Glucocorticoid amplifies vasopressin‐induced phosphoinositide hydrolysis in aortic smooth muscle cells

Watanabe, Yasuko; Tokuda, Harukuni; Suzuki, Atsushi; Shinoda, Junji; Kotoyori, Jun; Ito, Yoshiaki; Oiso, Yutaka; Kozawa, Osamu

doi:10.1002/jcb.240570317

Cited by 6 publications

(3 citation statements)

References 27 publications

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“…Cortisol potentiated NE-induced Ins(1,4,5)P 3 synthesis in both nonpregnant and pregnant uterine arteries. Glucocorticoid-mediated potentiation of Ins(1,4,5)P 3 production has been reported in vascular smooth muscle for angiotensin II, arginine vasopressin, endothelin-1, and catecholamines (24,30,43). The role of Ins(1,4,5)P 3 as the messenger of pharmacomechanical Ca 2ϩ mobilization in smooth muscle has been firmly established (35).…”

Section: Discussionmentioning

confidence: 96%

Effect of cortisol on norepinephrine-mediated contractions in ovine uterine arteries

Xiao

Huang

Pearce

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Cortisol potentiated norepinephrine (NE)-mediated contractions in ovine uterine arteries (UA). We tested the hypothesis that cortisol regulated alpha(1)-adrenoceptor-mediated pharmacomechanical coupling differentially in nonpregnant UA (NUA) and pregnant UA (PUA). Cortisol (10 ng/ml for 24 h) significantly increased contractile coupling efficiency of alpha(1)-adrenoceptors in NUA, but increased alpha(1)-adrenoceptor density in PUA. Cortisol potentiated NE-induced inositol 1,4,5-trisphosphate [Ins(1,4,5)P(3)] synthesis in both NUA and PUA, but increased coupling efficiency of alpha(1)-adrenoceptors to Ins(1,4,5)P(3) synthesis only in NUA. Carbenoxolone alone did not affect NE-mediated Ins(1,4,5)P(3) production, but significantly enhanced cortisol-mediated potentiation of NE-stimulated Ins(1,4,5)P(3) synthesis in PUA. In addition, cortisol potentiated the NE-induced increase in Ca(2+) concentration in PUA, but increased NE-mediated contraction for a given amount of Ca(2+) concentration in NUA. Collectively, the results indicate that cortisol potentiates NE-mediated contractions differentially in NUA and PUA, i.e., by upregulating alpha(1)-adrenoceptor density leading to increased Ca(2+) mobilization in PUA while increasing alpha(1)-adrenoceptor coupling efficiency and myofilament Ca(2+) sensitivity in NUA. In addition, the results suggest that pregnancy increases type 2 11 beta-hydroxysteroid dehydrogenase activity in the UA.

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Section: Discussionmentioning

confidence: 96%

Effect of cortisol on norepinephrine-mediated contractions in ovine uterine arteries

Xiao

Huang

Pearce

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…The elevation of mRNA levels precedes the rise in binding activity, suggesting a transcriptional effect. Furthermore, it has been reported that GC amplify the vasopressin-induced transduction signal (increased IP accumulation in the presence of dexamethasone) (312,313). At the protein level, GC have been shown to produce an early decrease in binding site density, followed later by an increase, which becomes more prevalent with time.…”

Section: A Tissue-specific Expression and Regulation Of Membrane Hormentioning

confidence: 99%

Ectopic and Abnormal Hormone Receptors in Adrenal Cushing’s Syndrome*

et al. 2001

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The mechanism by which cortisol is produced in adrenal Cushing's syndrome, when ACTH is suppressed, was previously unknown and was referred to as being "autonomous." More recently, several investigators have shown that some cortisol and other steroid-producing adrenal tumors or hyperplasias are under the control of ectopic (or aberrant, illicit, inappropriate) membrane hormone receptors. These include ectopic receptors for gastric inhibitory polypeptide (GIP), beta-adrenergic agonists, or LH/hCG; a similar outcome can result from altered activity of eutopic receptors, such as those for vasopressin (V1-AVPR), serotonin (5-HT4), or possibly leptin. The presence of aberrant receptors places adrenal cells under stimulation by a trophic factor not negatively regulated by glucocorticoids, leading to increased steroidogenesis and possibly to the proliferative phenotype. The molecular mechanisms responsible for the abnormal expression and function of membrane hormone receptors are still largely unknown. Identification of the presence of these illicit receptors can eventually lead to new pharmacological therapies as alternatives to adrenalectomy, now demonstrated by the long-term control of ectopic P-AR- and LH/hCGR-dependent Cushing's syndrome by propanolol and leuprolide acetate. Further studies will potentially identify a larger diversity of hormone receptors capable of coupling to G proteins, adenylyl cyclase, and steroidogenesis in functional adrenal tumors and probably in other endocrine and nonendocrine tumors.

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“…V1a receptor is located mainly in the central nervous system and cardiovascular organs including VSMC, while V1b and V2 are located in the central nervous system and kidney, respectively. As for intracellular signaling mechanisms, it has been reported that AVP mobilizes intracellular Ca 2+ and stimulates protein kinase C (PKC) through the activation of phospholipase (PL) C and PLD in VSMC [15][16][17], which is involved in the mechanism of AVP-induced proliferation of these cells [18]. Other important signaling pathways to mediate the mitogenic and differentiation processes are tyrosine kinases.…”

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confidence: 99%

Vasopressin Stimulates Na-dependent Phosphate Transport and Calcification in Rat Aortic Smooth Muscle Cells

et al. 2007

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Abstract. We investigated the effect of arginine vasopressin (AVP) on inorganic phosphate (Pi) transport in A-10 rat aortic vascular smooth muscle cells (VSMCs). AVP time-and dose-dependently stimulated Na-dependent Pi transport in A-10 cells. This stimulatory effect of AVP on Pi transport was markedly suppressed by V1 receptor antagonist. A protein kinase C (PKC) inhibitor calphostin C partially suppressed the stimulatory effect of AVP. The selective inhibitors of cJun-NH 2 -terminal mitogen-activated protein (MAP) kinase (Jun kinase) attenuated AVP-induced Pi transport, but Erk kinase or p38 MAP kinase inhibitors did not. Wortmannin, a phosphatidylinositol (PI) 3-kinase inhibitor, suppressed AVP-induced Pi transport. Rapamycin, a selective inhibitor of S 6 kinase, reduced this effect of AVP, while Akt kinase inhibitor did not. The combination of inhibitors for PKC, Jun kinase and PI 3-kinase completely suppressed the AVPenhanced Pi transport. Furthermore, AVP rescued the VSMC from high phosphate-induced cell death and enhanced mineralization of these cells. In summary, these results suggest that AVP stimulates both Na-dependent Pi transport and mineralization in VSMCs. The mechanism is mediated by the activation of multiple signaling pathways including PKC, PI 3-kinase, S 6 kinase and Jun kinase.

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Glucocorticoid amplifies vasopressin‐induced phosphoinositide hydrolysis in aortic smooth muscle cells

Cited by 6 publications

References 27 publications

Effect of cortisol on norepinephrine-mediated contractions in ovine uterine arteries

Effect of cortisol on norepinephrine-mediated contractions in ovine uterine arteries

Ectopic and Abnormal Hormone Receptors in Adrenal Cushing’s Syndrome*

Vasopressin Stimulates Na-dependent Phosphate Transport and Calcification in Rat Aortic Smooth Muscle Cells

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