Rod-cone-interactions in deuteranopic observers: models and dynamics.

We studied the interactions between rods and L-cones in deuteranopic human observers by stimulating the photoreceptors independently. Thresholds were determined using a PEST procedure for different ratios of rod to L-cone modulation without modulating the S-cones. Modulation frequency was either 2 or 10 Hz and the retinal illuminance ranged from 4.7 to 470 td (10.9-1090 scot td). We measured at 2, 7.5 and 20 degrees retinal eccentricity. The threshold data could be described by a model based on a vector addition of responses originating in the rods and the L-cones. The relative strength of rod signals relative to the L-cone signals increased with increasing retinal eccentricity and decreasing retinal illuminance. At 20 degrees eccentricity, rod and cone signals were of about equal magnitude at retinal illuminances as high as 470 td. Temporal frequency did not have a large effect on the ratio of rod to L-cone signal strength.

Ca2+ entry and vasoconstriction during osmotic swelling of vascular smooth muscle cells.

Exposure of aortic strips from guinea-pigs to hypotonic extracellular fluid is followed by marked vasoconstriction, which is inhibited by D-600 (3 microM), a blocker of voltage-sensitive Ca2+ channels. Conventional electrophysiology, patch-clamp studies, pH determination with 2',7' bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF) and Ca2+ measurements with Fura-2 have been performed on smooth muscle cells cultured either from rat or human aorta to further elucidate the underlying mechanisms. Exposure of the cells to a 25% hypotonic extracellular fluid leads to a rapid and fully reversible depolarization, paralleled by an increase of the selectivity and conductance of the cell membrane to Cl-, an acidification of the cytoplasm and an increase of intracellular Ca2+ concentration ([Ca2+]i). The latter is inhibited by the Ca2+ channel blocker D-600 (1-3 microM). It is concluded that osmotic cell swelling leads to the activation of an anion channel. The subsequent depolarization of the cell membrane activates voltage-sensitive Ca2+ channels which increases [Ca2+]i, thus stimulating the contraction of vascular smooth muscle cells.