Regulation of bradykinin receptor level by cholera toxin, pertussis toxin and forskolin in cultured human fibroblasts

Pharmacological characterization of bradykinin receptors in canine cultured tracheal smooth muscle cells

“…Cyclic AMP elevating agents have been shown to exert their effect by receptor up-regulation (Etscheid et al, 1991;Banno et al, 1993). We previously reported that pretreatment of TSMCs with cholera toxin, forskolin, and dibutyryl cyclic AMP enhanced bradykinin-induced inositol phosphates accumulation and a rise in [Ca2+]i through an increase in density of the bradykinin receptor (Yang et al, 1994c Moreover, preincubation with forskolin led to an increase in B. from 25.1 ± 0.3 to 218 ± 24 fmol mg'-protein without changing the KD value.…”

“…It has been shown that long-term cholera toxin treatment potentiates the bradykinin-stimulated phosphoinositide turnover in canine TSMCs, human foreskin fibroblasts, osteoblast-like cell line MC3T3-E1 and BALB/c/3T3 cells (Banno et al, 1993;Etscheid et al, 1991;Olashaw & Pledger, 1988;Yang et al, 1994c (Etscheid et al, 1991;Banno et al, 1993;Yang et al, 1994c). Although only B2 receptor density has been shown to increase in osteoblast-like MC3T3-E1 cells treated with cholera toxin (Banno et al, 1993) …”

The effect of cyclic AMP elevating agents on bradykinin‐ and carbachol‐induced signal transduction in canine cultured tracheal smooth muscle cells

“…These results suggest that prolonged treatment with CTX and forskolin might be required to induce protein synthesis in canine TSMCs. (Gardner et al, 1989;Guillon et al, 1989;Socorro et al, 1990;Etscheid et al, 1991;Banno et al, 1993 …”

“…The enhancing effect of CTX on the PI-PLC pathway may be due to the activation of the stimulatory G, protein, which in turn activates adenylate cyclase, and which leads to an increased intracellular cyclic AMP level (Gilman, 1984) Results are expressed as the mean ± s.e.mean of five separate experiments determined in triplicate. 25r increase in the concentration of cyclic AMP caused by CTX and forskolin is responsible for the enhancement of BKinduced IPs accumulation (Etscheid et al, 1991;Banno et al, 1993). In contrast, several lines of evidence have shown that CTX and forskolin exert a negative feedback regulation on receptor-activated signal transduction through activation of the cyclic AMP-dependent protein kinase.…”

“…This potentiating action was inhibited by cycloheximide. This response may therefore involve an increase in protein synthesis following elevation of the concentration of cyclic AMP, probably through BK receptors (Etscheid et al, 1991;Banno et al, 1993). Moreover, elevation of cyclic AMP concentration caused by CTX promotes transcription of mRNA encoding a protein that stimulates the release of arachidonic acid metabolites (Peterson et al, 1991).…”