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.