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Exp Eye Res. 1999 Oct;69(4):413-29.

Modulation of choroidal autoregulation in the rabbit.

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Department of Ophthalmology, University of Texas Health Science Center, San Antonio, Texas 78299-3900, USA.


Previous studies show that the choroid can maintain its blood flow despite changes in perfusion pressure, behaviour possibly mediated by an autoregulatory mechanism. However, the choroid's rich autonomic innervation suggests possible neural involvement in the response. To evaluate the potential neural contribution, choroidal blood flow was measured by laser Doppler flowmetry over a wide range of perfusion pressure before and after ganglionic blockade in anaesthetized rabbits. Although an upward shift in the pressure-flow (P-F) curve was anticipated due to loss of adrenergic tone, ganglionic blockade shifted the P-F curve downward, prompting a search for a neural vasodilator to explain the response. Cholinergic blockade with atropine failed to alter the P-F curve suggesting little parasympathetic involvement. By contrast, inhibition of nitric oxide (NO) synthase with nitro-L-arginine methyl ester (L-NAME) caused a dramatic downward shift in the P-F curve, suggesting the nitridergic nerves as the source of vasodilatory tone. However, the downward shift in the P-F curve with L-NAME was greater than seen with ganglionic blockade, indicating that endothelial NO rather than neural dilator tone predominates. Moreover, calcium channel blockade after L-NAME reversed the downward shift in the P-F curve suggesting that choroidal vascular tone is modulated by an interaction between NO and an unknown vasoconstrictor. Neither hexamethonium, losartan or a vasopressin antagonist given after L-NAME reversed the downward shift in the P-F curve, ruling out a neural vasoconstrictor, angiotensin II and vasopressin as the source of constrictor tone. Phentolamine given after L-NAME caused a small but significant reversal of the downward shift in the P-F curve, suggesting a minor adrenergic contribution. By contrast, the non-selective endothelin antagonist, A-182086, given after L-NAME significantly attenuated the choroidal constriction. These results indicate that an unknown neural dilator and locally produced NO and endothelin exert competing influences on the inherent reactivity of the choroidal resistance vessels as they respond to changes in perfusion pressure, and that this local regulation is likely modulated by extrinsic neurohumoral factors that are relatively quiet in the anesthetized rabbit.

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