Contribution of the vasopressin V1 receptor to its hydrosmotic response

Thomas Yorio, Nimman Satumtira

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Toad urinary bladder epithelial cells grown in culture (primary) show a significant increase in water-soluble inositol phosphates when treated with 10-8 M vasopressin (AVP), but not with (3-deamino-8-d-arginine)vasopressin (ddAVP), a V2-agonist. The increase in inositol phosphates was blocked by the V1-antagonist, d(CH2)5Tyr(Me)AVP, suggesting a V1-coupled phosphoinositide breakdown. The V1-antagonist had no effect on basal adenylate cyclase activity nor on that stimulated by AVP. However, the V1-antagonist was found to attenuate the hydrosmotic response of AVP, suggesting some role of the V1-receptor cascade in the water flow response. Mezerein (MZ), a non-phorbol activator of protein kinase C (PKC) increased osmotic water flow response. Mezerein (MZ), a non-phorbol activator of magnitude and occurred over a longer period (90 min) than that observed with AVP. In an attempt to emulate the V1-response, activation of PKC, and an increase in intracellular calcium, toad bladders were incubated with MZ and the calcium ionophore A23187 (IP). It was found that IP enhanced the water flow response to MZ at all times measured. Mz and IP were also found to enhance cAMP-mediated water flow, suggesting that apical membrane permeability may be regulated in part through V1-receptor stimulation and its respective second messengers. Collectively, these observations suggest that the V1 receptor may play a role not only as part of a negative feedback system, but also as an integral component of the enhanced water permeability that occurs at the apical membrane.

Original languageEnglish
Pages (from-to)7-12
Number of pages6
JournalBiology of the Cell
Volume66
Issue number1-2
DOIs
StatePublished - 1 Jan 1989

Fingerprint

Vasopressin Receptors
Water
Calcimycin
Inositol Phosphates
Ionophores
Anura
Protein Kinase C
Permeability
Urinary Bladder
Membranes
Calcium Ionophores
Arginine Vasopressin
Second Messenger Systems
Phosphatidylinositols
Vasopressins
Adenylyl Cyclases
Epithelial Cells
Calcium
mezerein

Keywords

  • AVP
  • V receptor
  • water flow

Cite this

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abstract = "Toad urinary bladder epithelial cells grown in culture (primary) show a significant increase in water-soluble inositol phosphates when treated with 10-8 M vasopressin (AVP), but not with (3-deamino-8-d-arginine)vasopressin (ddAVP), a V2-agonist. The increase in inositol phosphates was blocked by the V1-antagonist, d(CH2)5Tyr(Me)AVP, suggesting a V1-coupled phosphoinositide breakdown. The V1-antagonist had no effect on basal adenylate cyclase activity nor on that stimulated by AVP. However, the V1-antagonist was found to attenuate the hydrosmotic response of AVP, suggesting some role of the V1-receptor cascade in the water flow response. Mezerein (MZ), a non-phorbol activator of protein kinase C (PKC) increased osmotic water flow response. Mezerein (MZ), a non-phorbol activator of magnitude and occurred over a longer period (90 min) than that observed with AVP. In an attempt to emulate the V1-response, activation of PKC, and an increase in intracellular calcium, toad bladders were incubated with MZ and the calcium ionophore A23187 (IP). It was found that IP enhanced the water flow response to MZ at all times measured. Mz and IP were also found to enhance cAMP-mediated water flow, suggesting that apical membrane permeability may be regulated in part through V1-receptor stimulation and its respective second messengers. Collectively, these observations suggest that the V1 receptor may play a role not only as part of a negative feedback system, but also as an integral component of the enhanced water permeability that occurs at the apical membrane.",
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Contribution of the vasopressin V1 receptor to its hydrosmotic response. / Yorio, Thomas; Satumtira, Nimman.

In: Biology of the Cell, Vol. 66, No. 1-2, 01.01.1989, p. 7-12.

Research output: Contribution to journalArticle

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