Receptors for bradykinin in rabbit aortae

Regoli, Doménico; Barabé, J.; Park, W K

doi:10.1139/y77-115

Cited by 251 publications

(121 citation statements)

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“…21 However, it also induces contraction of arteries 22 and veins. 23 These different effects of bradykinin on arteries have been explained by the existence of bradykinin receptor subtypes.…”

Section: Discussionmentioning

confidence: 99%

“…23 These different effects of bradykinin on arteries have been explained by the existence of bradykinin receptor subtypes. 22 Endothelial cells possess low-affinity B, receptors and high-affinity B 2 receptors. 24 In this study, bradykinin-induced stimulation of NO production was inhibited by the B2 receptor antagonist but not by the B, receptor antagonist.…”

Section: Discussionmentioning

confidence: 99%

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Captopril inhibits endothelin-1 secretion from endothelial cells through bradykinin.

et al. 1993

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ET-1 induces a strong and sustained pressor response in vessels 1 and systemic hypertension in the rat.2 It also stimulates mitogenesis in vascular smooth muscle cells.3 These studies suggest the potential importance of endothelin in the pathophysiology of hypertension 2 -4 and atherosclerosis.3 Angiotensin I converting enzyme (ACE) inhibitors generally have been used as antihypertensive drugs. However, the precise mechanism of the antihypertensive effects of ACE inhibitors has not been fully elucidated. In addition, there is recent evidence for new important functions of ACE inhibitors in the cardiovascular field. ACE inhibitors can induce regression of intimal hyperplasia, whereas other antihypertensive drugs are ineffective in this regard.5 Clinical trials in patients with chronic congestive heart failure demonstrated a significant reduction in mortality with ACE inhibitor therapy. 6 Although ACE inhibition diminishes the formation of a pressor peptide, angiotensin II, 7 it also diminishes degradation of kinins, which are vasodepressor peptides.8 Bradykinin stimulates the synthesis of prostaglandin I 2 and endothelium-derived relaxing factor, 9 recently identified as nitric oxide (NO). 910 NO not only antagonizes the effects of ET-1 of vasoconstriction 11 and mitogenesis of

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Captopril inhibits endothelin-1 secretion from endothelial cells through bradykinin.

et al. 1993

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“…In the presence of the carboxypeptidase inhibitor mergetpa, responses to bradykinin were still inhibited by [Leu8,des-Argl-BK (1-30JiM; n = 6; data not shown). Regoli et al, 1977), rabbit mesenteric artery (Regoli et al, 1978;Boutillier et al, 1987) and rat duodenum (Boschcov et al, 1984). Once stabilized, responses to [des-Argl-BK in both the rabbit bladder and aorta preparations were competitively antagonized by B1 receptor-selective antagonists.…”

Section: Phosphatidylinositol Hydrolysis Measurementmentioning

confidence: 99%

Bradykinin B₁ receptors in the rabbit urinary bladder: induction of responses, smooth muscle contraction, and phosphatidylinositol hydrolysis

Butt

Dawson

Hall

1995

British J Pharmacology

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1 The aim of this study was to analyse the pharmacological characteristics, and second-messenger coupling-mechanisms, of bradykinin B1 receptors in an intact tissue, the rabbit urinary bladder; and to investigate the influence of inhibition of endogenous peptidases on kinin activities. 2 In preparations of rabbit mucosa-free urinary bladder, at 90 min after mounting of the preparations, bradykinin (1 nM-10 fM) evoked contractile responses. In contrast, the B1 receptor-selective agonist [des-Argl-BK (10 nM-10-JM) was only weakly active at this time. Contractile responses to [des-Argl-BK increased with time of tissue incubation in the organ bath, reaching a maximum after 3 h, when the pD2 estimates were 6.4 ± 0.3 for bradykinin, and 6.9 + 0.2 for [des-Arg9]-BK. [Leu8,des-Argj-BK inhibited responses to bradykinin under these conditions (n = 4). and B2 receptors, but does not require conversion by peptidases in order to activate B1 receptors. We demonstrate, for the first time, B. receptor-coupling to phosphatidylinositol hydrolysis in an intact tissue preparation.

