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Enzyme
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Query: UNIPROT:P01185 (
vasopressin
)
23,126
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
1. Vasopressin and phenylephrine markedly inhibited the glucuronidation of p-nitrophenol in isolated murine hepatocytes. 2. After longer preincubation of hepatocytes in the presence of
vasopressin
or phenylephrine the rate of conjugation began to return to the control values indicating the reversibility of the inhibition caused by these agents. 3. The inhibitory effect of both agents was dependent on the Ca2+ filled state of the intracellular stores. 4. The inhibition caused by the alpha 1 receptor agonist phenylephrine was receptor mediated because it could be prevented by the addition of alpha 1 antagonist prazosin. 5. The data support the theory that the maintenance of the intralumenal Ca2+ concentration is necessary for the optimal activity of p-nitrophenol
UDP
-glucuronosyl-transferase.
...
PMID:Inhibition of p-nitrophenol glucuronidation by calcium mobilizing hormones. 857 63
The present study aimed to investigate the reactivity of cultured pituicytes from adult neurohypophysis to various bioactive substances using Ca2+ indicator dye Fura-2. A transient increase of intracellular Ca2+ [Ca2+]i was observed when pituicytes were treated with nucleotides (ATP, ADP, UTP, and
UDP
) and amines (5-HT2 and alpha2-agonist). Treatment with peptides such as endothelin-1 (ET-1), endothelin-3 (ET-3), bradykinin (BK),
vasopressin
(AVP), and angiotensin II (Ang II) also induced [Ca2+]i increase in pituicytes. Prostaglandin E2 (PGE2) and F2alpha (PGF2alpha) increased [Ca2+]i, but amino acids of GABA, glutamate (Glu), and taurine had no effect. Serum-free culture condition augmented [Ca2+]i responses to ATP, Ang II and 5-HT within 24 h. These results indicate that pituicytes express many of receptors for neurotransmitters or neuromodulators.
...
PMID:Intracellular Ca2+ responses to nucleotides, peptides, amines, amino acids and prostaglandins in cultured pituicytes from adult rat neurohypophysis. 1046 4
ATP increases intracellular calcium concentration ([Ca(2+)](i)) in supraoptic nucleus (SON) neurons in hypothalamo-
neurohypophyseal
system explants loaded with the Ca(2+)-sensitive dye, fura 2-AM. Involvement of P2X purinergic receptors (P2XR) in this response was anticipated, because ATP stimulation of
vasopressin
release from hypothalamo-
neurohypophyseal
system explants required activation of P2XRs, and activation of P2XRs induced an increase in [Ca(2+)](i) in dissociated SON neurons. However, the ATP-induced increase in [Ca(2+)](i) persisted after removal of Ca(2+) from the perifusate ([Ca(2+)](o)). This suggested involvement of P2Y purinergic receptors (P2YR), because P2YRs induce Ca(2+) release from intracellular stores, whereas P2XRs are Ca(2+)-permeable ion channels. Depletion of [Ca(2+)](i) stores with thapsigargin (TG) prevented the ATP-induced increase in [Ca(2+)](i) in zero, but not in 2 mM [Ca(2+)](o), indicating that both Ca(2+) influx and release of intracellular Ca(2+) contribute to the ATP response. Ca(2+) influx was partially blocked by cadmium, indicating a contribution of voltage-gated Ca(2+) channels. PPADS (pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid), and iso-PPADS, P2XR antagonists, attenuated, but did not abolish, the ATP-induced increase in [Ca(2+)](i). Combined treatment with PPADS or iso-PPADS and TG prevented the response. A cocktail of P2YR agonists consisting of UTP,
UDP
, and 2-methylthio-ADP increased [Ca(2+)](i) (with or without tetrodotoxin) that was markedly attenuated by TG. 2-Methylthio-ADP alone induced consistent and larger increases in [Ca(2+)](i) than UTP or
UDP
. MRS2179, a specific P2Y(1)R antagonist, eliminated the response to ATP in zero [Ca(2+)](o). Thus, both P2XR and P2YR participate in the ATP-induced increase in [Ca(2+)](i), and the P2Y(1)R subtype is more prominent than P2Y(2)R, P2Y(4)R, or P2Y(6)R in SON.
...
PMID:ATP increases intracellular calcium in supraoptic neurons by activation of both P2X and P2Y purinergic receptors. 1697 29