Effect of Somatostatin on the Release of Gonadotropins in Male Rats

Abstract

Abstract

Since somatostatin, the growth hormone release–inhibiting hormone, has inhibitory actions in many cell types and is delivered to the anterior pituitary gland via the hypophysial portal vessels, as well as being synthesized by cells within the gland, we tested the hypothesis that it might inhibit the release of gonadotropins from anterior pituitaries in vitro. Consequently, the effect of somatostatin on gonadotropin release from incubated anterior pituitaries of male rats with and without the stimulatory action of luteinizing hormone–releasing hormone (LHRH) was studied. After a preincubation period of 1 hr, hemipituitaries from adult male rats were incubated in fresh Krebs-Ringer bicarbonate (KRB) buffer in a Dubnoff incubator with an atmosphere of 95% O₂-5% CO₂ at 37°C for 3 hr. Incubation with somatostatin (10⁻⁶, 10⁻⁷, and 10⁻⁸ M) had no effect on basal release of either LH or follicle-stimulating hormone (FSH). However, somatostatin (10⁻⁶-10⁻⁸ M) suppressed LHRH (1.7 x 10⁻⁸ M)-induced release of LH (P < 0.01 to P < 0.0001), but not FSH. Furthermore, somatostatin antiserum (1:1000) had no significant effect on basal LH or FSH release, whereas incubation with the antiserum plus LHRH (1.7 x 10⁻⁹ or 1.7 x 10⁻⁸ M) increased LH (P = 0.015 and P = .005, respectively), but not FSH release. In summary, our results suggest that somatostatin exerts a physiologically significant inhibitory effect on LH but not FSH release in the presence of LHRH in vitro. Presumably, somatostatin is secreted in vitro by pituitary cells since not only have anterior pituitaries of rats been shown to contain somatostatin, but also somatostatin mRNA. Somatostatin then diffuses to the LH gonadotropes, where it exerts its inhibitory action. However, the release of somatostatin is insufficient to alter basal in vitro release. On the other hand, at least at the concentrations employed, there was no significant effect either of somatostatin or the antiserum to alter basal or stimulated FSH release.