Assessment of the permeability of the blood-retinal barrier in hypertensive rats.

Abstract

SUMMARY We assessed the permeability surface area products at the blood-retinal barrier and blood-brain barrier to sucrose (molecular weight, 340) and microperoxidase (molecular weight, 2000) following acute hypertension induced by metaraminol in Wistar-Kyoto rats (controls) and during chronic hypertension in spontaneously hypertensive rats. In acute hypertension, the permeability surface area product for sucrose was increased at the blood-retinal barrier and at the blood-brain barrier over control values (p<0.02), and the vessels became leaky to microperoxidase. In chronic hypertension, the permeability of the blood-retinal barrier to sucrose was increased over that in control animals (p<0.02), whereas the permeability of the blood-brain barrier was unaffected. Neither barrier leaked microperoxidase. These results indicate that the blood-brain barrier and the blood-retinal barrier are similarly affected in acute hypertension and that in chronic hypertension, the blood-brain barrier is unaffected whereas the blood-retinal barrier is rendered more permeable to small, but not large, solutes. 1 Changes in retinal blood vessels are apparent on clinical examination in humans with acute and chronic hypertension. Following an acute pressure rise, the blood-retinal barrier (BRB) can be shown to be breached using fluorescein angiography, but fiuorescein leakage usually is not apparent in chronic benign hypertension. Spontaneously hypertensive rats (SHR) have been used as an animal model to examine the effects of chronic hypertension. They manifest the characteristic renal lesions of arteriolar nephrosclerosis, 3 and their cerebral blood vessels demonstrate the same increased media thickness and larger vessel to lumen wall ratio

Mechanistic links between systemic hypertension and open angle glaucoma

“…It is worth noting that oral administration of losartan and captopril reduces IOP in primary open angle glaucoma patients, 57,58 suggesting that systemic Renin-Angiotensin system may potentially affect the regulation of IOP by influencing ocular Renin-Angiotensin system. This is consistent with the finding that the blood-retinal barrier was shown to be more permeable in spontaneously hypertensive rats compared with that in Wistar Kyoto rats, 63 indicating that a disrupted blood-retinal barrier resulting from hypertension may enhance the effects of circulating Renin-Angiotensin system on the eye.…”

T/T homozygosity of the tenascin-C gene polymorphism rs2104772 negatively influences exercise-induced angiogenesis

“…This observation differs from those in studies assessing the role of tenascin-C in vascular growth in pathological blood vessel remodeling in chronic angiotensin-mediated hypertension and tumor growth [4, 5, 7] which are characterized by chronic inflammation and elevated microvascular permeability [55, 56]. The latter has been shown to reflect leaky blood vessels in association with the angiopoietin pathway [57].…”

Quantitative evaluation for blood-retinal barrier breakdown in experimental retinal vein occlusion produced by photodynamic thrombosis using a new photosensitizer

“…15,16 In previous reports, hypertensive animals have damaged vascular endothelial cells with increased capillary permeability before RVO. 25,26 Therefore, the BRB of SHR will be more damaged than that of WKY by RVO. According to our results, high EB values continued longer in SHR than in WKY, indicating that capillary endothelial cells and pericytes of SHR after RVO recovered from the damage later than those of WKY.…”