Bedi G S
Department of Oral Biology, School of Medicine, State University of New York, Buffalo 14214.
Crit Rev Oral Biol Med. 1993;4(3-4):565-71. doi: 10.1177/10454411930040034301.
The present investigation was undertaken to study the effect of adrenoreceptor modulators on the expression of salivary proteins. Sprague-Dawley rats were treated for 10 consecutive days with adrenergic agonists isoproterenol, dobutamine, terbutaline, salbutamol, methoxyphenamine, or methoxamine. Antiserum to selected salivary proteins was used to compare the concentration of these proteins in the submandibular and parotid glands of treated animals. Chronic treatments of rats (50 mumol/kg body weight for 10 d) with either isoproterenol or dobutamine induced synthesis of a cysteine-proteinase inhibitor (cystatin) in the submandibular glands. When isoproterenol was injected concomitantly with the mixed beta-antagonist propranolol or the beta 1-adrenergic antagonists metaprolol, protocol, or atenolol, the induction of cystatin was totally suppressed. However, the beta 2-antagonist, ICI-118551, produced only partial reduction in cystatin induction elicited by isoproterenol. On the contrary, rats treated with either isoproterenol or beta 1-agonists demonstrated a significantly reduced concentration of serine-proteinase kallikrein in submandibular glands. The decrease observed in submandibular kallikrein of rats treated with isoproterenol was prevented by concomitant treatment with beta 1-antagonists but not with beta 2-antagonists. Because kallikreins are produced by ductal cells and cystatins are produced by acinar cells of submandibular glands, these observations suggest that there may be differential control of expression of proteins synthesized by ductal and acinar cells. Chronic treatment of rats with nonselective beta-agonist isoproterenol or beta 1-selective agonists increased markedly the proline-rich proteins (PRP) in parotid glands, but the parotid amylase concentration was not significantly affected by beta-adrenergic agonists.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究旨在探讨肾上腺素能受体调节剂对唾液蛋白表达的影响。将Sprague-Dawley大鼠连续10天用肾上腺素能激动剂异丙肾上腺素、多巴酚丁胺、特布他林、沙丁胺醇、甲氧明或美沙明进行处理。使用针对特定唾液蛋白的抗血清来比较处理动物下颌下腺和腮腺中这些蛋白的浓度。大鼠(50 μmol/kg体重,持续10天)用异丙肾上腺素或多巴酚丁胺进行慢性处理可诱导下颌下腺中半胱氨酸蛋白酶抑制剂(胱抑素)的合成。当异丙肾上腺素与混合β拮抗剂普萘洛尔或β1肾上腺素能拮抗剂美托洛尔、普拉洛尔或阿替洛尔同时注射时,胱抑素的诱导被完全抑制。然而,β2拮抗剂ICI-118551仅部分降低了异丙肾上腺素引起的胱抑素诱导。相反,用异丙肾上腺素或β1激动剂处理的大鼠下颌下腺中丝氨酸蛋白酶激肽释放酶的浓度显著降低。用异丙肾上腺素处理的大鼠下颌下激肽释放酶的降低可通过与β1拮抗剂同时处理而预防,但不能通过与β2拮抗剂同时处理来预防。由于激肽释放酶由下颌下腺的导管细胞产生,而胱抑素由腺泡细胞产生,这些观察结果表明,导管细胞和腺泡细胞合成的蛋白质表达可能存在差异调控。用非选择性β激动剂异丙肾上腺素或β1选择性激动剂对大鼠进行慢性处理可显著增加腮腺中富含脯氨酸的蛋白质(PRP),但腮腺淀粉酶浓度不受β肾上腺素能激动剂的显著影响。(摘要截短于250字)