Inhibitory effect of somatostatin on the mechanosensitivity of articular afferents in normal and inflamed knee joints of the rat.

The effect of somatostatin on the sensory activity of primary afferents was studied in normal and acutely inflamed rat knee joints. Fine afferent nerve fibers with conduction velocities of 0.9-18.0 m/s were recorded as single units. All nerve fibers tested responded to local mechanical stimulation, movements of the joint and i.a. injections of KCl (10(-4) mol, 0.1 ml) close to the joint. Somatostatin (10(-4) mol, 0.2 ml) caused no direct response of the units. In normal joints, somatostatin did not change the discharges evoked by non-noxious movements but decreased the responses to noxious movements significantly to about 63% of the responses before the application. In acutely inflamed joints, somatostatin reduced the discharges of non-noxious and of noxious movements to about 55% and 52%, respectively. Injections of somatostatin with lower concentrations (10(-6) mol, 10(-8) mol) i.a. close to inflamed joints revealed shorter and less pronounced reductions of the responses to noxious movements. In a proportion of afferents, substance P (10(-4) mol) and bradykinin (10(-4) mol) were able to increase these responses again. These data indicate that the mechanosensitivity of articular afferents in normal joints may also be regulated by several neuropeptides based on a balance of pro-inflammatory peptides such as substance P, and anti-inflammatory peptides such as somatostatin. In an inflamed joint, pro-inflammatory peptides seem to predominate resulting in a sensitization of the peripheral nerve fibers. In this case, an application of somatostatin or its analogues could be used clinically to compensate this effect.