The effects of α‐adrenoceptor agonists on intracellular Ca<sup>2</sup>+ levels in freshly dispersed single smooth muscle cells from rat tail artery

Li, Xiaofang; Kargacin, Margaret E.; Triggle, Chris R.

doi:10.1111/j.1476-5381.1993.tb13760.x

Cited by 19 publications

(9 citation statements)

References 10 publications

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“…Our results support this hypothesis; in the Ca 2 +-free medium Epi still increased [Ca 2 +]i, and this increase was highly sensitive to yohimbine and WB 4101 but was resistant to prazosin. Our findings are distinct from those in reports on myocytes isolated from rat tail artery [26] and rat portal vein [7], in which the increase in [Ca2+]i by activation of a 2 -ARs was solely from the Ca 2 entry through VDCCs. These discrepancies may be due to the difference in preparations, because the rat myocytes contain both at-ARs and O 2 -ARs, with a-ARs outnumbering at 2 -ARs [27,28], whereas porcine myometrial cells contain predominantly a 2 -ARs with few al-ARs [2].…”

Section: Discussioncontrasting

confidence: 84%

α2-Adrenergic Receptor-Mediated Ca2+ Influx and Release in Porcine Myometrial Cells1

ZhuGe

Chen

et al. 1997

Biology of Reproduction

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We studied the mechanisms underlying alpha2-adrenergic receptor (AR)-mediated increase in intracellular free calcium ([Ca2+]i) in freshly dispersed myometrial cells from sows in the luteal phase of the estrous cycle. After the blockade of beta-ARs with propranolol, epinephrine increased [Ca2+]i dose-dependently in both the presence and absence of extracellular Ca2+. The rank order of alpha antagonists in inhibiting [Ca2+]i response to epinephrine was yohimbine > WB4101 >> prazosin in both the presence and absence of extracellular Ca2+, suggesting that epinephrine acts on alpha(2A)-ARs to increase Ca2+ influx as well as Ca2+ release from intracellular stores. Thapsigargin, the blocker of the Ca2+ pump in the sarcoplasmic reticulum, abolished the release but did not affect the influx. Pertussis toxin (PTX) inhibited the influx but failed to change the release. Nimodipine, an L-type Ca2+ channel blocker, nearly abolished the influx. The peak increase in [Ca2+]i caused by epinephrine was reached within 20 sec of administration. Intracellular cAMP concentrations were also decreased at 20 sec post-epinephrine. Epinephrine enhanced the L-type Ca2+ channel current, whereas forskolin suppressed it. Maximization of intracellular cAMP content by applying 8-bromo-cAMP (100 microM) blocked the effect of epinephrine on the current. U-73122, a phospholipase C inhibitor, reduced the Ca2+ release by epinephrine and oxytocin. Our results suggested that 1) activation of alpha2-ARs induces Ca2+ influx through opening L-type Ca2+ channels as well as inducing Ca2+ release from intracellular stores, and 2) a PTX-sensitive G protein couples negatively to adenylyl cyclase, leading to a decrease in cAMP formation which may be involved in the activation of Ca2+ channels. In addition, our results are consistent with the coupling of alpha2-ARs to a PTX-insensitive G protein (G(q)) to release Ca2+ from intracellular stores.

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Section: Discussioncontrasting

confidence: 84%

α2-Adrenergic Receptor-Mediated Ca2+ Influx and Release in Porcine Myometrial Cells1

ZhuGe

Chen

et al. 1997

Biology of Reproduction

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“…Radioligand binding assays with membranes from rat tail arteries (Gheung and Triggle 1988), isolated tissue preparations (Abe et al 19871, and freshly dispersed single vascular smooth muscle cells (Li et al 1993) have demonstrated that both aa-and a2-a&enoceptors are present on the postsynaptic cell membrane. In the present study, a differential sensitivity to PTX versus CTX was demonstrated, suggesting that at least one PTX-sensitive G-protein is involved in the regulation of a-adrenoeeptor-mediated vasoconstriction.…”

Section: Discussionmentioning

confidence: 98%

“…To address this questionS we have (i) investigated almd a2-adrenoceptor agonist stimulated contractile responses of rat tail artery rings from rats that were hypertensive (SHR) or nomotensive (WKY and Sprague -Dawley (SD)) and determined the effects of a-adrenocepterr antagonists and nifedipine on the responses to these agonists, and (ii) compared the effects of in vivs pretreatment with PTX or CTX on the contractile responses induced by al-and a2-adrenoceptor agonists in tail artery rings from these three strains of rats. The rat tail artery has the advantage that in comparison to most other arterial vessels, studies with radioligand binding assays (Cheung and Triggle 1988) and isolated tissue preparations (Abe et al 1987), as well as freshly dispersed single vascular smooth muscle cels (Li et al 1993), have demonstrated that postsynaptic al-and a2-adrensceptors are present in this tissue.…”

mentioning

confidence: 98%

Effects of pertussis and cholera toxins on α-adrenoceptor function in rat tail artery: differences in hypertension

Li¹,

Triggle²

1993

Can. J. Physiol. Pharmacol.

