Alpha-adrenoceptor activation induces rhythmic contractile activity in carotid arteries from young, not adult, rats.

Rhythmic contractions are produced by small arteries, arterioles and veins in several vascular beds, but they are often absent in large arteries. However, under certain conditions, and in certain disease states large arteries may produce rhythmic contractions. For this reason, the present study was undertaken to test the hypothesis that rhythmic contractions may be a 'normal' response in large arteries at some stage in development. We investigated this hypothesis by examining contractions of carotid arteries in male and female rats aged 15, 25 and 30 days and in adult rats. Rhythmic contractions were produced by exposure to, or during washout of alpha-adrenoceptor agonists in young, but not adult, rats. In particular, rhythmic activity was identified in 40, 95 and 50% of the arteries from, respectively, 15, 25 and 30-day-old rats. No differences were found in rhythmic activity between female and male rats. Furthermore, the rhythmic activity was not inhibited by the K+ channel blocker TEA (20 mM) or the Na+/K(+)-ATPase inhibitor, ouabain (32 microM). Nor was it inhibited by endothelial denudation. However, the Ca2+ channel blocker, nifedipine (0.1 microM), completely eliminated rhythmic contraction. These results suggest that receptor-induced rhythmic contractile activity is a 'normal' characteristic at approximately 25 days of development in carotid arteries of rats, but that this activity declines with age until it is completely absent by adulthood. We proposed that this difference was due to unfused and fused Ca2+ channel activities in, respectively, young and adult rat arteries, to differential expression of Ca2+ channel isotypes, or to differences in receptor-mediated signal transduction mechanisms 'upstream' from Ca2+ channels.