The present invention relates to novel antagonists to a B1-bradykinin (B1-BK) receptor which have a good affinity and selectivity therefor, some of which being at least partially resistant to enzymatic degradation. The synthesis of the B1 receptors is induced during inflammation. Symptoms associated with inflammation (elevated hydrostatic pressure and plasma leakage or extravasation) have been observed in diabetic animal models (streptozotocin-induced diabetes (STZ)) as well as in spontaneously hypertensive rats (SHR). The present inventors confirm the presence of B1-BK receptors in these two models. B1-BK antagonists abolished the vasocontraction induced by B1-BK in SHR and STZ, and reduced the glycemia of diabetic animals to normal levels. The present B1-antagonists are useful for treating any condition wherein B1-receptor is expressed, particularly during inflammation, and more particularly wherein B1-receptor expression results in diabetic vasculopathy, other diabetic symptoms associated with an insulitis and a post-capillary resistance building as a consequence of the presence of a B1-receptor.