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The alpha 1- and alpha 2-adrenoceptor-stimulated contractile responses of rat tail artery rings were compared in Sprague-Dawley (SD), spontaneously hypertensive (SHR), and Wistar-Kyoto (WKY) rats that were untreated, treated with pertussis toxin, or treated with cholera toxin. The maximal responses, expressed as milligrams of tension, induced by clonidine (an alpha 2-adrenoceptor agonist) and cirazoline (a selective alpha 1-adrenoceptor agonist) were significantly greater in SHR than in SD or WKY, and the tissues were more sensitive to the agonists in SHR or SD than in WKY. Yohimbine (0.1 microM), a selective alpha 2-adrenoceptor antagonist, shifted the dose-response curves for clonidine to the right. The effects of yohimbine were greater in SD than in WKY or SHR, but not different between WKY and SHR. Prazosin (0.05 microM), a selective alpha 1-adrenoceptor antagonist, shifted the dose-response curves of cirazoline to the right, but the effects of prazosin were not different among these three strains of rats. Nifedipine (0.05 microM) completely blocked the response to clonidine in SD and WKY; however, in SHR, approximately one-third of the response to clonidine was resistant to nifedipine. Nifedipine, at 0.05 microM, only partially inhibited responses to cirazoline in SD, SHR, and WKY, and no differences were noted between the strains. Pertussis toxin pretreatment (50 micrograms/kg, 3 days before experiment) almost completely blocked the responses to clonidine, but only partially inhibited those to cirazoline. After pertussis toxin pretreatment, the responses (maximal effects and EC50s) to clonidine and cirazoline were not significantly different in arteries from the three strains of rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Stimulation of al-adrenoceptors in rat aorta activates extracellular Ca2" influx and/or intracellular Ca2+ release for contraction (Cauvin & Malik, 1984). In rat tail artery al-adrenoceptors mediate a fast and transient increase in intracellular Ca2+ which is probably the result of the mobilization of intracellular calcium and Ca2" influx through receptor-operated channels (Li et al, 1993). In addition, direct studies in tail artery rings using Fura 2 (Thorin & Atkinson, 1994) or indirect studies using inositol phosphate accumulation (Labelle & Murray, 1990;Vila et al, 1993) (Chiu et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

Effect of N^G‐nitro‐L‐arginine methylester (L‐NAME) on functional and biochemical α₁‐adrenoceptor‐mediated responses in rat blood vessels

Tabernero¹,

Giraldo

Vila³

1996

British J Pharmacology

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1. The modulation by NG-nitro-L-arginine methylester (L-NAME) of alpha 1-adrenoceptor-mediated contraction was investigated on isolated segments of rat tail artery and aorta. The influence of L-NAME on inositol phosphates accumulation by alpha 1-adrenoceptor agonists was also investigated to elucidate the intracellular mechanism responsible for this modulation. 2. In aorta but not in tail artery L-NAME (30 microM) enhanced the sensitivity (3.3 times) and the maximum contraction (Emax) induced by the full agonist, phenylephrine. 3. St-587, a partial alpha 1-adrenoceptor agonist, behaved as a weak agonist in the aorta (22.2% of phenylephrine Emax). However, when the same agonist was studied in tail artery rings a maximum contraction that was 78.4% of the phenylephrine induced Emax was reached. 4. L-NAME increased (3.3 times) the Emax for St-587 contraction in the aorta but not in the tail artery. Sensitivity to St-587 was slightly but significantly (P < 0.001) enhanced (1.9 times) by L-NAME in tail artery segments. 5. Contractile responses to phenylephrine after partial alkylation with phenoxybenzamine were analyzed by the nested hyperbolic null method. To elicit 50% of Emax for contraction only 1.1% of the receptors in the tail artery and 21% of the receptors in the aorta need to be occupied. These results indicate a higher receptor reserve for the tail artery than the aorta. 6. In the tail artery but not in the aorta, St-587 activates phosphoinositide turnover. The presence of L-NAME was without effect on inositol phosphates accumulation induced by this partial alpha 1-adrenoceptor agonist. 7. The maximum contraction induced by phenylephrine, after partial alpha-adrenoceptor alkylation, was enhanced by L-NAME in tail artery rings. However, the NO synthase inhibitor was unable to modify the phenylephrine-induced accumulation of inositol phosphates in the presence of phenoxybenzamine. 8. These results indicate that the differences in St-587-induced contraction and the modulation by L-NAME of alpha 1-adrenoceptor-mediated contraction observed between the tail artery and aorta are associated with differences in receptor reserve. In addition, our biochemical studies indicate that the potentiating effect of L-NAME is independent of intracellular calcium release via phosphatidylinositol turnover.

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The effects of α‐adrenoceptor agonists on intracellular Ca²+ levels in freshly dispersed single smooth muscle cells from rat tail artery

Cited by 19 publications

References 10 publications

α2-Adrenergic Receptor-Mediated Ca2+ Influx and Release in Porcine Myometrial Cells1

α2-Adrenergic Receptor-Mediated Ca2+ Influx and Release in Porcine Myometrial Cells1

Effects of pertussis and cholera toxins on α-adrenoceptor function in rat tail artery: differences in hypertension

Effect of N^G‐nitro‐L‐arginine methylester (L‐NAME) on functional and biochemical α₁‐adrenoceptor‐mediated responses in rat blood vessels

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The effects of α‐adrenoceptor agonists on intracellular Ca2+ levels in freshly dispersed single smooth muscle cells from rat tail artery

Cited by 19 publications

References 10 publications

α2-Adrenergic Receptor-Mediated Ca2+ Influx and Release in Porcine Myometrial Cells1

α2-Adrenergic Receptor-Mediated Ca2+ Influx and Release in Porcine Myometrial Cells1

Effects of pertussis and cholera toxins on α-adrenoceptor function in rat tail artery: differences in hypertension

Effect of NG‐nitro‐L‐arginine methylester (L‐NAME) on functional and biochemical α1‐adrenoceptor‐mediated responses in rat blood vessels

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The effects of α‐adrenoceptor agonists on intracellular Ca²+ levels in freshly dispersed single smooth muscle cells from rat tail artery

Effect of N^G‐nitro‐L‐arginine methylester (L‐NAME) on functional and biochemical α₁‐adrenoceptor‐mediated responses in rat blood vessels