α-Adrenoceptor activation of polyphosphoinositide hydrolysis in the rat tail artery

Cheung, Y.-D.; Feltham, Ian; Thompson, Peter M.; Triggle, Chris R.

doi:10.1016/0006-2952(90)90082-v

Cited by 13 publications

(5 citation statements)

References 32 publications

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“…PTX had no e ect on the parameters generally taken as criteria for satisfactory use of this technique, namely, R' max , R' min , b' and the loading ratio F 360 /AF 360 . This absence of e ect of PTX on [Ca 2+ ] i is not surprising given the lack of e ect of PTX on either calcium channels or inositol phosphate metabolism (Cheung et al, 1990;LaBelle & Murray, 1990;Takuwa et al, 1990;Ohya & Sperelakis, 1991). The possibility exists that the PTX B-oligomer could modify [Ca 2+ ] i by triggering phospholipase C (Wong & Roso , 1996), but this does not appear to be the case in our preparation.…”

Section: Discussionmentioning

confidence: 54%

Pertussis toxin‐sensitive G_i‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

Spitzbarth-Régrigny¹,

Petitcolin

Bueb

et al. 2000

British J Pharmacology

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1 We studied the involvement of pertussis toxin (PTX)-sensitive G-proteins in the sensitivity of arterial constriction to intracellular calcium ([Ca 2+ ] i ) mobilization. 2 Vasoconstriction was measured in vitro in perfused, de-endothelialized rat tail arteries loaed with the calcium-sensitive dye, fura-2 and treated or not with PTX (30 ± 1000 ng ml 71 ). Arteries were stimulated with noradrenaline (NA, 0.1 ± 100 mM) or KCl (15 ± 120 mM). 3 KCl elicited a smaller vasoconstrictor response (E max =94+8 mmHg) than NA (E max =198+9 mmHg) although [Ca 2+ ] i mobilization was similar (E max =123+8 and 135+7 nM for KCl and NA, respectively). PTX (1000 ng ml 71 ) had no e ect on [Ca 2+ ] i mobilization but lowered NA-(but not KCl-) induced vasoconstriction (E max =118+7 mmHg). 4 G i/o -proteins were revealed by immunoblotting with anti-G ia and anti-G oa antibodies in membranes prepared from de-endothelialized tail arteries. [a 32 P]-ADP-ribosylation of G-proteins by PTX (1000 ng ml 71 ) was demonstrated in the intact rat tail artery (pixels in the absence of PTX: 3150, presence: 25053). 5 In conclusion, we suggest that smooth muscle cells possess a PTX-sensitive G i -protein-mediated intracellular pathway which ampli®es [Ca 2+ ] i sensitivity of contraction in the presence of agonists such as NA.

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Section: Discussionmentioning

confidence: 54%

Pertussis toxin‐sensitive G_i‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

Spitzbarth-Régrigny¹,

Petitcolin

Bueb

et al. 2000

British J Pharmacology

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“…Although possible, this would be surprising, since α 1 -adrenoceptors in caudal artery have been demonstrated to be coupled to phosphoinositide hydrolysis and to increase production of inositol phosphates (Cheung et al 1990;Gisbert et al 2003). Although not directly demonstrated in either of the latter studies, this would also be accompanied by production of diacylglycerol, the physiological activator of PKC.…”

Section: Discussionmentioning

confidence: 83%

Differential participation of protein kinase C and Rho kinase in α₁-adrenoceptor mediated contraction in rat arteries

Mueed¹,

Bains²,

Zhang³

et al. 2004

Can. J. Physiol. Pharmacol.

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The major functional alpha1-adrenoceptor in the rat aorta is of the alpha1Dsubtype and that in the caudal artery is of the alpha1A subtype. In the present study, the participation of protein kinase C (PKC) and Rho kinase (RhoK) in contractile responses to stimulation of the alpha1-adrenoceptors in these two arteries was investigated. Both the PKC inhibitor Ro-318220 and the RhoK inhibitor Y-27632 significantly blocked contractile responses of the aorta to phenylephrine (PE) and the selective alpha1A-adrenoceptor agonist A61603. When used in combination, the inhibitors had an additive blocking effect. In the caudal artery, Y-27632 but not Ro-318220 inhibited contractile responses to PE and A61603, and, in combination, the antagonism produced was no greater than that by Y-27632 alone. Contractile responses to direct activation of PKC with phorbol 12,13-dibutyrate were much smaller and levels of CPI-17 (PKC-activated protein phosphatase inhibitor of 17 kDa) were much lower in the caudal artery than the aorta. The results suggest that both PKC and RhoK contribute independently to contractile responses to stimulation of alpha1D-adrenoceptors in the aorta. However, RhoK, but not PKC, participates in contractile responses to stimulation of alpha1A-adrenoceptors in the caudal artery. This difference may largely be due to differences between the two arteries in the extent to which PKC participates in contraction.

