Does activation of cyclic AMP dependent phosphorylation induced by beta‐adrenergic agent control the tone of vascular muscle?

Hirata, Mario H.; Kuriyama, Hirosi

doi:10.1113/jphysiol.1980.sp013428

Cited by 11 publications

(5 citation statements)

References 33 publications

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“…a reciprocal interaction between Ca and cyclic AMP had been postulated (Kroeger, Teo, Ho & Wang, 1975;Webb & Bhalla, 1976; Thoren & Haeusler, 1978). However, Hirata & Kuriyama (1980) found that in the porcine coronary artery 80% of the total protein kinase binding sites were occupied by endogenous cyclic AMP in the cytosol fraction and 100 % in the particulate fraction, even when the concentration of cyclic AMP was markedly reduced in excess K. Although full saturation of cyclic AMP binding to the cytosol fraction was observed on treatment with isoprenaline, the phosphorylation was not enhanced. These observations in the porcine coronary artery differed from findings in the cardiac muscle of the same species, because the phosphorylation was increased in the cardiac muscles.…”

Section: Discussionmentioning

confidence: 99%

“…Although the role of cyclic AMP in relaxation of visceral smooth muscles has been an area ofgreat interest, a consistent link is lacking between changes in the tissue cyclic AMP and activated ATPase. For instance in vascular smooth muscles, the transport of Ca by microsomes was not increased by applied cyclic AMP (Zelck & Karnstedt, 1977), and the 476 SMOOTH MUSCLE RELAXATION BY fl-ACTIVATION phosphorylation activated by cyclic AMP and relaxation were not causally related (Hirata & Kuriyama, 1980). Increase in cyclic AMP mediated by f-receptor activation can also lead to competitive actions between cyclic AMP-dependent protein kinase (protein kinase) and calmodulin on the myosin light chain kinase.…”

Section: Introductionmentioning

confidence: 99%

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Mechanisms of relaxation induced by activation of β‐adrenoreceptors in smooth muscle cells of the guinea‐pig mesenteric artery

Itoh

Izumi

Kuriyama

1982

The Journal of Physiology

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SUMMARYRelaxation of smooth muscle cells induced by activation of fi-adrenoceptors was investigated in intact and skinned muscles of the guinea-pig mesenteric artery.1. In concentrations over 10-7 M, isoprenaline reduced the resting tone of intact preparations and also the amplitude of K contractions. When Ca was applied after previous superfusion with Ca-free solution, the amount of Ca accumulated into storage sites was increased by isoprenaline in polarized and depolarized ([K]0 128 mM) muscles. The amount of Ca stored increased even further when procaine and isoprenaline were applied simultaneously during store loading.2. Isoprenaline increased the concentration of cyclic AMP as determined by radioimmunoassay. Application of isoprenaline at a concentration of 10-7 M increased cyclic AMP from 2-2 + 0 3 to 2-8 + 0-6 p-mole/mg wet weight and at 10-6 M increased it to 4-5 + 08 p-mole/mg wet weight after 5 min incubation (n = 4).3. Application of cyclic AMP (3 x 10-6 M) with cyclic AMP-dependent protein kinase (50 jg/ml.) had no effect on the pCa-tension relationship in the skinned muscles. However, an increased concentration of cyclic AMP (> 10-5 M) suppressed the Ca-induced concentration only in the presence of protein kinase. This protein kinase (50 ,tg/ml.) alone had no effect on the Ca-induced contraction.4. In skinned fibres, the Ca store could be loaded by applying low concentrations of Ca. If cyclic AMP (3 x 10-6 M) with protein kinase (50 jug/ml.) was applied during the loading procedure, the amount of Ca accumulated by the store increased if the loading solution contained 10-6 M-Ca applied for 2 min or less, but if the loading solution was applied for 3 min, or if higher Ca concentrations were used, the presence of cyclic AMP with protein kinase decreased the store size, suggesting that a Cainduced Ca-release mechanism was also being activated.5. In skinned muscles, accumulation of Ca into the store site in the presence of cyclic AMP (3 x 10-6 M) with protein kinase (50 gg/ml.) was further accelerated by simultaneous applications of procaine (5 mM), as here the Ca-induced Ca-release mechanism was suppressed.6. These results indicate that activation of f-adrenoceptors by isoprenaline increases the amount of cyclic AMP in the intact muscles, and leads to an increase in Ca accumulation into the store site. In the skinned muscles, the Ca-induced

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mechanisms of relaxation induced by activation of β‐adrenoreceptors in smooth muscle cells of the guinea‐pig mesenteric artery

Itoh

Izumi

Kuriyama

1982

The Journal of Physiology

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“…However, the ability of fl-receptor activation to relax is not dependent on the occurrence of this hyperpolarization but is believed to depend on some biochemical consequences of f8-receptor activation; these are possibly associated with a rise in cyclic AMP which affects myosin phosphorylation, and also with calcium entry, storage or extrusion although ,-receptor activation generally seems not to alter the internal calcium ion concentration (Morgan & Morgan, 1984). In any event it is not a potential-dependent mechanism (Biulbring & den Hertog, 1980;Hirata & Kuriyama, 1980;Meisheri & van Breeman, 1982;Riiegg & Paul, 1982;Miller, Silver & Stull, 1983). Other agents such as vasoactive intestinal polypeptide (VIP) also relax tension and raise cyclic AMP (Frandsen, Krishna & Said, 1978) but produce little hyperpolarization (Bolton, Lang & Ottesen, 1981).…”

