Release of Pituitary Hormones, Cortisol, Testosterone and Insulin in Response to Prostaglandin F2 α Given during Intracarotid Infusion of Somatostatin in Bulls

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Abstract
A carotid artery and a jugular vein were cannulated in each of four 1-year-old bulls. In an experiment with latin square design, each bull was given 30-min intracarotid infusions of saline or .5 mg somatostatin, and each was given an intravenous (iv) injection of 0 (saline) or 20 mg PGF2α (26.6 mg PGF2α THAM salt) in saline at 5 min after beginning infusions. Blood serum growth hormone declined (P<.05) continuously from 4.8 ± .6 ng/ml at the outset of somatostatin infusion to 1.8 ± .4 ng/ml at the end, then increased (P<.05) to 8.7 ± 3.8 ng/ml within 10 min and remained relatively stable during the 1-hr period after somatostatin. In the absence of somatostatin, PGF2α caused a threefold increase in blood serum growth hormone. Intracarotid infusion of somatostatin abolished the growth hormone release in response to iv PGF2α until somatostatin infusion was terminated; then growth hormone increased (P2α. Blood serum thyroid stimulating hormone was unaltered by either somatostatin or PGF2α. Blood serum insulin decreased (P<.05) continuously from 5.5 ± .4 at the outset of the 30-min intracarotid infusion of somatostatin to 1.6 ± .3 ng/ml at the conclusion, then increased (P<.01) to pre-treatment concentrations within 10 min after cessation of somatostatin treatment. Prostaglandin did not significantly influence blood serum insulin. We conclude that somatostatin is a potent inhibitor of growth hormone and insulin secretion, but inhibition of growth hormone and insulin disappears completely within 10 min after somatostatin infusion. Somatostatin does not affect blood serum prolactin, Cortisol, LH or TSH in bulls. Copyright © 1977. American Society of Animal Science . Copyright 1977 by American Society of Animal Science.

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