Effects of Kinins on Organ Systems

Johnson, Alice

doi:10.1007/978-3-642-67301-6_10

Cited by 26 publications

(16 citation statements)

References 166 publications

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“…Bradykinin, adenosine triphosphate (ATP) and acetylcholine, despite being powerful systemic vasodilators (Dale, 1914; Rocha e Silva, Beraldo & Rosenfeld, 1949;Green & Stoner, 1950), often contract or have no effect on isolated vascular preparations (Furchgott & Bhadrakom, 1953;Furchgott, 1955;Kovalcik, 1962;Johnson, 1979). One possible explanation for this discrepancy was provided by Furchgott & Zawadzki (1980a) who demonstrated that relaxation of rabbit isolated aortic rings induced by acetylcholine was dependent upon the presence of the endothelium.…”

Section: Introductionmentioning

confidence: 99%

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Gordon

Martin

1983

British J Pharmacology

162

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1 Bradykinin, adenosine triphosphate (ATP) and acetylcholine each relaxed histamine-contracted strips of pig aorta in a dose-dependent manner. These relaxations were abolished when the endothelium was removed. 2 Relaxation induced by ATP was mimicked by adenosine diphosphate (ADP) but adenosine monophosphate (AMP) and adenosine were about 120 times less potent. 3 Relaxation induced by acetylcholine was antagonized by atropine in a competitive manner, and carbachol induced the same degree of relaxation as acetylcholine, but was about 10 times less potent. 4 The calcium ionophore, A23 187, also induced a dose-dependent relaxation of pig aortic strips provided the endothelium was present, suggesting that a rise in the level of ionized calcium within the endothelial cells is one means by which vascular smooth muscle relaxation can be triggered. 5 Bradykinin, ATP, ADP, AMP, adenosine and A23 187 each induced a dose-dependent increase in 86Rb efflux from preloaded pig aortic endothelial cells. The dose-response curves for stimulation of 86Rb efflux and for endothelium-dependent relaxation were similar for each individual compound. ADP was equipotent with ATP, but AMP and adenosine were about 120 times less potent. 6 Neither acetylcholine nor carbachol, in concentrations that induce endothelium-dependent relaxation, had any effect on 86Rb efflux from isolated aortic endothelial cells. 7 Lanthanum, which blocks calcium influx, abolished the increases in 86Rb efflux induced by bradykinin and ATP, and the calcium ionophore A23187 was the most effective stimulant of 86Rb efflux, suggesting that the potassium transport induced by these agents is calcium-activated. 8 It is concluded that endothelial responses to bradykinin and ATP can be assessed by monitoring 86Rb efflux, which probably reflects a calcium-activated efflux of potassium associated with the endothelium-dependent vascular relaxation induced by these agents. This pathway is apparently not involved in endothelial responses to acetylcholine.

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Section: Introductionmentioning

confidence: 99%

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Gordon

Martin

1983

British J Pharmacology

162

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“…Endogenous mediators of inflammation, such as bradykinin and prostaglandins (PG), are derived from the injured tissue. Bradykinin is formed by cleavage of kininogen by kallikrein (4), and during the inflammatory reaction acts as a vasodilator (5) and increases vascular permeability (6), thereby contributing to the edema. Bradykinin also elicits PG release from various intact organ systems (7) as well as different cell types such as fibroblasts (8) and endothelial cells (9).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of enhanced fibroblast arachidonic acid metabolism by mononuclear cell factor.

