Nitric oxide inhibits vasopressin- and serotonin-induced ca2+ signal through a cyclic gmp dependent pathway

Michèle R. Stone, Donald Gill, Cécile J. Favre

Research output: Contribution to journalArticle

Abstract

Vasopressin and serotonin are important mediators of vasoconstriction and Ca2+ signals in smooth musclo cells. Upon binding to their respective membrane receptor, cytosolic Ca2+ increases are mediated by release of Ca2+ from intracellular stores through the Iris(l,4,5)P3 pathway. The present studies investigated the action of NO donors and cyclic GMP on cytosolic Ca2+ increases induced by stimulation with vasopressin and serotonin in A7r5 smooth muscle cells. The two hormones show different effects and different sensitivities; con centratjons of vasopressin as low as 100 nM induced a transient cytosolic Ca2+ increase with a rapid deactivation. In contrast, 1 /zM serotonin induce sustained ('a2"" oscillations. Our results reveal a rapid and profound action of NO on Ca2"1 oscillations, Ca2+ release and (V+ influx. The potent NO donor GEA 3162, a l-aryl substituted oxatriazole. rapidly inactivated Ca2+ oscillations induced by serotonin. The action of vasopressin was also rapidly decreased upon addition of GKA 3162. Experiments investigating the effects of 8-Br-cyclic GMP, a non-hydrolyzable, membrane pi-rmeant cGMP analogue, showed a dramatic inhibitory effort on serotonin induced Ca24 oscillations. Absence of external Ca2+ did noi abolish Ca2+ oscillation, indicating that external Ca2+ is not required for l he maintenance of the oscillations. The results suggest that the action of nitric oxide through a cyclic GMP pathway, reflecting directed effects on Ca2+ release or Ca2+ storage. (Supported by MH Grant HL55426 and the Sv-iss XatiotMl Research Foundation).

Original languageEnglish (US)
JournalFASEB Journal
Volume12
Issue number8
StatePublished - Dec 1 1998

Fingerprint

vasopressin
Vasopressins
serotonin
nitric oxide
Serotonin
Nitric Oxide
calcium
Cyclic GMP
oscillation
cyclic GMP
Membranes
Iris
Vasoconstriction
Smooth Muscle Myocytes
Muscle
Cells
Maintenance
Hormones
Research
vasoconstriction

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

Cite this

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title = "Nitric oxide inhibits vasopressin- and serotonin-induced ca2+ signal through a cyclic gmp dependent pathway",
abstract = "Vasopressin and serotonin are important mediators of vasoconstriction and Ca2+ signals in smooth musclo cells. Upon binding to their respective membrane receptor, cytosolic Ca2+ increases are mediated by release of Ca2+ from intracellular stores through the Iris(l,4,5)P3 pathway. The present studies investigated the action of NO donors and cyclic GMP on cytosolic Ca2+ increases induced by stimulation with vasopressin and serotonin in A7r5 smooth muscle cells. The two hormones show different effects and different sensitivities; con centratjons of vasopressin as low as 100 nM induced a transient cytosolic Ca2+ increase with a rapid deactivation. In contrast, 1 /zM serotonin induce sustained ('a2{"}{"} oscillations. Our results reveal a rapid and profound action of NO on Ca2{"}1 oscillations, Ca2+ release and (V+ influx. The potent NO donor GEA 3162, a l-aryl substituted oxatriazole. rapidly inactivated Ca2+ oscillations induced by serotonin. The action of vasopressin was also rapidly decreased upon addition of GKA 3162. Experiments investigating the effects of 8-Br-cyclic GMP, a non-hydrolyzable, membrane pi-rmeant cGMP analogue, showed a dramatic inhibitory effort on serotonin induced Ca24 oscillations. Absence of external Ca2+ did noi abolish Ca2+ oscillation, indicating that external Ca2+ is not required for l he maintenance of the oscillations. The results suggest that the action of nitric oxide through a cyclic GMP pathway, reflecting directed effects on Ca2+ release or Ca2+ storage. (Supported by MH Grant HL55426 and the Sv-iss XatiotMl Research Foundation).",
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Nitric oxide inhibits vasopressin- and serotonin-induced ca2+ signal through a cyclic gmp dependent pathway. / Stone, Michèle R.; Gill, Donald; Favre, Cécile J.

In: FASEB Journal, Vol. 12, No. 8, 01.12.1998.

Research output: Contribution to journalArticle

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AU - Stone, Michèle R.

AU - Gill, Donald

AU - Favre, Cécile J.

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AB - Vasopressin and serotonin are important mediators of vasoconstriction and Ca2+ signals in smooth musclo cells. Upon binding to their respective membrane receptor, cytosolic Ca2+ increases are mediated by release of Ca2+ from intracellular stores through the Iris(l,4,5)P3 pathway. The present studies investigated the action of NO donors and cyclic GMP on cytosolic Ca2+ increases induced by stimulation with vasopressin and serotonin in A7r5 smooth muscle cells. The two hormones show different effects and different sensitivities; con centratjons of vasopressin as low as 100 nM induced a transient cytosolic Ca2+ increase with a rapid deactivation. In contrast, 1 /zM serotonin induce sustained ('a2"" oscillations. Our results reveal a rapid and profound action of NO on Ca2"1 oscillations, Ca2+ release and (V+ influx. The potent NO donor GEA 3162, a l-aryl substituted oxatriazole. rapidly inactivated Ca2+ oscillations induced by serotonin. The action of vasopressin was also rapidly decreased upon addition of GKA 3162. Experiments investigating the effects of 8-Br-cyclic GMP, a non-hydrolyzable, membrane pi-rmeant cGMP analogue, showed a dramatic inhibitory effort on serotonin induced Ca24 oscillations. Absence of external Ca2+ did noi abolish Ca2+ oscillation, indicating that external Ca2+ is not required for l he maintenance of the oscillations. The results suggest that the action of nitric oxide through a cyclic GMP pathway, reflecting directed effects on Ca2+ release or Ca2+ storage. (Supported by MH Grant HL55426 and the Sv-iss XatiotMl Research Foundation).

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