Terbutaline, forskolin and cAMP reduce secretion of aqueous humour in the isolated bovine eye.

TitleTerbutaline, forskolin and cAMP reduce secretion of aqueous humour in the isolated bovine eye.
Publication TypeJournal Article
Year of Publication2020
AuthorsShahidullah M, Wilson WStuart, Rafiq K, Sikder MHasan, Ferdous J, Delamere NAnthony
JournalPLoS One
Volume15
Issue12
Paginatione0244253
Date Published2020
ISSN1932-6203
KeywordsAnimals, Aqueous Humor, Bodily Secretions, Bronchodilator Agents, Calcium, Cattle, Cells, Cultured, Colforsin, Cyclic AMP, Cyclic AMP-Dependent Protein Kinases, Terbutaline
Abstract

In order to elucidate involvement of cyclic AMP and intracellular Ca2+,[Ca2+]i, in the modulation of aqueous humour formation (AHF), we studied the effects of terbutaline, forskolin and 8-Br-cAMP in the isolated bovine eye. We also studied the interaction of cAMP on calcium signaling in cultured ciliary epithelial (CE) cells. Drug effects on AHF were measured by fluorescein dilution. Drug effects on [Ca2+]i were studied by the fura-2 fluorescence ratio technique. Terbutaline (100 nmol-100 M), forskolin (30 nM-100 M) or 8-Br-cAMP (100 nM- 10 μM), administered in the arterial perfusate produced significant reductions in AHF. The AH reducing effect of terbutaline was blocked by a selective inhibitor of protein kinase A (KT-5720). ATP (100 M) caused a rapid, transient (peak) increase in [Ca2+]i followed by a sustained plateau phase lasting more than 5 minutes. Preincubation of the cells (6 min) with terbutaline, forskolin or 8-Br-cAMP significantly reduced the peak calcium response to ATP. The sustained plateau phase of the response, on the other hand, was augmented by each of the agents. KT-5720 partially reversed the inhibitory effect of terbutaline on the peak and totally inhibited its effect on the plateau phase. These data indicate: (a) that AHF in the bovine eye can be manipulated through cyclic AMP, operating via protein kinase A, (b) that protein kinase A can affect [Ca2+]i homeostasis, (c) that calcium release from the intracellular store, not the entry, affects AHF, and (d) that interaction of [Ca2+]i with cAMP plays a role in modulating AH secretion.

DOI10.1371/journal.pone.0244253
Alternate JournalPLoS One
PubMed ID33347508
PubMed Central IDPMC7751850
Grant ListR01 EY029171 / EY / NEI NIH HHS / United States