Differential effects of acetylcholine and bradykinin on prostanoid release from the rat mesenteric bed: role of endothelium and of nitric oxide

Peredo, Horacio A.; Feleder, Ethel; Adler‐Graschinsky, Edda

doi:10.1016/s0952-3278(97)90567-6

Cited by 13 publications

(7 citation statements)

References 22 publications

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“…Other mechanisms have been implicated in the vasorelaxant effect induced by BK, such as the generation of vasodilator prostanoids (Nwator et al, 1989;Peredo et al, 1997). This later possibility was evaluated by using indomethacin, a non-selective COX inhibitor.…”

Section: Discussionmentioning

confidence: 99%

Functional characterization of the mechanisms underlying bradykinin-induced relaxation in the isolated rat carotid artery

2007

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Section: Discussionmentioning

confidence: 99%

Functional characterization of the mechanisms underlying bradykinin-induced relaxation in the isolated rat carotid artery

2007

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“…This can be explained by acetylcholine releasing a vasodilator substance from the endothelium other than NO which opposes the direct vasoconstrictor actions of acetylcholine. Acetylcholine releases vasodilator prostacyclin from cultured endothelial cells of rabbit heart (Kan et al 1997) and the release of prostacyclin from rat mesenteric vasculature by acetylcholine has been shown to be entirely endothelium-dependent (Peredo et al 1997). Notwithstanding these issues, the fact that in the presence of L-NOARG, there is a vasoconstriction to acetylcholine after endothelium removal suggests that this method of endothelium removal is eOE ective.…”

Section: Discussionmentioning

confidence: 99%

Effects of adenosine receptor agonists on guinea-pig isolated working hearts and the role of endothelium and NO

Maddock

Broadley

Bril

et al. 2002

Journal of Pharmacy and Pharmacology

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The hypothesis that the coronary vasodilator effects of adenosine receptor agonists are independent of the vascular endothelium or mediators derived therefrom was examined in guinea-pig isolated working hearts. Adenosine receptor agonists, 5'-(N-ethylcarboxamido)-adenosine (NECA; two-fold selective for A2 over A1 receptors), 2-[p-(2-carboxyethyl)phenylethylamino]-5'-N-ethylcarboxamidoadenosine (CGS21680; A2A selective), N6-cyclopentyl-adenosine (CPA; A1 selective) and N6-(3-iodobenzyl)adenosine-5'-N-methyluronamide (IB-MECA; A3 selective), were infused (3 x 10(-7) M) after endothelium removal by passing oxygen through the coronary circulation. In spontaneously beating hearts, CGS21680 and NECA increased, while CPA decreased, coronary flow. NECA and CPA reduced heart rate, left ventricular pressure and aortic output. The nitric oxide synthase (NOS) inhibitor, N(G)-nitro-L-arginine (L-NOARG; 3 x 10(-5) M) abolished the vasodilatation by NECA but not CGS21680, indicating that nitric oxide (NO) of a non-endothelial source mediated the NECA response. Coronary vasodilatation by CGS21680 was inhibited bythe A2A receptor antagonist, 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo [2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM241385). Indometacin (10(-6) M) attenuated the coronary vasodilatation to CGS21680, suggesting a partial role for cyclooxygenase products. IB-MECA had no effect, indicating no A3 receptor involvement. In paced working hearts, the responses were similar except CPA had no effect on coronary flow or aortic output and CGS21680 increased left ventricular pressure and the maximum rate of ventricular pressure rise. This study has demonstrated functionally effective removal of the endothelium by a novel method of passing oxygen through the coronary vasculature. A coronary vasodilator action of adenosine receptor agonists mediated via A2A receptors is endothelium- and NO-independent, but partially involves cyclooxygenase products.

