The mechanism of bradykinin‐induced endothelium‐dependent contraction and relaxation in the porcine interlobar renal artery

Ihara, Eikichi; Hirano, Katsuya; Derkach, Dmitry N.; Nishimura, Junji; Nawata, Hajime; Kobayashi, Hideo

doi:10.1038/sj.bjp.0703141

Cited by 30 publications

(43 citation statements)

References 53 publications

(72 reference statements)

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“…Interestingly, the amount of PGI 2 evoked by ACh is above the concentration required to initiate a vasoconstrictor activity (1 ng/mg 6-keto-PGF 1␣ can be translated into 2.7 mol PGI 2 produced in 1 kg vessel tissue). In addition, PGH 2 , the intermediate of PGI 2 synthesis that may diffuse outside the endothelium, can also cause contraction by acting on TP receptors before being converted to PGI 2 in medial smooth muscle (10,13,52). Thus, the vasoconstrictor activity of COX-1 in diabetic aortas could be in an important part derived from PGI 2 synthesis, owing to limited function of IP receptors, as we have previously suggested in normal mouse arteries (23).…”

Section: Discussionmentioning

confidence: 80%

Vasoconstrictor role of cyclooxygenase-1-mediated prostacyclin synthesis in non-insulin-dependent diabetic mice induced by high-fat diet and streptozotocin

Zhu

Liu

Luo

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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. Vasoconstrictor role of cyclooxygenase-1-mediated prostacyclin synthesis in noninsulin-dependent diabetic mice induced by high-fat diet and streptozotocin. Am J Physiol Heart Circ Physiol 307: H319 -H327, 2014. First published May 30, 2014 doi:10.1152/ajpheart.00022.2014.-This study tested the hypothesis that in diabetic arteries, cyclooxygenase (COX)-1 mediates endothelial prostacyclin (PGI2) synthesis, which evokes vasoconstrictor activity under the pathological condition. Non-insulin-dependent diabetes was induced to C57BL/6 mice and those with COX-1 deficiency (COX-1 Ϫ/Ϫ mice) using a high-fat diet in combination with streptozotocin injection. In vitro analyses were performed 3 mo after. Results showed that in diabetic aortas, the endothelial muscarinic receptor agonist ACh evoked an endothelium-dependent production of the PGI2 metabolite 6-keto-PGF1␣, which was abolished in COX-1 Ϫ/Ϫ mice. Meanwhile, COX-1 deficiency or COX-1 inhibition prevented vasoconstrictor activity in diabetic abdominal aortas, resulting in enhanced relaxation evoked by ACh. In a similar manner, COX-1 deficiency increased the relaxation evoked by ACh in nitric oxide synthase-inhibited diabetic renal arteries. Also, in diabetic abdominal aortas and/or renal arteries, both PGI2 and the COX substrate arachidonic acid evoked contractions similar to those of nondiabetic mice. However, the contraction to arachidonic acid, but not that to PGI2, was abolished in vessels from COX-1 Ϫ/Ϫ mice. Moreover, we found that 3 mo after streptozotocin injection, systemic blood pressure increased in diabetic C57BL/6 mice but not in diabetic COX-1 Ϫ/Ϫ mice. These results explicitly demonstrate that in the given arteries from non-insulin-dependent diabetic mice, COX-1 remains a major contributor to the endothelial PGI2 synthesis that evokes vasoconstrictor activity under the pathological condition. Also, our data suggest that COX-1 deficiency prevents or attenuates diabetic hypertension in mice, although this could be related to the loss of COX-1-mediated activities derived from both vascular and nonvascular tissues. diabetes; arachidonic acid; metabolism; thromboxane prostanoid receptors; contraction CYCLOOXYGENASE (COX

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Section: Discussionmentioning

confidence: 80%

Vasoconstrictor role of cyclooxygenase-1-mediated prostacyclin synthesis in non-insulin-dependent diabetic mice induced by high-fat diet and streptozotocin

Zhu

Liu

Luo

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…Several studies reported that the cyclooxygenase products, prostaglandin (PG) H 2 (PGH 2 ), thromboxane A 2 (TXA 2 ), and PGF 2a , mediate the contraction evoked by the peptide (10 -12). Although the vasorelaxant effect of bradykinin is well known to be endothelium-and nitric oxide (NO)-dependent (3,7,13), the nature and role of its vasoconstrictor effect is unclear.…”

Section: Introductionmentioning

confidence: 99%

Different Prostanoids Are Involved in Bradykinin-Induced Endothelium-Dependent and -Independent Vasoconstriction in Rat Mesenteric Resistance Arteries