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“…In vascular smooth muscle, NaF in the presence of AlCl3 is thought to stimulate the G-protein coupled to PLC because of the consistent observation that NaF stimulates increases in accumulation of inositol phosphates and/or increases in productionof IP3 in tissues such as rat aortic myocytes (Berta et al, 1988), rat caudal artery (Zeng et al, 1989;Cheung et al, 1990), rabbit femoral artery (Ratz & Blackmore, 1990), and rat and rabbit aorta (Adeagbo & Triggle, 1991). Various lines of evidence suggest that NaF also activates Gproteins coupled to calcium channels.…”

Section: Discussionmentioning

confidence: 99%

Enhanced contractile responses of arteries from streptozotocin diabetic rats to sodium fluoride

Weber

Chow

Abebe

et al. 1996

British J Pharmacology

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1 Previous studies from this laboratory have demonstrated that cxl-adrenoceptor-mediated increases in tension and phosphoinositide metabolism are enhanced in the aorta and mesenteric arteries from diabetic rats. The purpose of the present investigation was to determine whether contractile responses to sodium fluoride (NaF), which directly stimulates GTP-binding proteins (G-proteins), are also enhanced in diabetic arteries. 2 NaF (1-20 mM) in the presence of 10 ,UM aluminium chloride produced slowly developing, concentration-dependent contractions in mesenteric arteries from three month streptozotocin-diabetic (60 mg kg-', i.v. ) male Wistar rats and age-matched control rats. The maximum contractile response but not the sensitivity to NaF was significantly greater in mesenteric arteries from diabetic than from control rats, as was the response to noradrenaline (NA). Maximum contractile responses of aorta and caudal artery from diabetic rats to NaF were also significantly enhanced. 3 Removal of the endothelium and denervation with 6-hydroxydopamine did not significantly alter the maximum contractile response of mesenteric arteries from either control or diabetic rats to NaF. Similarly, NaF had no effect on cyclic AMP levels in aorta, and no difference in cyclic AMP levels, either basally or in the presence of NaF, was detected between control and diabetic rat aorta. 4 Contractile responses of mesenteric arteries from both control and diabetic rats to NaF were diminished in calcium-free Krebs solution, but the NaF response remained significantly elevated in mesenteric arteries from diabetic rats compared to control.5 Ryanodine (30 gM) which depletes intracellular calcium stores, nifedipine (3 gM) which blocks dihydropyridine-sensitive calcium channels and calphostin C (0.5 gM) which selectively inhibits protein kinase C, all significantly inhibited maximum contractile responses of mesenteric arteries from control and diabetic rats to NaF. There were no significant differences between control and diabetic arteries in the relative magnitude of the inhibition produced by the three antagonists. 6 These data suggest that there may be increased activation of the same signalling processes that mediate NA-stimulated vasoconstriction, perhaps contraction-associated G-proteins or the effectors coupled to these G-proteins, in response to NaF in mesenteric arteries from diabetic rats. This may also be responsible for the enhanced contractile responses of these arteries to a,-adrenoceptor stimulation.

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α-Adrenoceptor activation of polyphosphoinositide hydrolysis in the rat tail artery

Cited by 13 publications

References 32 publications

Pertussis toxin‐sensitive G_i‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

Pertussis toxin‐sensitive G_i‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

Differential participation of protein kinase C and Rho kinase in α₁-adrenoceptor mediated contraction in rat arteries

Enhanced contractile responses of arteries from streptozotocin diabetic rats to sodium fluoride

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α-Adrenoceptor activation of polyphosphoinositide hydrolysis in the rat tail artery

Cited by 13 publications

References 32 publications

Pertussis toxin‐sensitive Gi‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

Pertussis toxin‐sensitive Gi‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

Differential participation of protein kinase C and Rho kinase in α1-adrenoceptor mediated contraction in rat arteries

Enhanced contractile responses of arteries from streptozotocin diabetic rats to sodium fluoride

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Product

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Pertussis toxin‐sensitive G_i‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

Pertussis toxin‐sensitive G_i‐proteins and intracellular calcium sensitivity of vasoconstriction in the intact rat tail artery

Differential participation of protein kinase C and Rho kinase in α₁-adrenoceptor mediated contraction in rat arteries