The effect of adrenergic agonists and antagonists on the expression of proteins in rat submandibular and parotid glands

Crit Rev Oral Biol Med. 1993;4(3-4):565-71. doi: 10.1177/10454411930040034301.

Abstract

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)

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adrenergic beta-Agonists / pharmacology*
  • Adrenergic beta-Antagonists / pharmacology*
  • Amylases / analysis
  • Amylases / drug effects
  • Amylases / genetics
  • Animals
  • Cystatins / analysis
  • Cystatins / genetics
  • Female
  • Gene Expression
  • Glycoproteins / analysis
  • Glycoproteins / drug effects
  • Glycoproteins / genetics
  • Isoproterenol / pharmacology
  • Kallikreins / analysis
  • Kallikreins / drug effects
  • Kallikreins / genetics
  • Parotid Gland / drug effects
  • Parotid Gland / enzymology
  • Parotid Gland / metabolism*
  • Peptides / analysis
  • Peptides / drug effects
  • Peptides / genetics
  • Proline / analysis
  • Proline / drug effects
  • Proline / genetics
  • Proline-Rich Protein Domains
  • Rats
  • Rats, Sprague-Dawley
  • Saliva / chemistry
  • Saliva / enzymology
  • Salivary Proteins and Peptides / analysis
  • Salivary Proteins and Peptides / drug effects*
  • Salivary Proteins and Peptides / genetics
  • Submandibular Gland / drug effects
  • Submandibular Gland / enzymology
  • Submandibular Gland / metabolism*

Substances

  • Adrenergic beta-Agonists
  • Adrenergic beta-Antagonists
  • Cystatins
  • Glycoproteins
  • Peptides
  • Salivary Proteins and Peptides
  • Proline
  • Amylases
  • Kallikreins
  • Isoproterenol