March 1994
Volume 35, Issue 3
Articles  |   March 1994
Effects of extracellular pH on agonist-induced vascular tone of the cat ophthalmociliary artery.
Author Affiliations
  • E N Su
    Lions Eye Institute, University of Western Australia, Nedlands.
  • D Y Yu
    Lions Eye Institute, University of Western Australia, Nedlands.
  • V A Alder
    Lions Eye Institute, University of Western Australia, Nedlands.
  • S J Cringle
    Lions Eye Institute, University of Western Australia, Nedlands.
Investigative Ophthalmology & Visual Science March 1994, Vol.35, 998-1007. doi:
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      E N Su, D Y Yu, V A Alder, S J Cringle; Effects of extracellular pH on agonist-induced vascular tone of the cat ophthalmociliary artery.. Invest. Ophthalmol. Vis. Sci. 1994;35(3):998-1007.

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      © ARVO (1962-2015); The Authors (2016-present)

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PURPOSE: To test whether changes in extracellular pH (pHe) in an in vitro preparation of the cat ophthalmociliary artery affect passive tone and agonist responses and whether the endothelial cells are mediators of any pH-induced effect. This will determine the ability of the ophthalmociliary artery to influence retinal and choroidal blood flow in response to metabolic stimuli. METHODS: The isometric tension generated by isolated ring segments preactivated by prostaglandin F2 alpha (PGF2 alpha), noradrenaline (NA), or 40 mM K+ was measured as the pHe of the bathing solution was changed stepwise from 6.0 to 8.0 by adjusting the bathing bicarbonate concentration in preparations with and without functioning endothelial cells. RESULTS: PGF2 alpha produces a concentration-dependent contraction that is insensitive to an alkaline shift from control pHe (7.4) in the bathing medium. For acidic shifts to pHe 7.0, there is no significant change in the magnitude of the PGF2 alpha contraction, whereas at pHe 6.0, the PGF2 alpha contraction is reduced to 23 +/- 4% (n = 23) of its value at pHe 7.4. Threshold response concentration remains unaffected. Deliberate damage to the endothelial cells does not significantly affect the magnitude of the 10(-5) M PGF2 alpha response at pHe 7.4 nor the effect of acidic pH on this response. The 10(-5) M NA response is reduced in a graded fashion to acidic shifts to pH 7.0 and 6.0 (40 +/- 4% [n = 23]) and also to alkaline shift to pH 8.0 (22 +/- 5% [n = 23]) when compared to the induced tension at pHe 7.4. For the acidic shift only, endothelial cell damage causes a further significant reduction in the NA response to 20 +/- 3% (n = 5). For vessels contracted with K(+)-Krebs solution, there is a small but significant reduction in response at pHe 6.0 to 84 +/- 6% (n = 25), whereas for pHe 8.0 there is a much larger reduction to 45 +/- 5% (n = 24). All pHe-induced relaxations of K+ are endothelium independent. Passive tension is unaffected by all pHe manipulations. CONCLUSIONS: Vessel responses to vasoactive agents are selectively mediated by pHe changes. Major acidic shifts cause reduced responses (relaxation) to NA, PGF2 alpha, or K+, whereas only vessels preactivated with NA and K+ relax to alkaline shifts. This implies that NA or K+ induced vascular responses are maximal close to neutral pHe with major shifts from neutrality in either the acidic or alkaline direction causing a reduced response. These results imply that the ophthalmociliary artery probably does not play a major role in controlling ocular blood flow in response to pHe changes within the normal metabolic range, but it may become important in ischemic conditions.


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