Kinin receptors are important regulators of — and potential therapeutic targets for — pain in fibromyalgia, a study in mice suggests.
The study with that finding, “Kinins and their B1 and B2 receptors are involved in fibromyalgia-like pain symptoms in mice,” was published in the journal Biochemical Pharmacology.
Kinins are peptides (small proteins) that typically are made by the body in response to injury. Moreover, these molecules can activate pain and inflammation by binding to receptors called B1 and B2.
In the study, researchers hypothesized that kinins and their receptors might play a role in fibromyalgia pain.
They used a mouse model of fibromyalgia, induced by treatment with the drug reserpine. In mice, treatment with reserpine causes symptoms similar to those of fibromyalgia, such as exacerbated pain responses to stimuli that shouldn’t be painful, such as light touching and cold. Moreover, the animals also stop burrowing behavior, which is sort of analogous to how fibromyalgia pain might interfere with normal daily activities.
Researchers first confirmed that their model worked; the mice given reserpine exhibited the expected behavioral responses, and they didn’t have other adverse side effects (e.g., weight loss, skin irritability, etc.) that might have affected the experiments.
The researchers also noted that just the administration of reserpine increased the amount of B1 and B2 receptors the mice made, lending credence to the idea that these receptors are involved in the pain response. They then assessed this involvement using several strategies.
First, they gave reserpine to mice that were engineered to lack either the B1 or B2 receptor. These mice exhibited much less sensitivity to non-painful touch stimuli, which is called mechanical allodynia.
The researchers then used drugs to block the activity of the kinin receptors in wild-type mice treated with reserpine. These mice had less sensitivity to both touch and cold than their counterparts that were given only reserpine. Additionally, mice treated with kinin receptor blockers had increased burrowing behavior, again indicative of a lessened pain response.
Interestingly, molecules that activate the B1 or B2 receptors (agonists) induced pain behaviors in mice if they had been previously given reserpine, but in mice that hadn’t been given reserpine, kinin receptor activators did not induce pain responses. This suggests those receptors are important for pain in this model of fibromyalgia, but not necessarily for more broad pain phenomena.
“Kinin B1 or B2 receptor antagonists might present therapeutic potential for the control of fibromyalgia-like pain symptoms, the most relevant clinical feature of the disease,” the researchers concluded.
The feasibility of this strategy in humans is further supported because some such drugs are already used for other conditions; for example, icatibant (Firazyr) is an injectable B2 receptor antagonist that is approved to treat hereditary angioedema.
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