QUANTITATIVE STRUCTURAL-ANALYSIS AND THE SECRETORY BEHAVIOR OF THE RAT PAROTID-GLAND AFTER LONG AND SHORT-TERM ISOPRENALINE TREATMENT

  • 1 January 1979
    • journal article
    • research article
    • Vol. 57  (4) , 224-233
Abstract
Isoprenaline (IPR) was administered as daily s.c. injections into newborn rats for a period of 9 wk (long-term treatment) and into 8 wk old rats for 10 days (short-term treatment). Both the parotid and the submandibular glands increased 5-6 fold in weight in the 2 groups due to hypertrophy and to hyperplasia. The parotid glands were subjected to EM stereological analyses and to in vitro secretory studies. The results were compared with nontreated controls. Whereas mean total cell volume in the latter was 807 .mu.m3 it amounted to 5804 .mu.m3 in glands from long-term IPR-treated rats. A striking increase in size and number of cytoplasmic granules was noted after IPR treatment; there was also a marked decrease in granule electron density compared with control cells. Granule volume density was 31.2 .+-. 1.8% in controls and 58.0 .+-. 1.5% in long-term IPR-treated rats. Volume density increase was accompanied by a relative decrease in amylase and cyclic[c]AMP contents. On a percentage basis, the basal secretion of amylase from incubated IPR-treated parotid glands was markedly higher (roughly twice) than control glands; the absolute release of amylase into the medium was only slightly increased. Basal secretion was not energy requiring, which would suggest a passive diffusion. Stimulation by .beta.-adrenoceptor agonists, including .beta.1 and .beta.2 selective agents, had no or only a small stimulatory effect in vitro on IPR-treated glands. Dibutyryl cAMP was effective in controls but not in treated glands. Cholinergic stimulation caused a considerable amylase release from glands of IPR-treated rats; this release was comparable to that obtained in controls. Superstimulation of the .beta.-adrenoceptor evidently leads to a decreased sensitivity for adrenergic agonists. This may be due to membrane changes (e.g., modified receptor sites) and/or to an altered intracellular metabolism (e.g., a modified turnover of cyclic nucleotides).