Rhythmic contractions of isolated small arteries from rat: role of calcium

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Abstract
In order to investigate the mechanisms behind rhythmic contractions in small arteries of the mesenteric arcade from Wistar rats, the calcium dependency of the oscillations in response to noradrenaline activation was tested on isolated vessels. Application of 1 μM ryanodine or 30 μM TMB‐8 (procedures known to inhibit Ca2+release from intracellular stores) totally abolished the rhythmic activity, even though the antagonists had opposite effects on the amplitude of the contractile response to noradrenaline. Verapamil (1 μ) or felodipine (1 μ M) (agents known to inhibit influx of extracellular Ca2+) also abolished the oscillations and reduced the maximal noradrenaline response by about 40%. Reducing the extracellular Ca2+concentration to 0.1 DIM reduced the amplitude of the noradrenaline response to a similar extent as 1 nM felodipine, but did not eliminate the oscillations. This may indicate that the effect of calcium entry blockers was to eliminate the voltage‐dependency of Ca2+inflow rather than just reducing the Ca8+level. Manoeuvres that would increase the cytosolic Ca2+concentration (exposure to caffeine or to the calcium agonist BAY‐K 8644) increased the frequency of the oscillations. These observations indicate an important role, not only for voltage‐operating channels, but also for intracellular calcium stores in the generation of rhythmic contractions in these small arteries. Oscillations appear to be generated by an interplay between membrane activation and intracellular calcium stores.