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We demonstrate contradirectional couplers in silicon-on-insulator rib waveguides using a CMOS compatible technology, in which a periodic dielectric perturbation is introduced in the coupling region between two different-sized rib waveguides. This structure enables high fabrication tolerances for narrow-bandwidth add-drop filters, using commercially available deep-ultraviolet lithography, that do not suffer from having a free spectral range. The simulation using coupled-mode theory and mode-profile calculations shows good agreement with experiment. A narrow bandwidth of 0.35 nm and a low loss of less than 1 dB have been achieved experimentally.

Acetylcholine (ACh)-induced membrane hyperpolarization was studied in freshly isolated endothelial cells from rabbit aorta. Ten µM ACh induced transient hyperpolarization due to the opening of Ca²⁺-sensitive K⁺ channels, sensitive to TEA and charybdotoxin (CTX). The membrane potential response was accompanied by an increase in intracellular Ca²⁺ [Ca²⁺]_i. Pretreatment of endothelial cells with 20 µM ATP, 0.2 µM bradykinin or 0.1 µM platelet-aggregating factor, which induced either a transient hyperpolarization or no response, changed the subsequent ACh-induced response to a large maintained hyperpolarization. This sustained membrane hyperpolarization was also due to the opening of Ca²⁺-activated K⁺ channels as confirmed by CTX and TEA blockade, and was related to elevated [Ca²⁺]_i measured by fura-2 fluorescence. Pertussis toxin blocked potentiation, indicating involvement of a G protein. The linkage to receptor-operated Ca²⁺ (ROC)-entry was suggested by observations that the maintained hyperpolarization during potentiation was dependent on extracellular Ca²⁺ and was abolished by the ROC blockers SKF-96365 and Ni²⁺. Inhibition of the Ca²⁺ pump of the endoplasmic reticulum mimicked the potentiating effect of the agonists. The results suggest that crosstalk between the agonists in endothelial cells involves Ca²⁺ movements and that this crosstalk is important for the generation of endothelial secretions.

In Fura-2-loaded, freshly isolated rabbit aortic endothelial cells the Ca²⁺ entry pathway was investigated using the Mn²⁺-quenching technique. Acetylcholine (ACh) interaction with muscarinic receptors activated Mn²⁺ influx through the plasma membrane. Sarcoplasmic-endoplasmic reticulum Ca²⁺ ATPase blockers such as cyclopiazonic acid (CPA), thapsigargin and BHQ, which block the endoplasmic reticulum Ca²⁺ pump and do not interact with receptors, also activated Mn²⁺ influx. Mn²⁺ influx activated by either ACh or CPA was blocked by the following agents: SKF96365, a receptor-operated Ca²⁺ channel (ROC) blocker; NCDC, a PLC and ROC blocker, and genistein, a tyrosine kinase inhibitor. D600, the L-type Ca²⁺ channel blocker, had no significant effect on Mn²⁺ influx. Caffeine blocked the ACh-induced Ca²⁺ release but had no effect on the ACh-induced Mn²⁺ influx. Similarly dantrolene, which blocked intracellular Ca²⁺ release induced by ACh, did not affect the ACh-activated Mn²⁺ influx. These data suggest that ACh can activate Ca²⁺ influx without depletion of the ACh-sensitive intracellular Ca²⁺ store. It is concluded (1) that in freshly isolated endothelial cells depletion of the intracellular Ca²⁺ store is not necessary for ACh-activated Ca²⁺ influx, and (2) that receptor activation and intracellular Ca²⁺ store depletion may activate the same Ca²⁺ entry pathway through parallel mechanisms.