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within the myocytes. In contrast, mammalian atrial myocytes do not have a well developed t-tubular system, and the coupling between the L-type Ca 2+ channels in the sarcolemma and the junctional SR occurs around the periphery of the myocytes [6][7][8]. A confocal imaging of [Ca 2+ ] i has shown that in mammalian atrial myocytes during E-C coupling, an increase in [Ca 2+ ] i can be observed in the peripheral regions of the cell before it spreads to the center [9][10][11]. Furthermore, in spite of a poorly developed t-tubular system, ryanodine receptors (RyR) are present at seemingly equal abundance through atrial myocytes [11][12][13]. These observations strongly suggest that many RyR in the central SR are not associated with L-type Ca 2+ channels. It has been proposed

The effects of carvedilol (an alpha.beta-blocker) on lipid metabolism were assessed in addition to its hypotensive effect. The subjects were 18 men and 18 women, 20 with hypertension and 16 normotensives with other conditions requiring carvedilol treatment. They were aged from 31 to 79 years and were given a daily dose of 5-20 mg carvedilol (average, 9.7 mg/day) for 12 weeks. Significant falls were seen in blood pressure and heart rate after 12 weeks in the hypertensive subjects (mean +/- SE) (systolic: from 164 +/- 2 to 141 +/- 2 mm Hg, P less than 0.001; diastolic: from 98 +/- 1 to 85 +/- 2 mm Hg, P less than 0.001; heart rate: from 71 to 65 beats/min, P less than 0.001). Smaller changes in blood pressure and heart rate were seen in the normotensive subjects, with the fall in systolic pressure being significant (from 143 +/- 3 to 135 +/- 2 mm Hg, P less than 0.01). There were no significant changes in the overall serum total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, and phospholipid levels. In the subgroup with a pretreatment serum triglyceride level of greater than 150 mg/dl, a significant fall of 52.1 mg/dl was seen (P less than 0.05). Lipoprotein analysis showed a significant fall in alpha-lipoprotein levels (P less than 0.05). The atherogenic index did not change significantly, and it was concluded that carvedilol was an effective antihypertensive agent that produced no adverse effects and possibly had beneficial effects on lipid metabolism.

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