Interaction of bradykinin and des-Arg9-bradykinin with isolated pig coronary arteries: mechanical and electrophysiological events

Bény, Jean‐Louis; Brunet, Pascale Claude; Huggel, H

doi:10.1016/0167-0115(87)90061-9

Cited by 51 publications

(34 citation statements)

References 18 publications

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“…Isolated coronary arteries from a number of species relax in an endothelium-dependent manner to BK (Beny et al, 1987;Toda et al, 1987;Baydoun & Woodward, 1991;Mombouli et al, 1992;Auch-Schwelk et al, 1993;Kilpatrick & Cocks, 1994;Holzmann et al, 1994;Stork & Cocks, 1994), yet do not relax in response to des-Arg9-BK (Beny et al, 1987;Baydoun & Woodward, 1991;Auch-Schwelk et al, 1993;Holzmann et al, 1994). These findings suggest the presence of B2 but not B. receptors on the endothelium of the coronary vasculature.…”

Section: Introductionsupporting

confidence: 49%

Endothelium‐dependent relaxations mediated by inducible B₁ and constitutive B₂ kinin receptors in the bovine isolated coronary artery

Drummond

Cocks

1995

British J Pharmacology

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1 Rings of bovine left anterior descending coronary artery (LAD) were contracted with the thromboxane A2-mimetic, U46619 (1-30 nM), to approximately 40% of their maximum contraction to 125 mM KCI Krebs solution (KPSSma,,) 6.27 + 0.11) and the B2 receptor antagonist Hoe-140 (pA2, 9.63 + 0.14), respectively. 3 At 3 h of in vitro incubation, the sensitivity (pEC5o, 7.45 + 0.10) and Rmax (84.6 + 3.3%) to des-Arg9-BK were significantly less than those obtained in the same tissues at 6 h (pEC50, 7.94±0.06; Rma,, 91.4 + 2.5%), whereas endothelium-dependent relaxations to BK and ACh were unaffected by incubation time. 4 Relaxation responses to des-Arg9-BK, but not BK, at both 3 h and 6 h were significantly attenuated by the protein synthesis inhibitors, cycloheximide (30 and 100 gM) and actinomycin D (2 gM).5 At 6 h, the nitric oxide (NO) synthase inhibitor, N0-nitro-L-arginine (L-NOARG, 100 ,M), caused a significant 2 fold decrease in pEC50 (9.58 + 0.03) but had no effect on Rmax for BK. For des-Arg9-BK, L-NOARG (100 gM) caused a marked and significant decrease in both the pEC50 and Rmax and revealed contractions to low concentrations of des-Arg9-BK. In both cases, L-NOARG inhibition was reversed in the presence of L-arginine (10 mM). 6 At 6 h, removal of the endothelium abolished relaxation responses to des-Arg9-BK and BK, and for des-Arg9-BK, but not BK, unmasked concentration-dependent contractions (pEC5o, 7.57+0.09; Rma, 83.4±9.1%). The sensitivity of contractions to des-Arg9-BK increased slightly from 3 h (pEC5o, 7.37 + 0.08) to 6 h (pEC50, 7.62 + 0.12) of in vitro incubation; however, there was a small but significant depression in the maximum response over this time (Rmax, 126.8 + 8.5% and 103.3 ± 8.6% for 3 h and 6 h of incubation respectively). 7 In conclusion, the bovine LAD contains inducible B1 and constitutive B2 endothelial cell kinin receptors, both of which mediate endothelium-dependent relaxation partly via the release of NO. B1receptors were also present on the smooth muscle layer of the bovine LAD.

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Section: Introductionsupporting

confidence: 49%

Endothelium‐dependent relaxations mediated by inducible B₁ and constitutive B₂ kinin receptors in the bovine isolated coronary artery

Drummond

Cocks

1995

British J Pharmacology

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“…A similar response has been documented repeatedly in animal blood vessels with bradykinin and other endothelial stimulants (10,25,26), and has been attributed to the release of a diffusible substance, EDHF (9,11,14). In the uterine artery of the guinea pig (27) and in small mesenteric arteries ofthe rat (20), nitric oxide can cause membrane hyperpolarization.…”

Section: Discussionmentioning

confidence: 72%

Endothelium-dependent hyperpolarization caused by bradykinin in human coronary arteries.

Nakashima¹,

Mombouli²,

Taylor³

et al. 1993

J. Clin. Invest.

216

123

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The present study was designed to determine whether bradykinin induces endothelium-dependent hyperpolarization of vascular smooth muscle in human coronary arteries, and if so, to define the contribution of this hyperpolarization to endothelium-dependent relaxations. The membrane potential of arterial smooth muscle cells (measured by glass microelectrodes) and changes in isometric force were recorded in tissues from six patients undergoing heart transplantation. In the presence of indomethacin and NG-nitro-L-arginine (NLA), the membrane potential was -48.3±0.6 and -46.9±0.6 mV, in preparations with and without endothelium, respectively, and was not affected by treatment with perindoprilat, an angiotensin-converting enzyme inhibitor. In the presence of both indomethacin and NLA, bradykinin evoked transient and concentration-dependent hyperpolarizations only in tissues with endothelium, which were augmented by perindoprilat and mimicked by the calcium ionophore A23187. Glibenclamide did not inhibit membrane hyperpolarization to bradykinin. In rings contracted with prostaglandin F2,, the cumulative addition of bradykinin caused a concentration-dependent relaxation during contractions evoked by prostaglandin F2, which was not abolished by NLA and indomethacin. The present findings demonstrate the occurrence of endothelium-dependent hyperpolarization, and its contribution to endothelium-dependent relaxations, in the human coronary artery. (J. Clin. Invest. 1993. 92:2867-2871

