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The paradoxical vascular interactions between endothelin‐1 and calcitonin gene‐related peptide in the rat gastric mucosal microcirculation

1 The interactions between local intra‐arterial infusion of endothelin‐1 (ET‐1) and rat α‐calcitonin gene‐related peptide (α‐CGRP) on gastric mucosal damage and blood flow have been investigated in the pentobarbitone‐anaesthetized rat. 2 Close‐arterial infusion of ET‐1 (2–200 pmol kg−1 min−1) induced a significant and dose‐dependent increase in gastric mucosal haemorrhagic injury. 3 Close‐arterial infusion of the higher doses of ET‐1 (100 and 200 pmol kg−1 min−1) resulted in a biphasic effect on mucosal blood flow, as determined by laser Doppler flowmetry (LDF). This consisted of an initial transient increase followed by a pronounced and sustained fall in LDF. 4 Local microvascular constriction may thus contribute to the mechanisms underlying the gastric injury induced by these higher doses of ET‐1. 5 However, close‐arterial infusion of lower doses of ET‐1 (2–50 pmol kg−1 min−1), that also provoked substantial mucosal damage, induced only a sustained and significant mucosal hyperaemia, which may be secondary to microvascular injury. 6 Concurrent close‐arterial administration of rat α‐CGRP (50 pmol kg−1 min−1) significantly inhibited the extent of gastric mucosal injury induced by ET‐1 (5 pmol kg−1 min−1). 7 Furthermore, concurrent close‐arterial infusion of this dose of α‐CGRP, which itself increased mucosal LDF, significantly inhibited the hyperaemic response induced by close‐arterial infusion of ET‐1 (5 pmol kg−1 min−1). 8 These results indicate a damaging action on the gastric mucosa by low doses of ET‐1 which is independent of local vasoconstriction, that may involve a direct injury of the microvascular endothelium. The protective action of α‐CGRP thus seems unlikely to be due to a local vasodilator effect but may reflect protective actions on the microvascular endothelium