Kallidin

Where it comes from

Made in

Cut from low-molecular-weight kininogen by tissue kallikrein in kidney, salivary gland, pancreas and skin

Sent out by

Local inflammation and gland activity

Acts on

• Vessels
• Pain nerves
• Kidney tubule

What it does

• Does what bradykinin does, at the same B2 receptor and with much the same potency ¹
• Converted to bradykinin by aminopeptidases, so the two are never cleanly separate ¹
• Increases kidney blood flow and sodium excretion, which is the effect most often attributed to it rather than to bradykinin ¹

In medicine

• The medicines for bradykinin cover it. Icatibant blocks the B2 receptor both peptides use, and the kallikrein inhibitors stop the enzymes upstream of both ²
• No clinical test separates them. Kinin assays measure the family, and kallidin converts to bradykinin so fast that the ratio in a tube says as much about the handling as about the patient ¹
• Its des-Arg form is the strongest natural agonist of the human B1 receptor, which matters wherever inflammation has gone on long enough for that receptor to appear ¹

Beyond the body’s own use

• Nothing is in trials for kallidin itself and nothing is claimed for it; the work that uses it is pharmacology aimed at the B1 receptor ¹
• The difference from bradykinin that would matter is where it is made: tissue kallikrein in kidney, gland and skin rather than the contact system in blood. That is why kallidin is the kinin invoked for local effects such as salivary and kidney blood flow ¹
• Whether inhibiting tissue kallikrein would help anyone is untested. Every approved kallikrein inhibitor is aimed at plasma kallikrein instead ²