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“…This results in release of nitric oxide 15,16 and endothelium-derived hyperpolarizing factor to produce vasorelaxation. 17,18 However, although inhibition of nitric oxide synthase with N Gmonomethyl-L-arginine attenuates the vasodilatation to bradykinin, it does not affect endothelial t-PA release. 13 This would suggest that bradykinin-stimulated t-PA release is mediated through a nitric oxide synthase-independent pathway and that the endothelium regulates blood flow and t-PA release through distinct pathways.…”

Section: Discussionmentioning

confidence: 99%

Bradykinin Receptor Antagonism and Endothelial Tissue Plasminogen Activator Release in Humans

Witherow

Dawson²,

Ludlam³

et al. 2003

ATVB

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Objective-We sought to assess pharmacodynamic responses to the bradykinin antagonist B9340 and to determine the contribution of the endothelial bradykinin receptor to stimulated tissue plasminogen activator (t-PA) release in humans. Methods and Results-Bilateral forearm blood flow and plasma fibrinolytic variables were measured in 8 volunteers during 100 minutes of intrabrachial infusions of saline placebo, B9340 at 4.5 nmol/min, or B9340 at 13.5 nmol/min. On each occasion, intra-arterial bradykinin (30 to 3000 pmol/min) and substance P (4 to 16 pmol/min) were coinfused for 10 minutes at each dose. To assess the onset and offset of action, 6 additional subjects on 2 occasions received intra-arterial bradykinin (100 pmol/min) for 60 minutes with a coinfusion of either saline placebo or B9340 (13.5 nmol/min) for 12 minutes. During placebo infusion, bradykinin and substance P caused dose-dependent vasodilatation in the infused forearm (PϽ0.001). B9340 caused a dose-dependent inhibition of bradykinin-induced forearm vasodilatation and t-PA release (PϽ0.001) without affecting substance P-induced vasodilatation or t-PA release (PϭNS). B9340 caused a reversible inhibition of bradykinin-induced vasodilatation (PϽ0.001) with a rapid onset and offset of action. radykinin is an endogenous, vasoactive, nonapeptide mediator involved in many physiologic processes. It is cleaved from high-molecular-weight kininogen during the contact phase of blood coagulation, 1 resulting in endothelium-dependent vasodilatation and stimulation of tissue plasminogen activator (t-PA) release from human endothelial cells. 2 It has a brief duration of action (plasma half-life of 15 to 30 seconds) owing to its rapid degradation by several enzymes, principally angiotensin-converting enzyme (ACE). Bradykinin appears to contribute to the vascular effects of ACE inhibitor therapy in hypertension 3 and heart failure. 4 Bradykinin receptor antagonists have been developed from peptide analogues of bradykinin. The most widely used bradykinin receptor antagonist is HOE-140, or icatibant, which demonstrates high selectivity for the B 2 receptor. Recently, a third-generation synthetic peptide antagonist of bradykinin, B9340, has been synthesized. It has a similar chemical structure to HOE-140 and differs by replacement of the ␣-(2-indanyl)glycine at position 7 of the molecule with a tetrahydroisoquiniline-3-carboxylic acid moiety. In comparison with HOE-140, B9340 retains similar potency of inhibition at the bradykinin B 2 receptor (median inhibitory concentration [IC 50 ] of 0.158 nmol/L for both) but has greater inhibition at the B 1 receptor (IC 50 of 1000 nmol/L and 7.9 nmol/L for HOE-140 and B9340, respectively). 5 The purpose of this study was to assess pharmacodynamic responses to the novel bradykinin antagonist B9340 and to determine the contribution of the endothelial bradykinin receptor to stimulated t-PA release in vivo in humans. To assess the selectivity of B9340, we compared the vasomotor and fibrinolytic responses of bradykinin with those of s...

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Interaction of bradykinin and des-Arg9-bradykinin with isolated pig coronary arteries: mechanical and electrophysiological events

Cited by 51 publications

References 18 publications

Endothelium‐dependent relaxations mediated by inducible B₁ and constitutive B₂ kinin receptors in the bovine isolated coronary artery

Endothelium‐dependent relaxations mediated by inducible B₁ and constitutive B₂ kinin receptors in the bovine isolated coronary artery

Endothelium-dependent hyperpolarization caused by bradykinin in human coronary arteries.

Bradykinin Receptor Antagonism and Endothelial Tissue Plasminogen Activator Release in Humans

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Interaction of bradykinin and des-Arg9-bradykinin with isolated pig coronary arteries: mechanical and electrophysiological events

Cited by 51 publications

References 18 publications

Endothelium‐dependent relaxations mediated by inducible B1 and constitutive B2 kinin receptors in the bovine isolated coronary artery

Endothelium‐dependent relaxations mediated by inducible B1 and constitutive B2 kinin receptors in the bovine isolated coronary artery

Endothelium-dependent hyperpolarization caused by bradykinin in human coronary arteries.

Bradykinin Receptor Antagonism and Endothelial Tissue Plasminogen Activator Release in Humans

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Product

Resources

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Endothelium‐dependent relaxations mediated by inducible B₁ and constitutive B₂ kinin receptors in the bovine isolated coronary artery

Endothelium‐dependent relaxations mediated by inducible B₁ and constitutive B₂ kinin receptors in the bovine isolated coronary artery