Regulatory role of bradykinin in the coronary and cerebral circulations and in systemic hemodynamics

Volpe, Anna; Fontecchio, G; Carmignani, M.

doi:10.1016/s0162-3109(99)00140-x

Cited by 11 publications

(12 citation statements)

References 8 publications

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“…Bradykinin is considered to play a major role in microvessels dilatation and in the genesis of vascular pain. It potently dilates arterial cerebral vessels and contributes to the vasodilatation, edema and pain during migraine (Volpe et al, 1999). The anti-migraine effect of ANE is probably through its action on bradykinin receptors (B1 or B2) and inhibiting PPE and vocalization in rats.…”

Section: Discussionmentioning

confidence: 99%

Anti-migraine effect of Areca Catechu L. nut extract in bradykinin-induced plasma protein extravasation and vocalization in rats

Bhandare

Vyawahare²,

Kshirsagar

2015

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 99%

Anti-migraine effect of Areca Catechu L. nut extract in bradykinin-induced plasma protein extravasation and vocalization in rats

Bhandare

Vyawahare²,

Kshirsagar

2015

Journal of Ethnopharmacology

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“…We have previously demonstrated that, at physiological plasma concentrations, ENKs strongly enhance the increases in plasma NO induced by BK, which supplies L-arginine for endothelial NO synthesis. The mechanism underlying this enhancement was the selective inhibition by ENKs of kininase II activity, but not that of kininase I, which cleaves the C-terminal arginine from bradykinin (19)(20)(21). Therefore, the ENK-induced increases in plasma NO observed in our model may well be the result of a kininase I-mediated increase in the availability of BK-derived L-arginine in the endothelium, but this is not the only mechanism involved.…”

Section: Discussionmentioning

confidence: 73%

“…It is interesting to note that arterial vasoconstriction and venous dilatation are influenced by NO-mediated ENK interactions with the reninangiotensin and kallikrein-kinin systems (18,43). The prevention of hypodynamic shock by the 0opioid receptor antagonist ICI 174864 can be attributed to its antagonism of cardiovascular responses to ENKs, which are the specific physiological activators of o-opioid receptors (16)(17)(18), and to ENK-induced increases in plasma NO (18)(19)(20)(21). Indeed, the increasing severity of the hypodynamic changes paralleled progressive increases in jugular plasma levels of ENKs and NO.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, opioid peptides, such as leu'i-and met'<enkephalins (ENKs), are abundant in intestinal tissues, and they are known to be released under conditions of splanchnic hypoperfusion (16)(17). Moreover, at physiological plasma concentrations, ENKs markedly increase plasma NO levels by stimulating itsendothelial production from L-arginine, and both NO and ENKs play physiologic roles in the reduction of blood pressure (BP), heart rate (HR) and cardiac inotropism (18)(19)(20)(21). Opioid and nitrergic mechanisms are reportedly involved in the hemodynamic impairment that characterizes endotoxin and acute hypovolemic shock states, and, at the central level, their actions appear to be synergistic.…”

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confidence: 99%

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Shock Induction by Arterial Hypoperfusion of the Gut Involves Synergistic Interactions between the Peripheral Enkephalin and Nitric Oxide Systems

Carmignani

Zucchetti

Sacco

et al. 2005

Int J Immunopathol Pharmacol

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To determine whether critical splanchnic artery hypoperfusion can provoke systemic shock and to identify the roles of the peripheral opioid and nitric oxide (NO) systems in this process, various degrees of superior mesenteric artery hypoperfusion (SMA-H) were produced in anesthetized adult rabbits (n=40), and hemodynamic and metabolic indices were measured. Metabolic acidosis and irreversible hypodynamic shock occurred with SMA-H at levels representing 25-20% of mean baseline SMA blood flow. In 112 other rabbits subjected to SMA-H at 20% (SMA-H20%), we studied plasma NO and enkephalin (ENK) levels, cardiovascular reactivity to selected physiological agonists, effects of ENKs on plasma NO levels, and effects of peripheral opioid receptor blockade and inducible NO synthase (iNOS) inhibition. SMA-H20% progressively increased systemic blood levels of NO and ENKs. Exogenous ENK administration accentuated SMA-H20%-induced increases in plasma NO levels, and their cardiovascular depressing effects were significantly greater when they were administered during SMA-H20% (vs. administration under baseline conditions). Selective blockade of cardiovascular delta-opioid receptors improved hemodynamics, prevented shock irreversibility and reduced plasma NO levels; similar effects were obtained by selective iNOS inhibition. These findings demonstrate that critical arterial hypoperfusion of the gut can induce hypodynamic systemic shock through ENK-induced hyperactivation of cardiovascular delta-opioid receptors, which leads to increased plasma levels of NO related in part to increased iNOS activity. Since pronounced splanchnic artery hypoperfusion occurs in all advanced systemic shock states, selective delta-opioid receptor antagonists and/or iNOS inhibitors may prove to be useful in improving shock hemodynamics and metabolic derangements and/or preventing progression toward irreversibility.

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“…Bradykinin may have a regulatory role on blood vessel functions as increased carotid blood flow and jugular NO level is found following common carotid artery administration of the peptide [124]. It would be important to investigate the potential implications of bradykinin receptors and their antagonists in migraine-related cerebrovascular dilatation, hyperalgesia and neurogenic inflammation.…”

Section: Further Targetsmentioning

confidence: 99%

Recent Advancements in Anti-Migraine Drug Research: Focus on Attempts to Decrease Neuronal Hyperexcitability

Bölcskei

Farkas²,

Kocsis³

et al. 2009

RPCN

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Migraine is a painful, sometimes debilitating disorder, which is frequently associated with various neurological symptoms. Its prevalence in the population is higher than that of any other neurological disorders, thus the burden of this disease on society is considerable. Although the introduction of triptans nearly two decades ago revolutionized the treatment of the disease there is still a huge unmet need regarding drugs with better properties. Formerly, migraine therapy primarily aimed at treating the pathological alterations of meningeal blood vessels that are thought to directly initiate a migraine headache attack. By now, it has been increasingly recognized by drug companies that abnormal neural function may be more important in the development of the disease and also in triggering an attack. Migraine is associated with an increased neuronal excitability and episodes of cortical spreading depression. Understanding the molecular mechanisms underlying the abnormal functioning of over-activated neuronal circuits may help to identify novel anti-migraine drug targets. Besides a general description of the pathophysiology and pharmacotherapy of migraine this review paper aims at discussing the possible drug targets through which migraine-related hyperexcitability and over-excitation can be attenuated. It will be shown how these new ideas appear in the recent patent literature.

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Regulatory role of bradykinin in the coronary and cerebral circulations and in systemic hemodynamics

Cited by 11 publications

References 8 publications

Anti-migraine effect of Areca Catechu L. nut extract in bradykinin-induced plasma protein extravasation and vocalization in rats

Anti-migraine effect of Areca Catechu L. nut extract in bradykinin-induced plasma protein extravasation and vocalization in rats

Shock Induction by Arterial Hypoperfusion of the Gut Involves Synergistic Interactions between the Peripheral Enkephalin and Nitric Oxide Systems

Recent Advancements in Anti-Migraine Drug Research: Focus on Attempts to Decrease Neuronal Hyperexcitability

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