Nawa¹,

Kurosaki²,

Kawasaki³

2004

J Pharmacol Sci

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Abstract. Mechanisms underlying bradykinin-induced vasoconstriction were investigated in rat perfused mesenteric vascular beds with active tone. In preparations with intact endothelium, bolus injections of bradykinin (1 to 1,000 pmol) dose-dependently produced three-phase vascular effects, which consisted of a first-phase vasodilation followed by a second-phase vasoconstriction and a subsequent third-phase vasodilation; these effects were abolished by FR172357 (bradykinin B 2 -receptor antagonist), but not by des-Arg 9 -[Leu 8 ]-bradykinin (bradykinin B 1 -receptor antagonist). In preparations with intact endothelium, indomethacin (cyclooxygenase inhibitor), seratrodast (thromboxane A 2 (TXA 2 )-receptor antagonist), ONO-3708 (TXA 2 / prostaglandin H 2 (PGH 2 )-receptor antagonist) or ozagrel (TXA 2 synthesis inhibitor) markedly inhibited the bradykinin-induced vasoconstriction. In preparations without endothelium, the bradykinin-induced vasoconstriction was abolished by indomethacin and ONO-3708, while seratrodast and ozagrel had no effect. These results suggest that the endothelium-dependent vasoconstriction of bradykinin is mainly mediated by TXA 2 and that prostanoids other than TXA 2 , probably PGH 2 , in mesenteric vascular smooth muscle are responsible for bradykinin-induced endothelium-independent vasoconstriction.

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“…In these systems, dosedependent changes in active muscular tension can be characterized in response to vasorelaxing agents such as bradykinin, 18,22,23 sodium nitroprusside, 19,24,25 nitroglycerin, [26][27][28] and NO. 20,[29][30][31][32][33] Adaptation of the isolated tissue bath model to drug delivery studies could provide relevant, real-time quantitative data on the drug release and delivery profiles triggered by ultrasound.…”

Section: Drug Delivery Quantificationmentioning

confidence: 99%

“…3,4,[15][16][17][18][19] Optical techniques, such as fluorescence 16,20,21 or luminescence, 18,22,23 take advantage of the native optical properties of the therapeutic or conjugation of tracer molecules. Electrophysiological approaches, such as voltage-clamp techniques, 19,24,25 directly assess the changes in membrane potential provoked during UMDD, but often require isolated cells cultured in vitro, where cellular processes can vary from in vivo conditions.…”

Section: Drug Delivery Quantificationmentioning

confidence: 99%

Pulsed ultrasound enhances the delivery of nitric oxide from bubble liposomes to ex vivo porcine carotid tissue

Sutton¹,

Raymond²,

Verleye³

et al. 2014

IJN

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Ultrasound-mediated drug delivery is a novel technique for enhancing the penetration of drugs into diseased tissue beds noninvasively. By encapsulating drugs into microsized and nanosized liposomes, the therapeutic can be shielded from degradation within the vasculature until delivery to a target site by ultrasound exposure. Traditional in vitro or ex vivo techniques to quantify this delivery profile include optical approaches, cell culture, and electrophysiology. Here, we demonstrate an approach to characterize the degree of nitric oxide (NO) delivery to porcine carotid tissue by direct measurement of ex vivo vascular tone. An ex vivo perfusion model was adapted to assess ultrasound-mediated delivery of NO. This potent vasodilator was coencapsulated with inert octafluoropropane gas to produce acoustically active bubble liposomes. Porcine carotid arteries were excised post mortem and mounted in a physiologic buffer solution. Vascular tone was assessed in real time by coupling the artery to an isometric force transducer. NO-loaded bubble liposomes were infused into the lumen of the artery, which was exposed to 1 MHz pulsed ultrasound at a peak-to-peak acoustic pressure amplitude of 0.34 MPa. Acoustic cavitation emissions were monitored passively. Changes in vascular tone were measured and compared with control and sham NO bubble liposome exposures. Our results demonstrate that ultrasound-triggered NO release from bubble liposomes induces potent vasorelaxation within porcine carotid arteries (maximal relaxation 31%±8%), which was significantly stronger than vasorelaxation due to NO release from bubble liposomes in the absence of ultrasound (maximal relaxation 7%±3%), and comparable with relaxation due to 12 μM sodium nitroprusside infusions (maximal relaxation 32%±3%). This approach is a valuable mechanistic tool for assessing the extent of drug release and delivery to the vasculature caused by ultrasound.

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The mechanism of bradykinin‐induced endothelium‐dependent contraction and relaxation in the porcine interlobar renal artery

Cited by 30 publications

References 53 publications

Vasoconstrictor role of cyclooxygenase-1-mediated prostacyclin synthesis in non-insulin-dependent diabetic mice induced by high-fat diet and streptozotocin

Vasoconstrictor role of cyclooxygenase-1-mediated prostacyclin synthesis in non-insulin-dependent diabetic mice induced by high-fat diet and streptozotocin

Different Prostanoids Are Involved in Bradykinin-Induced Endothelium-Dependent and -Independent Vasoconstriction in Rat Mesenteric Resistance Arteries

Pulsed ultrasound enhances the delivery of nitric oxide from bubble liposomes to ex vivo porcine carotid tissue

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