Premium
Effects of calcium and sodium on ATP ‐induced vasopressin release from rat isolated neurohypophysial terminals
Author(s) -
Custer E. E.,
Knott T. K.,
OrtizMiranda S.,
Lemos J. R.
Publication year - 2018
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12605
Subject(s) - purinergic receptor , ppads , extracellular , vasopressin , medicine , endocrinology , calcium , p2 receptor , chemistry , receptor , sodium , receptor antagonist , antagonist , biology , biochemistry , organic chemistry
ATP receptors (P2X2, P2X3, P2X4 and P2X7) are found in neurohypophysial terminals ( NHTs ). These purinergic receptor subtypes are known to be cation selective. In the present study, we confirm that both sodium (Na + ) and calcium (Ca 2+ ) are permeable through these NHT purinergic receptors, although to varying degrees (91% vs 9%, respectively). Furthermore, extracellular calcium inhibits the ATP ‐current magnitude. Thus, the present study aimed to determine the effects of extracellular Na + vs Ca 2+ on ATP ‐induced vasopressin ( AVP ) release from populations of rat isolated NHTs . ATP (200 μmol L ‐1 ) perfused exogenously for 2 minutes in Normal Locke's buffer caused an initial transient increase in AVP release followed by a sustained increase in AVP release that lasted for the duration of the ATP exposure. Replacing extracellular NaCl with N‐methyl‐ d ‐glucamine chloride had no apparent effect on the ATP ‐induced transient increase in AVP release, although it abolished the sustained AVP release induced by ATP . Furthermore, removal of extracellular calcium resulted in no ATP ‐induced transient increase in AVP release but had no effect on the delayed, sustained increase in AVP release. The ATP ‐induced calcium‐dependent transient increase in AVP release was inhibited by >95% using 10 μmol L ‐1 of the P2X purinergic receptor antagonist PPADS (pyridoxal‐phosphate‐6‐azophenyl‐2,4‐disulphonic acid), which is a dose sufficient to block P2X2 and P2X3 receptors but not P2X4 or P2X7 receptors. Interestingly, the ATP ‐induced calcium‐independent, sodium‐dependent sustained increase in AVP release was not affected by 10 μmol L ‐1 PPADS . The ATP ‐induced calcium‐dependent transient increase in AVP release was not affected by the P2X7 receptor antagonist Brilliant Blue‐G (100 nmol L ‐1 ). However, the ATP ‐induced sodium‐dependent sustained AVP release was inhibited by 50%. Therefore, these results show that rat isolated NHTs exhibit a biphasic response to exogenous ATP that is differentially‐dependent on extracellular calcium and sodium. Furthermore, the initial transient release appears to be through P2X2 and/or P2X3 receptors and the sustained release is through a P2X7 receptor.