Section: Voltage-independent Mechanisms and Relaxationmentioning

confidence: 99%

Are Junction Potentials Essential? Dual Mechanism of Smooth Muscle Cell Activation by Transmitter Released From Autonomic Nerves

Bolton

Large

1986

Exp Physiol

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Stimulation of autonomic nerves supplying smooth muscle tissues often evokes either an e.j.p. or an i.j.p. which involves a shift in the membrane potential such that the entry of calcium into the cell through voltage-sensitive calcium channels is likely to be increased or decreased respectively. In smooth muscle which freely discharges action potentials either spontaneously or in response to excitatory influences in vivo, the change in membrane potential will alter the rate of action potential discharge and so the tension developed by the smooth muscle. In this way there is modulation of the rate of entry of calcium, or its release within the cell, by a voltage-dependent mechanism entrained by the junction potential, as the action potential represents the operation of voltage-dependent calcium channels. In smooth muscles not freely discharging action potentials, the numbers of open calcium channels may change with depolarization, or even hyperpolarization, so the junction potential again brings into play a voltage-dependent mechanism of calcium entry. However, a dual mechanism of neurotransmission seems to operate at many autonomic nerve-smooth muscle junctions such that voltage-independent mechanisms coexist with voltage-dependent mechanisms. It is now generally accepted that activation of receptors on smooth muscle cells caused by bathing smooth muscles in solutions containing excitatory transmitters can bring into operation processes which are not voltage-dependent and which do not depend on modulation of the rate of action potential discharge. Up to the present it has been by no means certain that when released from autonomic nerves these excitatory transmitters (ACh, noradrenaline, substance P and n.a.n.c. excitatory transmitters) could also act in the same voltage-independent way - not least because studies of smooth muscle cells at the cellular level have been dominated by membrane potential recording (by micro-electrode) which has revealed the e.j.p. or some form of depolarization as a seemingly ubiquitous feature of excitatory autonomic junctions of nerve and smooth muscle cells. However, experiments show that under conditions when the e.j.p. and/or the action potential are abolished or severely impaired by drug application, substantial nerve-evoked smooth muscle contractions may occur at many autonomic junctions. Conversely, severe impairment of nerve-evoked contraction may occur in some cases with excitatory-receptor antagonists without loss, or even in some cases any impairment, of the e.j.p. which presumably depends on a different receptor type.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…For tension recording, the guinea-pig taenia coli and the porcine coronary artery were prepared in strips, 0 5 mm in width and 10 mm in length. Tension was recorded using a strain gauge, as described by Hirata & Kuriyama (1980).…”

Section: Mechanical Recordingsmentioning

confidence: 99%

Effects of external cations on calcium efflux from single cells of the guinea‐pig taenia coli and porcine coronary artery.

Hirata¹,

Itoh²,

Kuriyama³

1981

The Journal of Physiology

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SUMMARY1. Single smooth muscle cells were prepared from the guinea-pig taenia coli and the porcine coronary artery by treatment with collagenase, in order to measure the 45Ca flux with special reference to the effects of external cations.2. In excess [K]o solution, cell suspensions prepared from both tissues showed an increased 45Ca uptake within 3-5 min. In Na-free solution, the cells prepared from taenia coli, but not from coronary artery showed an increased 45Ca uptake. The Ca uptake of the cells paralleled with the tension increase recorded from tissues of both species.3. The efflux of 45Ca into Ca-free EGTA containing solution was markedly increased by [Na] 7. In cells from the taenia coli, 45Ca efflux could still be observed in nominally Naand Ca-free solution. This residual 45Ca efflux made a large contribution to the total 45Ca efflux.8. When 45Ca uptake was measured in Na-free (Tris) solution, the [Na]o-activated, [Ca]o-activated and residual 45Ca effluxes of cells from the taenia coli were accelerated, non-selectively.9. These results obtained with cells prepared from the guinea-pig taenia coli are comparable to the Ca2+ efflux mechanism seen in the squid axon. However, maintenance of low concentrations of [Ca]i seems to require not only the above three 45Ca efflux mechanisms, but also Ca sequestering mechanisms in the cell.0022-3751/81/3240-0912 $07.50

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Does activation of cyclic AMP dependent phosphorylation induced by beta‐adrenergic agent control the tone of vascular muscle?

Cited by 11 publications

References 33 publications

Mechanisms of relaxation induced by activation of β‐adrenoreceptors in smooth muscle cells of the guinea‐pig mesenteric artery

Mechanisms of relaxation induced by activation of β‐adrenoreceptors in smooth muscle cells of the guinea‐pig mesenteric artery

Are Junction Potentials Essential? Dual Mechanism of Smooth Muscle Cell Activation by Transmitter Released From Autonomic Nerves

Effects of external cations on calcium efflux from single cells of the guinea‐pig taenia coli and porcine coronary artery.

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