Autoregulation but Disturbed Cyclo-Oxygenase and Nitric Oxide Effects on Retinal Arterioles during Acute Hypoxia in Diabetic Patients without Retinopathy

Bioelectric impact of pathological angiogenesis on vascular function

Lack of effect of nitroglycerin on the diameter response of larger retinal arterioles in normal persons during hypoxia

Contact Info

Product

Resources

About