Characterization of adenosine action in isolated rat renal artery

Grbović, Leposava; Radenković, Miroslav; Prostran, Milica; Pesic, Srdjan

doi:10.1016/s0306-3623(01)00087-8

Cited by 20 publications

(20 citation statements)

References 37 publications

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“…We showed that adenosine had a negligible effect on this contraction. Similar observation has been made before in rat renal artery (10). In contrast, some investigators found that adenosine relaxed high K ϩ -induced contraction in other blood vessels, such as coronary artery (31,32).…”

Section: Discussionsupporting

confidence: 86%

Role of store-operated Ca²⁺ entry in adenosine-induced vasodilatation of rat small mesenteric artery

Wang¹,

Zhang²,

Wier³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Store-operated Ca(2+) entry (SOCE) has recently been proposed to contribute to Ca(2+) influx in vascular smooth muscle cells (VSMCs). Adenosine is known for its protective role against hypoxia and ischemia by increasing nutrient and oxygen supply through vasodilation. This study was designed to examine the hypothesis that SOCE have a functional role in adenosine-induced vasodilation. Small mesenteric resistance arteries and mesenteric VSMCs were obtained from rats. Isometric tensions of isolated artery rings were measured by a sensitive myograph system. Laser-scanning confocal microscopy was used to determine the intracellular Ca(2+) concentration of fluo 3-loaded VSMCs. Adenosine (0.1-100 microM) relaxed artery rings that were precontracted by phenylephrine in a concentration-dependent manner. In cultured mesenteric VSMCs, passive store depletion by thapsigargin and active store depletion by phenylephrine both induced Ca(2+) influx due to SOCE. Adenosine inhibited SOCE-mediated increases in cytosolic Ca(2+) levels evoked by the emptying of the stores. In isolated artery rings, adenosine inhibited SOCE-induced contractions due to store depletion. A(2A) receptor antagonism with SCH-58261 and adenylate cyclase inhibition with SQ-22536 largely attenuated adenosine responses. The cAMP analog 8-bromo-cAMP mimicked the effects of adenosine on SOCE. Our results indicate a novel mechanism of vasodilatation by adenosine that involves regulation of SOCE through the cAMP signaling pathway due to activation of adenosine A(2A) receptors.

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Section: Discussionsupporting

confidence: 86%

Role of store-operated Ca²⁺ entry in adenosine-induced vasodilatation of rat small mesenteric artery

Wang¹,

Zhang²,

Wier³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…The abolished vasodilatation in the superficial vascular bed by ZM-241385 indicates that NO formation is primarily the result of A2aAR activation. These conclusions agree with previous studies in excised renal and nonrenal vessel preparations showing consistent increases in NOS activity and NO release in response to adenosine, usually through an A2AR-mediated process (Zanzinger and Bassenge, 1993 ; Martin TABLE 5 Effect of intravenous infusion of adenosine at 5, 10, and 20 g/min after injection of the nonspecific NOS inhibitor L-NAME on MAP, SBF, and SVR in wild-type (A1ARϩ/ϩ), A1 adenosine receptor knockout mice (A1ARϪ/Ϫ), and mice deficient in endothelial NOS (eNOSϪ/Ϫ) and Potts, 1994; Abebe et al, 1995;Grbovic et al, 2000). Adenosine has also been shown to dilate rabbit renal arteries through an undefined endothelial relaxing factor that does not seem to be NO (Rump et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Vasoconstrictor and Vasodilator Effects of Adenosine in the Mouse Kidney due to Preferential Activation of A1 or A2 Adenosine Receptors

