Does endothelin mobilize calcium from intracellular store sites in rat aortic vascular smooth muscle cells in primary culture?

Miasiro, Nobuco; Yamamoto, Hiromichi; Kobayashi, Hideo; Nakamura, Motoomi

doi:10.1016/s0006-291x(88)80841-6

Cited by 101 publications

(28 citation statements)

References 7 publications

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“…Here we confirm that the response to this peptide in the human bladder muscle is nifedipine-resistant and also substantially unaffected by Bay K 8644. Van Renterghem et al (1988) showed that endothelin acts in a complex manner on the cell membrane: it stimulates metabolism of inositol phosphates (see also Sugiura et al, 1989;Marsden et al, 1989), inducing mobilization of Ca from intracellular stores (Miasiro et al, 1988;Kai et al, 1989), it opens both a Casensitive K channel (transient hyperpolarization) and a non-specific cation channel (prolonged depolarization) which in turn may activate L-type voltage-dependent Ca channels (Van Renterghem et al, 1988). Thus, the contribution of L-type Ca channels to tension generation by endothelin might vary from one smooth muscle to another depending upon the relative role of the various mechanisms involved.…”

Section: Discussionmentioning

confidence: 99%

Multiple sources of calcium for contraction of the human urinary bladder muscle

Maggi

Giuliani

Patacchini

et al. 1989

British J Pharmacology

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1 KC1, carbachol, neurokinin A and endothelin produced concentration-dependent contractions of mucosa-free muscle strips from the dome of the human urinary bladder. The maximal response to carbachol or neurokinin A exceeded that to KCI, while the maximal response to endothelin approached that to KCI.2 Nifedipine (1 gM) abolished the response to KCI, reduced the response to carbachol or neurokinin A but had no effect on the response to endothelin. Bay K 8644 (1 gM) markedly potentiated the response to KCl but had little or no effect on the response produced by the other stimulants. 3 Superfusion of the strips with a nominally calcium (Ca)-free medium containing EDTA (1 mM) for 30min markedly reduced the response to carbachol, neurokinin A and endothelin, although a small response was still evident at high concentrations. Likewise, after a prolonged (60min) superfusion of the strips with a high K (80mM) Ca-free medium plus EDTA (1 mM) these three agonists still produced a small contractile response.4 The nifedipine (1 gM) resistant response to carbachol, neurokinin A or endothelin was markedly depressed by LaCl3 (1 mM). In contrast, the nifedipine-(1 gM) resistant response to carbachol was not modified by NiCl2 (0.1 mM) or co-conotoxin (0.1 Mm). 5 Caffeine produced divergent effects depending upon the temperature of incubation: a relaxation at 370C-and a concentration-dependent (2.5-20mM) contraction at 250C. The latter was markedly inhibited by procaine (3mM) but unaffected by nifedipine (1 gM).6 After a prolonged (60 min) superfusion with a high K, Ca-free medium containing EDTA the response to carbachol (100 Mm) was abolished by previous exposure to procaine (3mM). Conversely, the response to endothelin (1 MM) was unaffected by procaine. The response to endothelin in these experimental conditions was also resistant to LaCl3 (1 mM).7 These findings indicate that multiple sources of Ca age mobilized for contraction of the human bladder muscle by different stimulants. Dihydropyridine-and voltage-sensitive Ca channels provide the major if not the sole source of Ca for the response to KCI, play some role in the response to muscarinic (carbachol) or NK-2 tachykinin receptor stimulation but are not involved in the response to endothelin. Carbachol, neurokinin A and endothelin all mobilize a Ca pool (either extracellular or located at membrane level) which is LaCl3-sensitive but nifedipine-resistant. Neither T-nor N-type channels appear to be involved in the response to carbachol. In addition, these agents mobilize a tightly bound Ca pool independently from membrane depolarization. This latter pool is probably a procaine-sensitive intracellular source of activator Ca mobilized by caffeine and carbachol. The failure of procaine to prevent the response to endothelin in high K, Ca-free medium raises the possibility that this peptide mobilizes an intracellular source of activator Ca, distinct from the caffeine-and carbachol-sensitive pool.

