Inositol trisphosphate and the contraction of vascular smooth muscle cells

Popescu, L. M.; Hinescu, Mihail Eugen; Musat, Sorin; Ionescu, Mihai; Pistritzu, F.

doi:10.1016/0014-2999(86)90701-6

Cited by 25 publications

(4 citation statements)

References 3 publications

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“…Ca2+ reequilibration after Ca2+ entry (Popescu et al, 1986), IP, deserves consideration as a candidate second messenger for the effects of ol,-receptors on Ca2+-dependent conductances. Rat brain a,-adrenoceptors are known to be positively coupled to PI tumover (Brown et al, 1984;Janowsky et al, 1984;Minneman and Johnson, 1984;Schoepp et al, 1984;Gonzales and Crews, 1985;Kemp and Downes, 1986); however, this has not been demonstrated specifically in the dorsal raphe.…”

Section: Discussionmentioning

confidence: 99%

Role of phosphoinositide metabolites in the prolongation of afterhyperpolarizations by alpha 1-adrenoceptors in rat dorsal raphe neurons

Freedman

Aghajanian

1987

J. Neurosci.

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Afterhyperpolarizations and outward tail currents of rat dorsal raphe neurons were measured by intracellular recording and single-electrode voltage clamping in the brain slice preparation. The alpha 1-agonist phenylephrine, and (in the presence of propranolol) norepinephrine, elicited an increase in the duration, but not of the initial amplitude, of afterhyperpolarizations and associated outward tail currents which followed depolarizing pulses. These effects were antagonized by prazosin, indicating that they were mediated by alpha 1-adrenoceptors. The outward tail currents were sensitive to apamin, a blocker of certain Ca2+-activated K+ currents. A prolongation of afterhyperpolarizations would offset the major excitatory alpha 1 effects, which were associated with suppression of resting K+ currents and of the A-current. Since polyphosphoinositide metabolites have been reported to be second messengers for Ca2+-dependent receptor actions, we compared their effects with those of alpha 1-receptor stimulation on these cells. Intracellular ejection of the putative second messenger myo-inositol-1,4,5-trisphosphate from the recording electrode transiently mimicked the actions of alpha 1-agonists on the afterhyperpolarization. Superfusion with 1 mM LiCl, simulating therapeutic levels of lithium, had no effect on the rate of recovery from inositol trisphosphate ejection. Superfusion with water-soluble phorbol esters (which mimic actions of another phosphoinositide metabolite, 1,2-diacylglycerol) suppressed rather than mimicked the activation of raphe cell firing by phenylephrine; this occurred with a rank-order potency consistent with activation of protein kinase C and was associated with suppression of a slow inward current and of the outward tail current. Our results suggest that phosphoinositide turnover is more likely to mediate modulatory or negative-feedback effects of alpha 1-adrenoceptors than to mediate the major excitatory effects.

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Section: Discussionmentioning

confidence: 99%

Role of phosphoinositide metabolites in the prolongation of afterhyperpolarizations by alpha 1-adrenoceptors in rat dorsal raphe neurons

Freedman

Aghajanian

1987

J. Neurosci.

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“…Since the calcium pump seems to require the presence of inositol lipids, the decrease in Ptdlns4,5P2 content that occurs during stimula tion may result in a damping of the pump, thus enhancing the influx com ponent of the plasma membrane calcium cycle. There is evidence to suggest that Ins I ,4,5P3 inhibits the calcium pump on the sarcolemma of coronary arteries (157).…”

Section: Calcium Entry Across the Plasma Membranementioning

confidence: 99%

Inositol Trisphosphate and Diacylglycerol: Two Interacting Second Messengers

Berridge¹

1987

Annu. Rev. Biochem.

3,259

1,335

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“…Another possibility is that second messengers directly activate non-voltage gated Ca channels and thus augment Ca 2+ influx as observed with IP 3 in Tlymphocytes (Kuno & Gardner, 1987 ). Another possibility is that a second messenger (IP 3 ) blocks Ca 2+ extrusion (Popescu, Hinescu, Musat, Ionescu & Pistritzu, 1986) and hence causes a rise in [Ca2+]i by virtue of a maintained or elevated Ca 2+ influx.…”

Section: Discussionmentioning

confidence: 96%

A delayed all-or-none hyperpolarisation induced by a single Ca action potential in hamster eggs

et al. 1988

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A transient change of membrane potential and resistance could be evoked after a long latency (ca. 9 s) by a single calcium action potential in some unfertilized hamster eggs. The estimated reversal potential for the delayed response was close to EK supporting the conclusion that K channels were opened indirectly by the Ca2+ influx through voltage-gated channels. A second action potential elicited after the first did not induce a similar response. A number of treatments (insertion of a Ca2+ pipette, application of Na+-free solution, La3+ or high external pH) likely to raise [Ca2+]i also induced similar large changes of potential and resistance after which a single action potential failed to evoke a large delayed response. The evidence indicates that a small rise in [Ca2+]i activates a slow process leading to a further large increase in [Ca2+]i.

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Inositol trisphosphate and the contraction of vascular smooth muscle cells

Cited by 25 publications

References 3 publications

Role of phosphoinositide metabolites in the prolongation of afterhyperpolarizations by alpha 1-adrenoceptors in rat dorsal raphe neurons

Role of phosphoinositide metabolites in the prolongation of afterhyperpolarizations by alpha 1-adrenoceptors in rat dorsal raphe neurons

Inositol Trisphosphate and Diacylglycerol: Two Interacting Second Messengers

A delayed all-or-none hyperpolarisation induced by a single Ca action potential in hamster eggs

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