Mechanisms underlying spontaneous rhythmical contractions in irideal arterioles of the rat

Abstract

1. Mechanisms underlying spontaneous rhythmical contractions have been studied in irideal arterioles of the rat using video microscopy and electrophysiology. 2. Rhythmical contractions (4 min-1) were more common during the second and third postnatal weeks and were always preceded by large, slow depolarizations (5-40 mV). 3. Spontaneous contractions were unaffected by tetrodotoxin (1 μM), neurotransmitter receptor antagonists, the sympathetic neurone blocker, guanethidine (5 μM) or sensory neurotoxin, capsaicin (1 μM). 4. Stimulation of sensory nerves inhibited spontaneous activity and this was not prevented by L-NAME (10 μM). 5. L-NAME (10 μM) caused an increase in frequency of spontaneous contractions, while forskolin (30 nM), in the presence of L-NAME, abolished spontaneous, but not nerve-mediated, contractions. 6. Spontaneous activity was not affected by felodipine (1 nM) or nifedipine (1 μM), but was abolished by cadmium chloride (1 μM) or superfusion with calcium-free solution. 7. Caffeine (1 mM), thapsigargin (2 μM) and cyclopiazonic acid (3 μM), but not ryanodine (3 μM), abolished spontaneous and nerve-mediated contractions. After preincubation in L-NAME (10 μM), cyclopiazonic acid abolished spontaneous contractions only. 8. Spontaneous depolarizations and contractions were abolished by 18α-glycyrrhetinic acid (20 μM). 9. Results suggest that spontaneous rhythmical contractions are myogenic and result from the cyclical release of calcium from intracellular stores, without a contribution from voltage-dependent calcium channels. Intercellular coupling through gap junctions appears to be essential for co-ordination of these events which could be modulated by nitric oxide and increases in cAMP. The possibility that different intracellular stores underly spontaneous and nerve-mediated contractions is discussed.