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“…The B1 receptor is stimulated selectively by kinin fragments of BK and Lys-BK without the C-terminal arginine residue such as des-Arg9-BK and Lys-des-Arg9-BK. The development of competitive, potent and selective antagonists (prototype [Leu8]des-Arg9-BK) has consolidated the pharmacological identity of the receptors of the B, type (Regoli et al, 1977). Agonists and antagonists for B, receptors are conveniently assayed on the rabbit aortic preparation, which exhibits a prostaglandinindependent contractile response to kinins solely via this receptor type (Regoli et al, 1977).…”

Section: Introductionmentioning

confidence: 99%

Vascular mode of action of kinin B₁ receptors and development of a cellular model for the investigation of these receptors

Lévesque

Drapeau

Grose

et al. 1993

British J Pharmacology

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1 Kinins exert a contractile effect on rabbit aortic rings via the stimulation of B, receptors. Des-Arg9-bradykinin (BK) is more potent than BK on this receptor type. The mode of action of des-Arg9-BK on rabbit aortic tissue has been studied by both the aortic ring contractility assay and a cellular model using cultured aortic smooth muscle cells (SMCs). 2 The des-Arg9-BK-induced contractions in rabbit aortic rings were unaffected by pretreatments with nifedipine, indomethacin, REV-5901 (a 5-lipoxygenase blocker) and LY-83583 (a guanylyl cyclase inhibitor); however, the protein kinase inhibitors H-7 and H-9 significantly reduced the maximal effect of des-Arg9-BK. 3 The contractile responses to des-Arg9-BK in calcium-free Krebs solution were slightly but not significantly attenuated in amplitude, as compared to paired control tissues bathed in Krebs solution, and sustained plateaus of contraction were observed in the absence of Ca2 . However, Ca2+ replenishment further increased the kinin-induced contraction measured in Ca2'-free bathing fluid. 4 Despite the lack of evidence of a mediating role for prostaglandin in the mechanical response to des-Arg9-BK, the kinin stimulated the release of prostacyclin from rabbit aorta rings measured as immunoreactive 6-keto-prostaglandin Fl,a (6-keto-PGF1,,).5 Smooth muscle cells (SMCs) derived from the rabbit aorta exhibit functional responses to des-Arg9-BK in acute release of 6-keto-PGF1, and of inositol phosphate turnover which were inhibited by pretreatment with the B1 receptor antagonist, Lys[Leu8]des-Arg9-BK, but not by the B2 receptor antagonist, Preincubation of the cells with interleukin-1 (IL-1) 20 h before stimulation with the kinin had no effect on basal inositol phosphate turnover, but potentiated the acute effect of des-Arg9-BK.6 These results suggest that second mesengers derived from the action of phospholipase C are produced by SMCs when B1 receptors are activated in rabbit aortic tissue. Intracellular calcium stores are primarily mobilized by des-Arg9-BK, although receptor-controlled calcium influx has not been ruled out, and may contribute to initiate the contractile responses. The maintenance of the contractile state involves protein kinase C activity and is consistent with a current model of SMC function. The cell model retains some of the cardinal properties of B1 receptor-mediated vascular responses: endotheliumindependent PGI2 release and up-regulation by the cytokine IL-1. PGI2 is not involved in the mechanical response, possible because the rabbit aorta is refractory to this prostaglandin.

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Receptors for bradykinin in rabbit aortae

Cited by 251 publications

References 3 publications

Captopril inhibits endothelin-1 secretion from endothelial cells through bradykinin.

Captopril inhibits endothelin-1 secretion from endothelial cells through bradykinin.

Bradykinin B₁ receptors in the rabbit urinary bladder: induction of responses, smooth muscle contraction, and phosphatidylinositol hydrolysis

Vascular mode of action of kinin B₁ receptors and development of a cellular model for the investigation of these receptors

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Receptors for bradykinin in rabbit aortae

Cited by 251 publications

References 3 publications

Captopril inhibits endothelin-1 secretion from endothelial cells through bradykinin.

Captopril inhibits endothelin-1 secretion from endothelial cells through bradykinin.

Bradykinin B1 receptors in the rabbit urinary bladder: induction of responses, smooth muscle contraction, and phosphatidylinositol hydrolysis

Vascular mode of action of kinin B1 receptors and development of a cellular model for the investigation of these receptors

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Bradykinin B₁ receptors in the rabbit urinary bladder: induction of responses, smooth muscle contraction, and phosphatidylinositol hydrolysis

Vascular mode of action of kinin B₁ receptors and development of a cellular model for the investigation of these receptors