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Section: Discussionmentioning

confidence: 99%

Multiple sources of calcium for contraction of the human urinary bladder muscle

Maggi

Giuliani

Patacchini

et al. 1989

British J Pharmacology

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“…Future studies should be aimed at determining whether the apparent receptor subtypes described here are associated with different second messenger systems. It has already been shown that one of them, which binds ET-1 and SRTX-b with high affinity [1,2,14,15] and appears to correspond to the E-S,, subtype, is associated with phosphoinositide hydrolysis [1,3,4] and Ca 2+ mobilization [16,17]. It would also be of interest to identify the endogenous agonist for the E-Sa receptors, for which SRTX-c appears to be a selective agonist, and to determine whether or not there exists a selective natural agonist for E-St receptor.…”

Section: Discussionmentioning

confidence: 99%

Three apparent receptor subtypes for the endothelin/sarafotoxin family

et al. 1989

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Competition binding experiments performed with 125 I-sarafotoxin (SRTX)-b and SRTX-b, SRTX-c and endothelin (ET-1 and ET-3) using homogenates of rat right and left atria, aorta, uterus, cerebellum and candate putamen indicated heterogeneity of the ET/SRTX receptor. The evidence pointed to the existence of three receptor subtypes: a high-atfmity ET-1/ SRTX-b subtype typical of smooth muscle (E-S~ receptor), a high-affinity SRTX-c subtype typical of the cerebellum (E-S# receptor), and a less selective subtype typical of the caudate putamen that binds all of these peptides with high affinity (E-S r receptor).

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“…These data are consistent with the postulate of Yanagisawa et al (1988) that endothelin may be an agonist for the dihydropyridine-sensitive calcium channel. Miasiro et al (1988) have shown that endothelin increases 45Ca2 + efflux even in calcium-free solution, and propose, conversely, that the peptide causes the release of calcium from intracellular stores.…”

Section: Introductionmentioning

confidence: 99%

“…Endothelin, in studies using porcine tissue, is synthesized from a precursor molecule, preproendothelin, by proteolytic cleavage (Itoh et al, 1988) and exhibits effects both on intact tissue ) and a culture derived from vascular smooth muscle cells Miasiro et al, 1988). These actions are mediated through binding sites which are specific for endothelin and distinct from catecholamine receptors or sites sensitive to dihydropyridines Hirata et al, 1988;Kanse et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

The pharmacological properties of the peptide, endothelin

Eglen¹,

Michel²,

Sharif³

et al. 1989

British J Pharmacology

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1 The effect of endothelin (ET-1) has been studied on isolated vascular and non-vascular preparations, using both functional and competition radioligand binding techniques. The effects of endothelin on blood pressure were studied in both anaesthetised, chemically denervated normotensive and spontaneously hypertensive rats (SHR). 2 Endothelin elicited contractile responses in the rat thoracic aorta, perfused mesenteric bed, rabbit mesenteric artery and portal vein. The maximal responses in the rat aorta were enhanced by removal of the endothelium, and were reduced in the presence of either a cyclo-oxygenase inhibitor (indomethacin) or a thromboxane receptor antagonist (SQ 29,548). In terms of potency, the most sensitive preparation was the rat endothelium-denuded aorta and rat perfused mesenteric bed (-log EC50 values = 8.2 + 0.07 and 8.2 + 0.12, mean + s.e.mean, n = 4, respectively). In the perfused mesenteric bed of the rat the maximum response to endothelin (219 + 12 mmHg, n = 4) was greater than that to either phenylephrine (maximal response = 67 + 9 mmHg; n = 4) or KCl (maximal response = 110 + 6 mmHg, n = 4).3 Endothelin elicited contractile responses of the guinea-pig isolated ileum, oesophageal muscularis mucosae and uterus. Responses were also observed in the rat fundic strip and paced left atria. The guinea-pig urinary bladder, trachea, rat vas deferens and anococcygeus exhibited little or no response to endothelin at the concentrations studied (1 x 10 -2-3.2 x 10 -8M). Of the above preparations, the ileum and oesophageal muscularis mucosae were the most sensitive to endothelin (-log EC50 = 8.5 + 0.11 and 8.4 + 0.06, n = 6, respectively), exhibiting potencies similar to those observed in the endothelium-denuded aorta of the rat. 4 In competition-radioligand binding studies, endothelin did not displace either [3H]-PN 210-100 or [125I]< -)-co-conotoxin GVIA from binding sites in membranes from rat cerebral cortex and, skeletal muscle or from guinea-pig cerebral cortex and hippocampus, respectively. This indicates a lack of direct interaction of endothelin at the dihydropyridine binding site and the N-type calcium channel, respectively. However, in functional studies, contractile responses to endothelin (1 x 10-8M) in the endothelium-denuded aorta of the rat were potently reversed by nifedipine, verapamil, and prenylamine (-log IC50 values = 8.0 + 0.13, 7.2 + 0.09 and 6.6 + 0.08, n = 4-8,

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Does endothelin mobilize calcium from intracellular store sites in rat aortic vascular smooth muscle cells in primary culture?

Cited by 101 publications

References 7 publications

Multiple sources of calcium for contraction of the human urinary bladder muscle

Multiple sources of calcium for contraction of the human urinary bladder muscle

Three apparent receptor subtypes for the endothelin/sarafotoxin family

The pharmacological properties of the peptide, endothelin

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