Ca2+ handling mechanisms underlying neuropeptide Y-induced contraction in canine basilar artery

Tanaka, Yoshio; Nakazawa, Tomoo; Ishiro, Hiromi; Saito, Masanori; Uneyama, Hisayuki; Iwata, Seiichi; Ishii, Kunio; Nakayama, Koichi

doi:10.1016/0922-4106(95)90168-x

Cited by 11 publications

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References 26 publications

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“…Thus, the major [Ca 2+ ] i mobilizing action of NPY in mesenteric small arteries is due to a transmembrane influx of Ca 2+ . This is in agreement with results reported for canine basilar (Tanaka et al ., 1995) and bovine retinal (Prieto et al ., 1995) arteries, where the NPY‐induced contraction also is produced mainly by Ca 2+ influx through L‐type channels. However, data obtained in porcine aortic smooth muscle cells (Mihara et al ., 1989; Erdbrüger et al ., 1993; Shigeri et al ., 1995) and other cell systems (Herzog et al ., 1992; Selbie et al ., 1995), indicate that the NPY‐elicited rises in [Ca 2+ ] i are fully or partially due to mobilization of Ca 2+ from intracellular stores.…”

Section: Discussionsupporting

confidence: 94%

“…The ability of NPY to promote rises in [Ca 2+ ] i is well documented in vascular smooth muscle (Mihara et al ., 1989; Erdbrüger et al ., 1993; Shigeri et al ., 1995; Tanaka et al ., 1995). In the mesenteric small arteries studied here, NPY elicits moderate increases in basal [Ca 2+ ] i and tension which probably are consequent to depolarization (Prieto et al ., 1997), in particular since these responses are markedly inhibited by the L‐type calcium channel blocker, nifedipine (Prieto et al ., 1997).…”

Section: Discussionmentioning

confidence: 99%

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Neuropeptide Y regulates intracellular calcium through different signalling pathways linked to a Y₁‐receptor in rat mesenteric small arteries

Prieto

Buus

Mulvany

et al. 2000

British J Pharmacology

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1 Simultaneous measurements of intracellular calcium concentration ([Ca 2+ ] i ) and tension were performed to clarify whether the mechanisms which cause the neuropeptide Y (NPY)-elicited contraction and potentiation of noradrenaline contractions, and the NPY inhibition of forskolin responses are linked to a single or dierent NPY receptor(s) in rat mesenteric small arteries. ] i to resting levels. NPY completely inhibited these eects. The contractile responses to NPY in arteries maximally relaxed with either sodium nitroprusside (SNP) or nifedipine were not signi®cantly higher than those evoked by the peptide at resting tension, in contrast to the contractions to NPY in forskolin-relaxed arteries. BIBP 3226 competitively antagonized the contraction to NPY in forskolin-relaxed arteries with a pA 2 of 7.92+0.29. 5 Electrical ®eld stimulation (EFS) at 8 ± 32 Hz caused large contractions in arteries relaxed with either forskolin or noradrenaline in the presence of phentolamine. These responses to EFS were inhibited by BIBP 3226. Similar EFS in resting, non-activated arteries did not produce any response. 6 The present results suggest that dierent intracellular pathways are linked to a single NPY Y 1 receptor in intact rat mesenteric small arteries, and provide little support for involvement of other postjunctional NPY receptors in the contractile responses to NPY. Neurally released NPY also seems to act through Y 1 receptors, and may serve primarily as an inhibitor of vasodilatation.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y regulates intracellular calcium through different signalling pathways linked to a Y₁‐receptor in rat mesenteric small arteries

Prieto

Buus

Mulvany

et al. 2000

British J Pharmacology

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“…TXA 2 and its stable breakdown metabolite, TXB 2 , are known to be pulmonary vasoconstrictors (Friedman et al , 1979). We showed previously that 9,11‐dideoxy‐11α,9α‐epoxymethano prostaglandin F 2α (U46619), a stable TXA 2 analogue, increased not only the release of Ca 2+ from the intracellular storage sites but also the sensitivity of the myofilament to Ca 2+ in the canine cerebral artery (Tanaka et al , 1995), similar to data obtained in other vascular smooth muscle cells, such as the rabbit pulmonary artery (Himpens et al , 1990). Furthermore, we showed that U46619 increased the Ca 2+ sensitivity of the contractile elements in the canine basilar artery permeabilized by Staphylococcus aureus toxin (α‐toxin) in the presence of gua‐nosine 5′‐triphosphate (GTP).…”

Section: Discussionsupporting

confidence: 77%

Stretch‐induced contraction of rabbit isolated pulmonary artery and the involvement of endothelium‐derived thromboxane A₂

Nakayama

Ueta

Tanaka

et al. 1997

British J Pharmacology

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1 The mechanism of stretch-induced contraction of the intrapulmonary artery of rabbit was studied with special regard to the endothelium-dependence and production of prostanoids. 2 Isolated intrapulmonary artery of rabbits in ring form produced contraction when stretched slowly up to 180% of its initial muscle length (=100%) at a rate of 0.44 mm s 71, with a stimulus period of 5 min. 3 The stretch-induced contraction was attenuated by the mechanical removal of the endothelium, inhibitors of cyclo-oxygenase such as aspirin and indomethacin, [1S-[1a,2a(Z) (SQ 29,548), which is a thromboxane A 2 /prostaglandin H 2 receptor antagonist, or by ozagrel, an inhibitor of thromboxane A 2 synthase. 4 Biochemical assay indicated that the production of thromboxane B 2 , a stable metabolite of thromboxane A 2 , was increased 17 times in response to stretch only when the endothelium was intact. The production of thromboxane B 2 was also inhibited by aspirin or ozagrel. 5 The production of 6-keto prostaglandin F 1a , a stable metabolite of prostacyclin, was also increased in response to stretch in the preparation with intact endothelium. However, ozagrel showed no apparent eect on the production of 6-keto prostaglandin F 1a .6 These results suggest that a mechanical stimulus like stretch can act on endothelial cells of rabbit pulmonary artery to cause contraction by activation of arachidonic acid metabolism via the cyclooxygenase pathway and subsequent release of thromboxane A 2 and/or an increase in the ratio of thromboxane A 2 /prostacyclin.