Whiteley¹,

Needleman²

1984

J. Clin. Invest.

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Abstract. Chronic inflammation is associated with an infiltration of mononuclear cells, fibroblast proliferation, and elevated levels of prostaglandin (PG) E2. Mononuclear cell conditioned factor (MNCF) medium (5%) stimulated a 100-fold increase in basal human dermal fibroblast PGE2 release over 48 h as compared with fibroblasts that were incubated with control medium (conditioned medium prepared without cells). The MNCF-induced PGE2 production was suppressed by protein synthesis inhibitors. Fibroblasts pretreated with control medium released PGE2 only modestly in response to 1 nM bradykinin for 1 h (basal, 50±7 pg PGE2/,g protein; stimulated, 104±12 pg PGE2flsg protein), whereas cells that had been pretreated with MNCF showed a greatly facilitated bradykinin-induced release of PGE2. (basal, 297±59 pg PGE2/,g protein; stimulated, 866±85 pg PGE2/Ag protein). The exaggerated agonist response is not specific for bradykinin because plateletderived growth factor elicits a similar response. Exogenous arachidonic acid conversion to PGE2 was also facilitated (two-to threefold) by MNCF pretreatment as compared with control. Both the enhanced agoniststimulated and exogenous arachidonic acid-induced PGE2 release from the MNCF pretreated cells were inhibited by actinomyin D or cycloheximide. A kinetic study of microsomal cyclooxygenase prepared from fibroblasts pretreated with MNCF showed a threefold increase in the maximum velocity (Vmax) but the same Michaelis constant (Kin) as control-treated cells. This augmented arachidonic acid metabolism and subsequent enhanced PGE2 production may play an important role

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“…The kinins are a group of biologically active peptides known to affect smooth muscle and sensory neurons, as well as other cell types (16). In certain cases, kinins may be stored as neurotransmitters (17 (20).…”

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confidence: 99%

Bradykinin-stimulated electrolyte secretion in rabbit and guinea pig intestine. Involvement of arachidonic acid metabolites.

Musch¹,

Kachur²,

Miller³

et al. 1983

J. Clin. Invest.

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A B S T R A C T Bradykinin (BK) increases short-circuit current (Isc) when added to the serosal side of rabbit or guinea pig ileum or rabbit colon. Significant effects on Isc are seen at concentrations as low as 10-' M. Anion substitution experiments and unidirectional 36C flux measurements indicate that this effect of BK on Isc is due to Cl secretion. The effect of BK on Isc can be partially blocked (60-70% inhibition) by cyclooxygenase inhibitors (indomethacin and/or naproxen) and completely blocked by the phospholipase inhibitor, mepacrine. The combined cyclooxygenase/lipoxygenase inhibitors BW 755 and eicosa-5,8,11,14-tetraynoic acid (ETYA) also completely block the effect of BK on Isc but the slow-reacting substance of anaphylaxis (SRS-A) antagonist FPL 55712 has no effect. None 5 January 1983. this effect can be blocked by prior addition of either indomethacin or mepacrine. These effects of BK are similar to those of exogenously added arachidonic acid (AA). AA also stimulates Cl secretion and increases PGE2 synthesis and its effect on Isc can be inhibited by prior desensitization to PGE2 or by prior addition of indomethacin. The above results indicate that BK stimulates active Cl secretion in both small and large intestine and suggest that this effect is due to the intracellular release of AA. Although the prostaglandins appear to be the major products of AA metabolism contributing to the secretory response, lipoxygenase products may also play a role.

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Effects of Kinins on Organ Systems

Cited by 26 publications

References 166 publications

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Mechanism of enhanced fibroblast arachidonic acid metabolism by mononuclear cell factor.

Bradykinin-stimulated electrolyte secretion in rabbit and guinea pig intestine. Involvement of arachidonic acid metabolites.

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Effects of Kinins on Organ Systems

Cited by 26 publications

References 166 publications

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of 86Rb efflux from isolated endothelial cells

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of 86Rb efflux from isolated endothelial cells

Mechanism of enhanced fibroblast arachidonic acid metabolism by mononuclear cell factor.

Bradykinin-stimulated electrolyte secretion in rabbit and guinea pig intestine. Involvement of arachidonic acid metabolites.

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Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells

Endothelium‐dependent relaxation of the pig aorta: relationship to stimulation of ⁸⁶Rb efflux from isolated endothelial cells