Effects of atrial natriuretic factor (ANF) on phenylephrine‐triggered intra‐ and extracellular calcium dependent contraction in rat aorta

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Abstract
1. The ability of atrial natriuretic factor (ANF) to alter the different Ca++ events in phenylephrine (PE)-triggered contraction was tested ion isolated rat aorta. Isometric contraction of endothelium-free rat aortic ring was recorded in Ca++ free medium containing 1 mM EGTA. 2. PE (1 .mu.M) induced a phasic contraction and a sustained contraction following addition of CA++ (2.5 mM) to the medium. The phasic contaction is due to intracellular Ca++ release whereas the sustained one is dependent on extracellular Ca++. The Ca++ antagonist D600 (1 .mu.M) reduced by 39% the sustained contraction without affecting the phasic one. 3. ANF (0.3-3 nM) reduced both contractions, but spasmodic contractions were observed during the sustained phase. A similar effect was noted with sodium nitroprusside (NaNP: 10-100 nM) and forskolin (1 .mu.M) but not with prazosin (1 nM). 4. When D600 was added to the medium either before or after the initial contraction, the spasmodic contractions were completely abolished. Nifedipine (0.1 .mu.M) had a similar effect when added during the sustained phase, while in contrast, addition of the Ca++ agonist BAY K8644 (0.1 .mu.M), increased the frequency of the spasmodic contractions. 5. It can be concluded that in rat aorta ring, PE induces Ca++ release and Ca++ influx via receptor linked channels and potential dependent channels. ANF, NaNP but also forskolin inhibit both Ca++ release and Ca++ influx via receptor linked channels, while unlike prazosin, these agents are less effective in preventing Ca++ influx via potential dependent channel.