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“…There is evidence that NPY may promote the entry of extracellular Ca 2+ by opening membrane channels [33], and that this entry may be how NPY potentiates the effects of other vasoconstrictors [1,5,34]. Our results agree with these studies, and also suggest that L-type Ca 2+ channels may be involved, because the nonspecific Ca 2+ channel blocker NiCl 2 and the L-type-specific Ca 2+ channel blocker verapamil both reduced the NPY-induced potentiation of the ear artery's response to electrical stimulation with similar potency.…”

Section: Discussionmentioning

confidence: 99%

Effect of neuropeptide Y on the sympathetic contraction of the rabbit central ear artery during cooling

Garcı́a-Villalón

Padilla

Fernández

et al. 2000

Pflugers Arch - Eur J Physiol

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In order to analyse the effect of neuropeptide Y (NPY) on the cutaneous vascular response to sympathetic nerve stimulation during cooling, the isometric response of isolated 2-mm segments of the rabbit central ear (cutaneous) artery was recorded at 37 degrees C and during cooling (30 degrees C). Electrical field stimulation (4-16 Hz) at 37 degrees C produced a frequency-dependent contraction, which was reduced during cooling (45% for 16 Hz) and potentiated by NPY (10(-8), 3x10(-8) and 10(-7) M), this potentiation being greater at 30 degrees C than at 37 degrees C. The NPY-induced potentiation of the contraction elicited by electrical field stimulation (8 Hz) was abolished by an antagonist of Y1 subtype NPY receptors, BIBP3226 (10(-6) M), at 37 degrees C and 30 degrees C, reduced by phentolamine (10(-6) M) at 30 degrees C but not at 37 degrees C, was not modified by the purinoceptor antagonist PPADS (3x10(-5) M) and was reduced by application of both phentolamine and PPADS at both temperatures. Both NiCl2 (10(-3) M) and verapamil (10(-5) M) abolished the potentiating effect of NPY at 37 degrees C and reduced it at 30 degrees C. Neither application of an inhibitor of nitric oxide synthesis, L-Nomega-nitro-arginine (L-NOARG, 10(-4) M), nor endothelium removal modified the potentiating effect of NPY at 37 degrees C or 30 degrees C. NPY (10(-8), 3x10(-8) and 10(-7) M) potentiated in a concentration-dependent way the arterial contraction in response to exogenous noradrenaline (10(-8)-10(-4) M) at 30 degrees C but not at 37 degrees C, and it increased the response to ATP (10(-4)-10(-2) M) at both temperatures. Therefore, in cutaneous (ear) arteries: (1) NPY potentiates the sympathetic response at 37 degrees C and at 30 degrees C, (2) this potentiating effect of NPY was more marked at 30 degrees C than at 37 degrees C, probably because of greater potentiation of the alpha-adrenoceptor response during cooling, and (3) the potentiating effect of NPY at both temperatures is mediated by NPY receptors of the Y1 subtype, is dependent of Ca2+ channels and is independent of the release of endothelial nitric oxide.

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Ca2+ handling mechanisms underlying neuropeptide Y-induced contraction in canine basilar artery

Cited by 11 publications

References 26 publications

Neuropeptide Y regulates intracellular calcium through different signalling pathways linked to a Y₁‐receptor in rat mesenteric small arteries

Neuropeptide Y regulates intracellular calcium through different signalling pathways linked to a Y₁‐receptor in rat mesenteric small arteries

Stretch‐induced contraction of rabbit isolated pulmonary artery and the involvement of endothelium‐derived thromboxane A₂

Effect of neuropeptide Y on the sympathetic contraction of the rabbit central ear artery during cooling

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Ca2+ handling mechanisms underlying neuropeptide Y-induced contraction in canine basilar artery

Cited by 11 publications

References 26 publications

Neuropeptide Y regulates intracellular calcium through different signalling pathways linked to a Y1‐receptor in rat mesenteric small arteries

Neuropeptide Y regulates intracellular calcium through different signalling pathways linked to a Y1‐receptor in rat mesenteric small arteries

Stretch‐induced contraction of rabbit isolated pulmonary artery and the involvement of endothelium‐derived thromboxane A2

Effect of neuropeptide Y on the sympathetic contraction of the rabbit central ear artery during cooling

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Neuropeptide Y regulates intracellular calcium through different signalling pathways linked to a Y₁‐receptor in rat mesenteric small arteries

Neuropeptide Y regulates intracellular calcium through different signalling pathways linked to a Y₁‐receptor in rat mesenteric small arteries

Stretch‐induced contraction of rabbit isolated pulmonary artery and the involvement of endothelium‐derived thromboxane A₂