An examination of the sources of calcium for contractions mediated by postjunctional α1‐ and α2‐adrenoceptors in several blood vessels isolated from the rabbit

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Abstract
The roles of intracellular and extracellular‐derived Ca2+ in α‐adrenoceptor‐mediated contractions to noradrenaline (NA) have been investigated in several isolated blood vessels from the rabbit by examining responses in the presence of a modified Krebs‐Henseleit saline with 2.5 mm Ca2+ and a Ca2+‐buffered saline with 0.1 μm free Ca2+. NA was tested in preparations of the abdominal aorta, distal saphenous artery, renal vein, lateral saphenous vein, plantaris vein and ear vein exposed to a Ca2+‐buffered saline with 0.1 μm [Ca2+]. A concentration of NA which was maximally effective in modified Krebs‐Henseleit saline, produced an initial transient contraction (ITC) followed by a relaxation towards baseline. This is evidence that α‐adrenoceptor‐mediated responses in all these blood vessels depend upon calcium from both sources. The ITC was particularly pronounced in the arteries and was associated more closely with the α1‐receptor subtype. In the abdominal aorta, distal saphenous artery and renal vein the ITC can almost exclusively be attributed to an α1‐adrenoceptor (prazosin‐sensitive, rauwolscine‐resistant). In the ear vein, and to a lesser extent the plantaris vein, the ITC was mediated in part by an α2‐adrenoceptor (prazosin‐resistant, rauwolscine‐sensitive). α2‐Adrenoceptors in the lateral saphenous vein largely account for the response to NA in modified Krebs‐Henseleit saline, but α1‐adrenoceptors mediate the ITC in Ca2+‐buffered saline. After selective inactivation of α1‐adrenoceptors with a combination of phenoxybenzamine and rauwolscine, responses to NA in modified Krebs‐Henseleit saline are slow in onset and there is no ITC in Ca2+‐buffered saline. The possible significance of the coupling of postjunctional α2‐adrenoceptors to dual sources of Ca2+ is discussed in relation to the interaction between α‐adrenoceptor subtypes and the ease of demonstrating functional α2‐adrenoceptors in isolated blood vessels.

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