Norepinephrine stimulates the production of inositol trisphosphate and inositol tetrakisphosphate in rat aorta

Pijuan, Vivian; Litosch, Irene

doi:10.1016/s0006-291x(88)80831-3

Cited by 13 publications

(5 citation statements)

References 17 publications

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“…The mechanism involved in the sustained contractions induced by IP3 (Yamamoto & van Breemen, 1985;Chiu et al, 1987a,b;Pijvan & Litosch, 1988). However, activation of PI turnover per se is not always a necessary condition for contraction in the aorta (Suba & Roth, 1987).…”

Section: Discussionmentioning

confidence: 99%

Ryanodine reveals multiple contractile and relaxant mechanisms in vascular smooth muscle: simultaneous measurements of mechanical activity and of cytoplasmic free Ca²⁺ level with fura‐2

Hisayama

Takayanagi

Okamoto

1990

British J Pharmacology

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1 The effects of ryanodine on changes in cytoplasmic Ca2+ level ([Ca2+]i) and muscle tension induced by maximum concentrations of phenylephrine (Phe; 1 pM), prostaglandin F2, (PGF2,, 10UM), caffeine (Caf, 30 mM) and isoprenaline (Iso, 1 M) were examined in rat aortic strips using fura-2. Treatment of the preparation with ryanodine had no effect on the concentration-response curves for Iso in relaxing the 0.1 M Phe-or 40 mm K+-induced precontraction.7 It is suggested that Phe and Caf mobilize Ca2 + from a ryanodine-sensitive Ca2 + store and that PGF2.releases Ca2+ from a ryanodine-insensitive Ca2+ store. The former contributes to the transient contraction through a Ca2'-dependent process, while the latter seems not to be directly associated with the contraction. The sustained contraction under Ca2 +-free conditions might involve a Ca2 '-independent process or a change in the sensitivity of the contractile filaments to Ca2 + 8 In addition to lowering cytoplasmic Ca2+ concentration, it is suggested that Iso counteracts the apparently Ca2 +-independent process. The ryanodine-sensitive Ca2+ store plays no substantial role in active relaxation by Iso, although it does play a major role in the maintenance of cytoplasmic Ca2+ in a quiescent muscle.

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Section: Discussionmentioning

confidence: 99%

Ryanodine reveals multiple contractile and relaxant mechanisms in vascular smooth muscle: simultaneous measurements of mechanical activity and of cytoplasmic free Ca²⁺ level with fura‐2

Hisayama

Takayanagi

Okamoto

1990

British J Pharmacology

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“…The vasoconstrictor effects of ET were initially ascribed as being due to a direct opening of voltagedependent Ca2+ channels [25]. However, subsequent data showed that ET stimulated release of Ins(1,4,5)P3 and release of intracellular Ca2+ in vascular smooth-muscle cells [26], mechanisms which are similar to those described for many other vasoconstrictors, including angiotensin II (AII), vasopressin (VP) and a-adrenergic agonists [27][28][29]. However, detailed analysis of the responses to ET and other vasoconstrictors has raised a number of questions about the role of PtdIns turnover in mediating its effects.…”

Section: Introductionmentioning

confidence: 99%

Inositol phosphate release and steroidogenesis in rat adrenal glomerulosa cells. Comparison of the effects of endothelin, angiotensin II and vasopressin

