Maintenance of quantal size and immediately releasable granules in rat chromaffin cells by glucocorticoid.

Glucocorticoid is reported to regulate catecholamine synthesis and storage. However, it is not clear whether the actual amount of catecholamine released from individual granules (quantal size, Q) in mature chromaffin cells is affected by glucocorticoid. Using carbon fiber amperometry, we found that dexamethasone did not affect mean cellular Q or the proportional release from different populations of granules in rat chromaffin cells cultured for 1 day in a serum-free defined medium. After two extra days of culture in the defined medium, there was a rundown in mean cellular Q, and it was associated with a shift in the proportional release from the different granule populations. This phenomenon could not be rescued by serum supplementation but could be prevented by dexamethasone via an action that was independent of changes in voltage-gated Ca(2+) channel (VGCC) density. Using simultaneous measurements of membrane capacitance and cytosolic Ca(2+) concentration, we found that for cells cultured in defined medium dexamethasone enhanced the exocytotic response triggered by a brief depolarization (50 ms) without affecting the VGCC density or the fast exocytotic response triggered via flash photolysis of caged Ca(2+). Thus glucocorticoid may regulate the number of immediately releasable granules that are in close proximity to a subset of VGCC. Because chromaffin cells in vivo are exposed to high concentrations of glucocorticoid, our findings suggest that the paracrine actions of glucocorticoid maintain the mean catecholamine content in chromaffin cell granules as well as the colocalization of releasable granules with VGCCs.

Clinical utility of ST-segment depression in lead AVR in acute myocardial infarction.

The present study evaluated the prevalence and significance of ST-segment depression (STD) in lead aVR on the admission 12-lead electrocardiogram in 307 consecutive patients with an acute myocardial infarction (AMI) with ST-segment elevation. STD in aVR was present in a significantly higher proportion of patients with inferior/posterior AMIs. Within inferior/posterior AMIs those with STD in aVR had significantly more concomitant STD in V(1), V(2), V(3) and more concomitant STesegment elevation in V(5), V(6) and right precordial leads. These data suggests that STD in aVR may point to a coronary artery with a large area of supply as the culprit vessel responsible for the AMI.