Hansen

Hashimoto²,

Oppermann³

et al. 2005

J Pharmacol Exp Ther

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The present experiments in mice were performed to determine the steady-state effects of exogenous adenosine on the vascular resistance of the whole kidney, of superficial blood vessels, and of afferent arterioles. The steady-state effect of an intravenous infusion of adenosine (5, 10, and 20 g/min) in wild-type mice was vasodilatation as evidenced by significant reductions of renal and superficial vascular resistance. Resistance decreases were augmented in adenosine 1 receptor -nitro-L-arginine methyl ester (L-NAME) adenosine was unable to alter superficial blood flow and resistance significantly indicating that adenosine-induced dilatation is NO-dependent. Absence of a dilatory effect in endothelial nitric-oxide synthase (NOS) Ϫ/Ϫ mice suggests endothelial NOS as the source of NO. When infused into the subcapsular interstitium, adenosine reduced superficial blood flow through A1AR activation. Adenosine (10 Ϫ7 M) constricted isolated perfused afferent arterioles when added to the bath but not when added to the luminal perfusate. Luminal adenosine caused vasoconstriction in the presence of L-NAME or the A2AR antagonist 3,7-dimethyl-1-(2-propynyl)xanthine. Our data show that global elevation of renal adenosine causes steady-state vasorelaxation resulting from adenosine 2 receptor (A2AR)-mediated generation of NO. In contrast, selective augmentation of adenosine around afferent arterioles causes persistent vasoconstriction, indicating A1AR dominance. Thus, adenosine is a renal constrictor only when it can interact with afferent arteriolar A1AR without affecting the bulk of renal A2AR at the same time.

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“…At the beginning of each experiment, endothelium functional integrity was examined by precontraction of isolated RRA with submaximal concentration (EC 70 ) of phenylephrine (1 µM), followed by addition of acetylcholine (1 µM) (17). This procedure was repeated three times in 20-min intervals.…”

Section: Methodsmentioning

confidence: 99%

“…During this period the organ baths were washed with fresh (37°C) buffer solution every 15 min. After 45 min, each ring was gradually stretched to the previously established optimal point of the resting tension for RRA, 2 g (17). Once at their optimal length, the segments were allowed to equilibrate for 30 min before experimentation.…”

Section: Vascular Preparationsmentioning

confidence: 99%

Analysis of the Vasorelaxant Action of Angiotensin II in the Isolated Rat Renal Artery

et al. 2008

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Abstract. Taking into consideration that mechanisms involved in the vasodilatator actions of angiotensin II have not yet been completely elucidated, the present study was undertaken in order to examine the mechanisms underlying the angiotensin II-induced relaxation of rat renal artery (RRA). Angiotensin II produced concentration-dependent and endothelium-independent relaxation of isolated RRA. Angiotensin II-induced relaxation was partially reduced by inhibitors of nitric oxide synthase and guanylyl cyclase. The remaining dilatation was inhibited by a potassium channel blocker, charybdotoxin. Precontraction of RRA with high concentration of K + partially reduced angiotensin II-evoked relaxation, while indomethacin, glibenclamide, apamin and barium did not alter the angiotensin II concentration-response curve. Losartan had no effect on angiotensin II effect. Oppositely, HOE 140 and PD123319, separately or in combination, partially antagonized vasorelaxation induced by angiotensin II. Complete blockade of RRA response was obtained after simultaneous incubation of all three receptor antagonists HOE-140, PD123319, and losartan; L-NOARG plus HOE-140; or PD123319 plus charybdotoxin. These results indicate that angiotensin II produces endothelium-independent relaxation of RRA, which is most probably mediated by the interaction of the NO-cGMP pathway and K + channels. Moreover, we can assume that AT 1 , AT 2 , and B 2 receptors are involved in the vasorelaxant effect of angiotensin II.

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Characterization of adenosine action in isolated rat renal artery

Cited by 20 publications

References 37 publications

Role of store-operated Ca²⁺ entry in adenosine-induced vasodilatation of rat small mesenteric artery

Role of store-operated Ca²⁺ entry in adenosine-induced vasodilatation of rat small mesenteric artery

Vasoconstrictor and Vasodilator Effects of Adenosine in the Mouse Kidney due to Preferential Activation of A1 or A2 Adenosine Receptors

Analysis of the Vasorelaxant Action of Angiotensin II in the Isolated Rat Renal Artery

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Characterization of adenosine action in isolated rat renal artery

Cited by 20 publications

References 37 publications

Role of store-operated Ca2+ entry in adenosine-induced vasodilatation of rat small mesenteric artery

Role of store-operated Ca2+ entry in adenosine-induced vasodilatation of rat small mesenteric artery

Vasoconstrictor and Vasodilator Effects of Adenosine in the Mouse Kidney due to Preferential Activation of A1 or A2 Adenosine Receptors

Analysis of the Vasorelaxant Action of Angiotensin II in the Isolated Rat Renal Artery

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Role of store-operated Ca²⁺ entry in adenosine-induced vasodilatation of rat small mesenteric artery

Role of store-operated Ca²⁺ entry in adenosine-induced vasodilatation of rat small mesenteric artery