1. Mechanisms underlying spontaneous rhythmical contractions hare been stud
ied in irideal arterioles of the rat using video microscopy and electrophys
iology.
2. Rhythmical contractions (4 min(-1)) were more common during the second a
nd third postnatal weeks and were always preceded by large, slow depolariza
tions (5-40 mV).
3. Spontaneous contractions were unaffected by tetrodotoxin (1 mu M), neuro
transmitter receptor antagonists, the sympathetic neurone blocker, guanethi
dine (5 mu M) or sensory neurotoxin, capsaicin (1 mu M).
4. Stimulation of sensory nerves inhibited spontaneous activity and this wa
s not prevented by L-NAME (10 mu M).
5. L-NAME (10 mu M) caused an increase in frequency of spontaneous contract
ions, while forskolin (30 nM), in the presence of L-NAME, abolished spontan
eous, but not nerve-mediated, contractions.
6. Spontaneous activity was not affected by felodipine (1 nM) or nifedipine
(1 mu M), but was abolished by cadmium chloride (1 mu M) or superfusion wi
th calcium-free solution.
7. Caffeine (1 mM), thapsigargin (2 mu M) and cyclopiazonic acid (3 mu M),
but not ryanodine (3 mu M), abolished spontaneous and nerve-mediated contra
ctions. After preincubation in L-NAME (10 mu M), cyclopiazonic acid abolish
ed spontaneous contractions only.
8. Spontaneous depolarizations and contractions were abolished by 18 alpha-
glycyrrhetinic acid (20 mu M)
9. Results suggest that spontaneous rhythmical contractions are myogenic an
d result from the cyclical release of calcium from intracellular stores, wi
thout a contribution from voltage-dependent calcium channels. Intercellular
coupling through gap junctions appears to be essential for co-ordination o
f these events which could be modulated by nitric oxide and increases in cA
MP. The possibility that different intracellular stores underly spontaneous
and nerve-mediated contractions is discussed.