Woodcock

Little

Tanner

1990

Biochemical Journal

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Endothelin has steroidogenic activity in adrenal glomerulosa cells, as do two other vasoconstrictor peptides, angiotensin II and vasopressin. The steroidogenic activities of angiotensin II and vasopressin are probably mediated via the phosphatidylinositol-turnover pathway and associated changes in cytosolic Ca2+ concentration. Endothelin caused a steroidogenic response, which was small compared with that to angiotensin II and quantitatively similar to the vasopressin response. Cytosolic free Ca2+ responses were similarly higher to angiotensin II than to either of the other two peptides. However, total inositol phosphate responses to endothelin and angiotensin II were similar when these were measured over 20 min, and were quantitatively greater than the vasopressin response. A detailed study has been made of the phosphatidylinositol-turnover response to endothelin in comparison with responses to angiotensin II and vasopressin. Each of the three peptides produced a rapid and transient rise in Ins(1,4,5)P3 (max. 5-15 s), followed by a slow sustained rise. Ins(1,4,5)P3 was metabolized by both dephosphorylation and phosphorylation pathways, but the relative importance of the two metabolic pathways was different under stimulation by each of the three peptides. These findings show that adrenal glomerulosa cells can distinguish between the stimulation of phosphatidylinositol turnover by three different effectors. These differences in the pathway may be associated with the observed different steroidogenic and Ca2+ responses to the three peptides.

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“…Recently, a putative high-affinity InsP4 receptor was purified from pig cerebellar membranes (Donie & Reiser, 1991). While a role for InsP4 action in smooth muscle has not been established, generation of InsP4 in smooth muscle has been described by ourselves Schiemann et al, 1991) and others (Bielkiewicz-Vollrath et al, 1987;Pijuan & Litosch, 1988;Salmon & Bolton, 1988) although the location and nature of smooth muscle InsP4 receptors have not been described. It is still unknown whether InsP4 acts at the plasma membrane, on internal Ca2" stores, or on a structural element which connects the plasma membrane and the Ca2" store.…”

Section: Introductionmentioning

confidence: 99%

Inositol 1,4,5‐trisphosphate and inositol 1,3,4,5‐tetrakisphosphate binding sites in smooth muscle

Zhang

Bradley

Khoyi

et al. 1993

British J Pharmacology

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1 We have previously demonstrated that activation of M3 muscarinic receptors increases inositol 1,4,5-trisphosphate (InsP3) and inositol 1,3,4, 6 These results suggest the existence of distinct and specific InsP3 and InsP4 binding sites which may represent the physiological receptors for these second messengers; differences in the subcellular distribution of these receptors may contribute to differences in their putative physiological roles.

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Norepinephrine stimulates the production of inositol trisphosphate and inositol tetrakisphosphate in rat aorta

Cited by 13 publications

References 17 publications

Ryanodine reveals multiple contractile and relaxant mechanisms in vascular smooth muscle: simultaneous measurements of mechanical activity and of cytoplasmic free Ca²⁺ level with fura‐2

Ryanodine reveals multiple contractile and relaxant mechanisms in vascular smooth muscle: simultaneous measurements of mechanical activity and of cytoplasmic free Ca²⁺ level with fura‐2

Inositol phosphate release and steroidogenesis in rat adrenal glomerulosa cells. Comparison of the effects of endothelin, angiotensin II and vasopressin

Inositol 1,4,5‐trisphosphate and inositol 1,3,4,5‐tetrakisphosphate binding sites in smooth muscle

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Norepinephrine stimulates the production of inositol trisphosphate and inositol tetrakisphosphate in rat aorta

Cited by 13 publications

References 17 publications

Ryanodine reveals multiple contractile and relaxant mechanisms in vascular smooth muscle: simultaneous measurements of mechanical activity and of cytoplasmic free Ca2+ level with fura‐2

Ryanodine reveals multiple contractile and relaxant mechanisms in vascular smooth muscle: simultaneous measurements of mechanical activity and of cytoplasmic free Ca2+ level with fura‐2

Inositol phosphate release and steroidogenesis in rat adrenal glomerulosa cells. Comparison of the effects of endothelin, angiotensin II and vasopressin

Inositol 1,4,5‐trisphosphate and inositol 1,3,4,5‐tetrakisphosphate binding sites in smooth muscle

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Ryanodine reveals multiple contractile and relaxant mechanisms in vascular smooth muscle: simultaneous measurements of mechanical activity and of cytoplasmic free Ca²⁺ level with fura‐2

Ryanodine reveals multiple contractile and relaxant mechanisms in vascular smooth muscle: simultaneous measurements of mechanical activity and of cytoplasmic free Ca²⁺ level with fura‐2