Endothelium‐dependent and ‐independent effects of exogenous ATP, adenosine, GTP and guanosine on vascular tone and cyclic nucleotide accumulation of rat mesenteric artery

Vuorinen, Pauli; Pörsti, Ilkka; Metsä‐Ketelä, T.; Manninen, Vesa; Vapaatalo, Heikki; Laustiola, Kai

doi:10.1111/j.1476-5381.1992.tb14246.x

Cited by 37 publications

(31 citation statements)

References 40 publications

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“…In this vessel, ATP acts on purinergic receptors on smooth muscle to produce contraction via P2X receptors and additionally endothelium-independent relaxation via P2Y receptors (Mathieson and Burnstock, 1985;Burnstock and Warland, 1987b). Striking evidence for species differences between rabbit and rat mesenteric arterial purinergic signaling was presented in later studies, with the observation that ATP relaxation of rat mesenteric arteries was elicited largely via the endothelium (Vuorinen et al, 1992). Similarly, hyperpolarizations to ATP in hamster mesenteric arteries were endothelium dependent (Thapaliya et al, 1999), as were relaxations to ATP, ADP, and UTP in the hamster mesenteric arterial bed (Ralevic and Burnstock, 1996b).…”

Section: Mesenteric Vesselsmentioning

confidence: 86%

Purinergic Signaling and Blood Vessels in Health and Disease

2013

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Section: Mesenteric Vesselsmentioning

confidence: 86%

Purinergic Signaling and Blood Vessels in Health and Disease

2013

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“…Few in vitro studies have already shown that ATP exerts vasodilation partially via endothelium independent mechanisms (Mathieson & Burnstock, 1985;Vuorinen et al, 1992;McMillan et al, 1999). Vascular smooth muscle cells express P2y receptors which may mediate vasodilation (Wang et al, 2002).…”

Section: Why Was Atp-induced Vasodilation Not Inhibited By Any Of Thementioning

confidence: 99%

ATP‐induced vasodilation in human skeletal muscle

Ginneken

Meijer

Verkaik

et al. 2004

British J Pharmacology

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1 The purine nucleotide adenosine-5 0 -triphosphate (ATP) exerts pronounced effects on the cardiovascular system. The mechanism of action of the vasodilator response to ATP in humans has not been elucidated yet. The proposed endothelium-derived relaxing factors (EDRFs) were studied in a series of experiments, using the perfused forearm technique. 2 Adenosine 5 0 -triphosphate (0.2, 0.6, 6 and 20 nmol dl À1 forearm volume min À1 ) evoked a dosedependent forearm vasodilator response, which could not be inhibited by separate infusion of the nonselective COX inhibitor indomethacin (5 mg dl À1 min À1 , n ¼ 10), the blocker of Na þ /K þ -ATPase ouabain (0.2 mg dl À1 min À1 , n ¼ 8), the blocker of K Ca channels tetraethylammonium chloride (TEA, 0.1 mg dl À1 min À1 , n ¼ 10), nor by the K ATP -channel blocker glibenclamide (2 mg dl À1 min À1 , n ¼ 10). All blockers, except glibenclamide, caused a significant increase in baseline vascular tone. The obtained results might be due to compensatory actions of unblocked EDRFs. Combined infusion of TEA, indomethacin and L-NMMA (n ¼ 6) significantly increased the baseline forearm vascular resistance. The ATP-induced relative decreases in forearm vascular resistance were 4875, 6773, 8872, and 9272% in the absence and 2377, 6274, 8972, and 9371% in the presence of the combination of TEA, indomethacin and L-NMMA (Po0.05, repeated-measures ANOVA, n ¼ 6). A similar inhibition was obtained for sodium nitroprusside (SNP, Po0.05 repeated-measures ANOVA, n ¼ 6), indicating a nonspecific interaction due to the blocker-induced vasoconstriction. 3 ATP-induced vasodilation in the human forearm cannot be inhibited by separate infusion of indomethacin, ouabain, glibenclamide or TEA, or by a combined infusion of TEA, indomethacin, and L-NMMA. Endothelium-independent mechanisms and involvement of unblocked EDRFs, such as CO, might play a role, and call for further studies.

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“…Its vascular actions are not restricted to the coronary circulation since it causes vasodilatation in most vascular beds, although vasoconstriction may also occur in the kidney (Rossi et al, 1987). Vuorinen et al (1992Vuorinen et al ( , 1994 recently reported that rat mesenteric artery rings were relaxed by adenosine and that this action was blocked by the non-selective Al and A2 receptor antagonist, 8-phenyltheophylline (8-PT). Removal of the endothelium in these rings slightly attenuated the action of adenosine.…”

Section: Introductionmentioning

confidence: 99%

Effects of pH on responses to adenosine, CGS 21680, carbachol and nitroprusside in the isolated perfused superior mesenteric arterial bed of the rat

Bottrill

Warnock

Richardson

1995

British J Pharmacology

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1 The receptors mediating the vasodilator responses to adenosine in the isolated mesenteric arterial bed of the rat were identified by use of selective agonists and antagonists and the involvement of the endothelium was examined. 2 Adenosine-mediated dilatation of the mesentery was potentiated by the nitric oxide synthase inhibitor, N0-nitro-L-arginine methyl ester (L-NAME, 100 gM), but in contrast, removal of the endothelium substantially reduced the responses to adenosine. 3 The order of potency of adenosine receptor agonists was: 5'-N-ethylcarboxamidoadenosine (NECA) > 2-p-(-2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680) > 2-chloro-N6-cyclopentyl-adenosine (CCPA) > adenosine, suggesting the presence of A2A receptors.4 Adenosine-mediated dilatation was inhibited by the non-selective adenosine receptor antagonist, 8-phenyltheophylline (3 gM) and by the A2 receptor antagonist 8-(3-chlorostyryl)caffeine (500 nM), but was unaffected by the Al receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX; 10 nM).5 Reducing the pH of the perfusate to 6.8 potentiated the actions of both CGS 21680 and adenosine, but the vasodilator effects of carbachol were the same at both pH values. The adenosine response at the lower pH as at pH 7.4, was unaffected by DPCPX. The actions of the nitrovasodilator, sodium nitroprusside, were also potentiated at pH 6.8 relative to those at the higher pH value but smaller responses were obtained at the lower pH value with forskolin, a stimulator of adenylyl cyclase, than at pH 7.4. 6 It is concluded that the adenosine receptor mediating dilatation of the rat mesenteric arterial bed is of the A2A subtype, that the response, under the conditions used, is apparently partly dependent on the endothelium (but not due to the release of nitric oxide), and that the response to activation of this receptor is potentiated by a reduction in pH which is similar to that seen in ischaemic conditions.

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Endothelium‐dependent and ‐independent effects of exogenous ATP, adenosine, GTP and guanosine on vascular tone and cyclic nucleotide accumulation of rat mesenteric artery

Cited by 37 publications

References 40 publications

Purinergic Signaling and Blood Vessels in Health and Disease

Purinergic Signaling and Blood Vessels in Health and Disease

ATP‐induced vasodilation in human skeletal muscle

Effects of pH on responses to adenosine, CGS 21680, carbachol and nitroprusside in the isolated perfused superior mesenteric arterial bed of the rat

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