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“…Bradykinin is known also to act at BK B 2 receptors in the kidney (Maeda et al, 1996) and in mesenteric vascular beds (Peredo et al, 1997) to stimulate formation of eicosanoids and nitric oxide. Stimulation of phospholipase A 2 and formation of arachidonic acid in the signal transduction pathway for BK accounts for the prostaglandin production in these preparations.…”

Section: Discussionmentioning

confidence: 99%

Metabotropic Signal Transduction for Bradykinin in Submucosal Neurons of Guinea Pig Small Intestine

Gao

Liu

et al. 2004

J Pharmacol Exp Ther

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Intracellular recording methods with "sharp" microelectrodes were used to study signal transduction mechanisms underlying the excitatory action of bradykinin (BK) in morphologically identified neurons in the small intestinal submucosal plexus. Exposure to BK evoked slowly activating membrane depolarization and enhanced excitability associated with increased input resistance in AH-type and decreased input resistance in S-type neurons. Preincubation with pertussis toxin did not affect the BK-evoked responses. Pretreatment with the cyclooxygenase inhibitors indomethacin or piroxicam suppressed or abolished the BK-evoked responses. Application of prostaglandin (PG) E 2 or PG analogs evoked BK-like depolarizing responses in the submucosal plexus with a potency order of PGE 2 Ͼ PGE 1 Ͼ 17-phenyl trinor-PGE 2 Ͼ PGI 2 Ͼ sulprostone Ͼ PGF 2␣ . Depolarizing responses to bradykinin or PGE 2 in S-type neurons were suppressed in the presence of the phospholipase C inhibitor U73122 [(1-6-The inositol-1,4,5-trisphosphate receptor antagonist 2-aminoethoxydiphenylborane and the calmodulin inhibitor W-7, but not ryanodine, suppressed both bradykinin-and PGE 2 -evoked responses. KN-62, an inhibitor of calmodulin kinases, or GF109203X, a specific protein kinase C inhibitor, suppressed both BK-and PGE 2 -evoked depolarizing responses. Selective protein kinase A inhibitors did not alter BKor PGE 2 -evoked depolarizing responses in S neurons. The results suggest that BK stimulates synthesis and release of PGE 2 , which acts at EP 1 receptors to evoke depolarizing responses in submucosal neurons. The postreceptor transduction cascade includes activation of phospholipase C, inositol-1,4,5-trisphosphate production, intraneuronal Ca 2ϩ mobilization, activation of protein kinase C and/or calmodulin kinases, and phosphorylation of cationic channels.Exposing neurons in the guinea pig small intestinal myenteric or submucosal plexus to bradykinin (BK) in vitro evokes slowly activating depolarization of the membrane potential and enhanced excitability characterized by increased firing frequency during intraneuronal injection of depolarizing current pulses in both AH-and S-type neurons and the appearance of anodal break excitation at the offset of hyperpolarizing current pulses in AH neurons (Hu et al., 2003(Hu et al., , 2004. The depolarizing responses are associated with increased input resistance (i.e., decreased conductance) in AH neurons and with decreased input resistance (i.e., increased conductance) in S neurons. Selective BK B 2 receptor antagonists, but not BK B 1 antagonists, suppress the actions of BK in both myenteric and submucosal plexuses (Hu et al., 2003(Hu et al., , 2004. Binding studies with a fluorescently labeled, selective BK B 2 receptor antagonist reveal expression of BK B 2 receptors on a majority of the ganglion cells in the myenteric and submucosal plexuses. RT-PCR and Western blot analysis confirms the expression of BK B 2 receptor mRNA and protein in both plexuses (Hu et al., 2003(Hu et al., , 2004.Inhibition...

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Differential effects of acetylcholine and bradykinin on prostanoid release from the rat mesenteric bed: role of endothelium and of nitric oxide

Cited by 13 publications

References 22 publications

Functional characterization of the mechanisms underlying bradykinin-induced relaxation in the isolated rat carotid artery

Functional characterization of the mechanisms underlying bradykinin-induced relaxation in the isolated rat carotid artery

Effects of adenosine receptor agonists on guinea-pig isolated working hearts and the role of endothelium and NO

Metabotropic Signal Transduction for Bradykinin in Submucosal Neurons of Guinea Pig Small Intestine

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