Received February 16, 2006
Revised March 13, 2006
Accepted after revision March 23, 2006
GI & Epithelial Physiology [230]
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Pentagastrin-induced protein synthesis in the parotid gland of the anaesthetized rat, and its dependence on CCK-A and -B receptors and nitric oxide generation
Hülya Çevik Aras 1
J. Ekström 1*
1 Sahlgrenska Academy at Göteborg University
* To whom correspondence should be addressed. E-mail: jorgen.ekstrom{at}pharm.gu.se.
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Abstract |
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In parotid glands of pentobarbitone-anaesthetized rats, the incorporation of [3H]leucine into trichloroacetic acid-insoluble materials, reflecting protein synthesis, increased by 17% (compared to saline-treated rats) in response to infusion of pentagastrin (20 µg kg-1, I.V. for one hour) under muscarinic and a- and b-adrenoceptor blockade. Both the CCK-A receptor antagonist lorglumide (48 mg kg-1, I.V.) and the CCK-B receptor antagonist itriglumide (5.5 mg kg-1, I.V.), given separately, prevented the expected increase to pentagastrin and, in addition, reduced the glandular protein synthesis by 16% and 12%, respectively, below the level of saline-treated rats. In just saline-treated rats, the glandular protein synthesis was lowered by 22% by the CCK-A receptor antagonist and by 17% by the CCK-B receptor antagonist; combined, the two antagonists caused no further reduction (20%). There was no increase in the glandular protein synthesis of pentagastrin-treated rats as compared to those of the saline-treated rats, when both groups of rats were exposed to a combination of the two types of CCK receptor antagonists. In pentagastrin-treated rats, the protein synthesis in the parotid glands was 23% less in the presence of the nonselective nitric oxide(NO)-synthase inhibitor L-NAME (30 mg kg-1, I.V.) than in its absence; the result was the same (23%) when the neuronal NO-synthase inhibitor N-PLA (30 mg kg-1, I.V.) replaced L-NAME. The protein synthesis in just saline-treated rats was not reduced by L-NAME; neither were the protein synthesis of saline-treated rats different from that of pentagastrin- and L-NAME-treated rats. Thus, under "basal" condition a portion of the glandular protein synthesis as well as the whole increase in synthesis in response to administration of pentagastrin engaged both types of CCK-receptors. Furthermore, NO generation, due to neuronal NO-synthase activity, was required for the increase to occur in response to pentagastrin, whereas a non-NO-dependent pathway was responsible for the protein synthesis under "basal" condition.
Key Words:
Gastrin, Nitric oxide, Salivary gland
