TY - JOUR
T1 - Contribution of the vasopressin V1 receptor to its hydrosmotic response
AU - Yorio, Thomas
AU - Satumtira, Nimman
N1 - Funding Information:
This research was supported in part by a grant from the American Heart Association, Texas Affiliate. The authors would like to thank Dr. P. Cammarata for his assistance with the tissue cultures.
PY - 1989
Y1 - 1989
N2 - 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.
AB - 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.
KW - AVP
KW - V receptor
KW - water flow
UR - http://www.scopus.com/inward/record.url?scp=0024472816&partnerID=8YFLogxK
U2 - 10.1111/j.1768-322X.1989.tb00809.x
DO - 10.1111/j.1768-322X.1989.tb00809.x
M3 - Article
C2 - 2529941
AN - SCOPUS:0024472816
SN - 0248-4900
VL - 66
SP - 7
EP - 12
JO - Biology of the Cell
JF - Biology of the Cell
IS - 1-2
ER -