The vascular endothelium as a regulator of the ocular circulation: A new concept in ophthalmology?

Haefliger, Ivan O.; Meyer, Peter; Flammer, Josef; Lüscher, Thomas F.

doi:10.1016/0039-6257(94)90157-0

Cited by 175 publications

(89 citation statements)

References 84 publications

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“…Endothelial-derived molecules, ie; endothelins, thromboxane A2, prostaglandins and nitric oxide play a role in autoregulation by modulating vascular tone. 38 Breakdown of autoregulation occurs with rise or fall of perfusion pressure beyond a critical range. In hypertensives, where the autoregulation range is set to higher levels, episodic hypotension (spontaneously, as during sleep or due to overtreatment), changes in the tone of the precapillary arterioles (mediated by angiotensin or antihypertensive drugs) and vascular endothelial changes (leading to reduced nitric oxide synthesis) lead to breakdown of autoregulation.…”

Section: Pathophysiologymentioning

confidence: 99%

Hypertension and the eye: changing perspectives

et al. 2002

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Systemic hypertension is a common condition associated with significant morbidity and mortality. Hypertension confers cardiovascular risk by causing target-organ damage that includes retinopathy in addition to heart disease, stroke, renal insufficiency and peripheral vascular disease. The recognition of hypertensive retinopathy is important in cardiovascular risk stratification of hypertensive individuals. This review reevaluates the changing perspectives in the pathophysiology, classification and prognostic significance of fundal lesions in hypertensives.

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Section: Pathophysiologymentioning

confidence: 99%

Hypertension and the eye: changing perspectives

et al. 2002

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“…The vascular area of the optic nerve head which is critical in the pathogenesis of glaucoma also lacks autonomic innervation and is to some extent autoregulated [26,28,31]. However, blood supply of the optic nerve head mainly depends on the perfusion of the posterior ciliary arteries, which are regulated in a way similar to coronary and peripheral arteries [14]. In particular, all these ocular and extraocular vessels have in common that they are rather sensitive to the vasoconstrictor effects of endothelin-1 [4,22,23].…”

Section: Discussionmentioning

confidence: 99%

Inverse correlation between endothelin-1-induced peripheral microvascular vasoconstriction and blood pressure in glaucoma patients

Gass

Flammer

Linder

et al. 1997

Graefe's Arch Clin Exp Ophthalmol

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Abstract• Background: The potent vasoconstrictor peptide endothelin-I has been shown to participate in the control of peripheral vascular tone and in the regulation of ocular perfusion. In glaucoma patients vasospasms and arterial hypotension have been identified as risk factors for the progression of glaucomatous damage, and the regulation of endothelin-1 release is disturbed in some of these patients. The aim of this study was to assess the relationship between resting blood pressure and cutaneous vascular responsiveness to endothelin-1 and phenylephrine in patients with glaucoma and in matched controls. • Methods: In 9 patients with primary open-angle glaucoma (POAG), 7 patients with normal tension glaucoma (NTG), and 16 age-and sex-matched controls, endothelin-1 and phenylephrine responses were assessed in the human forearm microcirculation using laser Doppler flowmetry during intra-arterial drug administration. Blood pressure was measured intraarterially.• Results: In contrast to a~-adrenergic effects, endothelin-1 responses were inversely correlated to both systolic (r e = 0.27, P = 0.05) and diastolic (re =-0.54, P = 0.001) blood pressure in glaucoma patients, whereas there was no such correlation in controls. Patients with lower blood pressure values were more sensitive to the vasoconstrictor effects of endothelin-1. Cutaneous responsiveness to endothelin-1 and phenylephrine was similar in glaucoma patients and in controls.• Conclusion: These results reveal that glaucoma patients appear to have peripheral microvascular abnormalities which are exhibited as altered responsiveness to endothelin-1. Thus, this study supports the hypothesis that endothelin-l-related microvascular dysfunction may be involved in the pathogenesis of glaucomatous damage.

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“…7 Taken together, these observations suggest that vascular dysfunction or, more specifically, abnormalities of endothelial-derived vasodilator production may underlie the pathologic process. 8 In most vascular beds, nitric oxide (NO) is an important vasodilator produced by the endothelium through the action of nitric oxide synthase (NOS). Prostacyclin (PGI 2 ) is another significant vasodilator, for example in the coronary circulation.…”

Section: Introductionmentioning

confidence: 99%

Role of cyclooxygenase and haemoxygenase products in nitric oxide-independent vasodilatation in the porcine ciliary artery

Quinn

O’Brien

McLoughlin

2003

Eye

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Purpose Vascular endothelial cell dysfunction has been noted in patients with normal pressure glaucoma. Although nitric oxide (NO) accounts for a large proportion of vasorelaxation in the posterior ciliary artery, considerable relaxation remains unexplained. We investigated the roles of haemoxygenase (HO) and cyclooxygenase (COX), which produce the vasodilators carbon monoxide (CO) and prostacyclin, respectively, in NO-independent endothelium-dependent vasodilatation in porcine posterior ciliary arteries. Methods Isolated vascular rings were mounted in a Mulvaney-Halpern small vessel myograph for the measurement of isometric tension development. Vasodilator responses to bradykinin (BK) were elicited in each ring on three separate occasions following preconstriction with prostaglandin F 2a : first in the absence of inhibitors, second in the presence of the NO synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME, 10 -3 M), and third in the presence of L-NAME and either a COX (indomethacin, 10 -6 M) or an HO inhibitor (tin protoporphyrin-IX 10 -5 M). Results were expressed as a percentage of the maximal relaxation in the presence of L-NAME alone.Results Incubation with indomethacin (n ¼ 6), in the presence of L-NAME, significantly reduced (Po0.01) maximum BK-induced relaxation (À103.578.8%) compared to paired rings in the presence of L-NAME alone (À130.878.8%). HO inhibition did not reduce NO-independent, BK-induced relaxation when compared to paired control vessels.Conclusions These data suggest that in the presence of L-NAME, a COX product accounts for a significant proportion of NO-independent vasodilatation. In contrast, endogenous CO production does not have a functionally significant role in the porcine ciliary artery.

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The vascular endothelium as a regulator of the ocular circulation: A new concept in ophthalmology?

Cited by 175 publications

References 84 publications

Hypertension and the eye: changing perspectives

Hypertension and the eye: changing perspectives

Inverse correlation between endothelin-1-induced peripheral microvascular vasoconstriction and blood pressure in glaucoma patients

Role of cyclooxygenase and haemoxygenase products in nitric oxide-independent vasodilatation in the porcine ciliary artery

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