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Query: UMLS:C0595921 (intraocular pressure)
 11,750 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The importance of considering the effect of a possible flow out of the anterior chamber before inferring any mechanism of aqueous humor formation from the relative concentration of a substance in the aqueous humor and plasma under equilibrium conditions has been stressed. Several processes to account for the chemical equilibria between aqueous humor and blood based on the ultrafiltration and secretion hypotheses with a possible simultaneous loss of aqueous humor by flow have been outlined. On the basis of these processes, equations were formulated which would relate the rates of transfer into and out of the anterior chamber to the ratio of concentration of a substance in the aqueous to that in the blood at various intervals after its introduction into the blood. The explanation of equilibrium ratios above and below one for aqueous constituents is made apparent from the mathematical formulations. For each substance tested a determination was made of the best fit when the concentration in the aqueous humor is plotted against time. This fit was obtained by plotting the rate of transfer in against the rate of transfer out of the anterior chamber for all of the experimentally found concentration ratios on the basis of both the ultrafiltration and secretory hypotheses. Two sets of values were obtained from these calculations, one set for each hypothesis. The substantial agreement of all the experimental data with an assumed rate of leakage out of the anterior chamber of approximately 4 c. mm. per minute was shown to be compatible only with the idea that all the monovalent electrolytes tested entered the anterior chamber as a result of secretory process. It could not be decided from these chemical studies whether the non-electrolytes and the one multivalent electrolyte tested enter the anterior chamber by ultrafiltration or secretion. Experimental findings from other sources were cited which would suggest that non-electrolytes enter the anterior chamber as a result of ultrafiltration. The implications of the mechanism outlined in the paper with respect to intraocular pressure have been discussed. Supplementary evidence from the literature has been given in support of the conclusions presented here.
J Gen Physiol 1942 Nov 20
PMID:THE MECHANISM OF AQUEOUS HUMOR FORMATION INFERRED FROM CHEMICAL STUDIES ON BLOOD-AQUEOUS HUMOR DYNAMICS. 1987 33

Mechanotransduction by the trabecular meshwork (TM) is an essential component of intraocular pressure regulation in the vertebrate eye. This process is compromised in glaucoma but is poorly understood. In this study, we identify transient receptor potential vanilloid isoform 4 (TRPV4) and TWIK-related potassium channel-1 (TREK-1) as key molecular determinants of TM membrane potential, pressure sensitivity, calcium homeostasis, and transcellular permeability. We show that resting membrane potential in human TM cells is unaffected by "classical" inhibitors of voltage-activated, calcium-activated, and inwardly rectifying potassium channels but is depolarized by blockers of tandem-pore K+ channels. Using gene profiling, we reveal the presence of TREK-1, TASK-1, TWIK-2, and THIK transcripts in TM cells. Pressure stimuli, arachidonic acid, and TREK-1 activators hyperpolarize these cells, effects that are antagonized by quinine, amlodipine, spadin, and short-hairpin RNA-mediated knockdown of TREK-1 but not TASK-1. Activation and inhibition of TREK-1 modulates [Ca2+]TM and lowers the impedance of cell monolayers. Together, these results suggest that tensile homeostasis in the TM may be regulated by balanced, pressure-dependent activation of TRPV4 and TREK-1 mechanotransducers.
J Gen Physiol 2018 12 03
PMID:TREK-1 channels regulate pressure sensitivity and calcium signaling in trabecular meshwork cells. 3116 65


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