Modulatory effect of bradykinin on noradrenaline release in isolated atria from normal and B2 knockout transgenic mice

Chulak, Chantal; Couture, Réjean; Foucart, Sylvain

doi:10.1016/s0014-2999(98)00060-0

Cited by 21 publications

(14 citation statements)

References 26 publications

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“…This observation is consistent with the finding of diminished norepinephrine release from isolated atria of BK 2 r Ϫ/Ϫ mice. 30 Taken together, these findings raise the possibility of a differential effect of BK accumulation in the cardiac interstitium, where it interacts directly with nerve terminals and fibroblasts and may have a deleterious effect by promoting norepinephrine release and perivascular/myocardial fibrosis, versus at the luminal surface of the vasculature, where it interacts with endothelial cells and may have a beneficial effect by promoting NO synthesis. Further study is needed to test this intriguing hypothesis.…”

Section: See P 2359mentioning

confidence: 82%

Bradykinin in the Heart

Dell’Italia

Oparil

1999

Circulation

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H ypertension and heart failure are marked by activation of both the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system. These forms of neurohumoral activation, in turn, have deleterious effects on the heart, kidney, and other target organs, worsening the prognosis in these disease states. Pharmacological agents that interrupt the RAAS are useful in both improving hemodynamics and preventing morbidity and mortality in such patients. In particular, treatment with ACE inhibitors has been shown to improve survival in patients with advanced heart failure and after myocardial infarction. It is hypothesized that ACE inhibitors exert beneficial effects by inhibiting both circulating and cardiac tissue ACE, thus attenuating unfavorable remodeling of the left ventricle (LV), reducing afterload, and improving the balance between thrombotic and thrombolytic factors. It remains unclear whether the dominant mechanism of action of ACE inhibitors in the setting of LV dysfunction relates to their global hemodynamic effects (which result in improved loading conditions), to reduced production of angiotensin (Ang) II with subsequent diminished Ang II type 1 (AT 1 ) receptor activation, or to alteration of other neurohormonal systems, such as the kallikrein-kinin system. See p 2359Importantly, in addition to generating Ang II from Ang I, ACE catalyzes the degradation of bradykinin (BK) to inactive metabolites. 1 Studies of recombinant full-length ACE have shown that the apparent K m of ACE for BK is substantially lower than for Ang I, which indicates more favorable kinetics for hydrolysis of BK than for conversion of Ang I to Ang II. 2 Furthermore, site-directed mutagenesis demonstrated that the K m for BK was lower than that for Ang I at both N and C active sites of ACE, which suggests that at physiological concentrations, BK could be a preferential substrate over Ang I at both active sites of ACE. 2 The biological effects of BK and other kinins are mediated by stimulation of specific receptors, classified as BK 1 and BK 2 , both of which have been cloned and extensively characterized. 3 BK 1 receptors are expressed mainly in pathological conditions such as tissue injury and are thought to mediate the inflammatory and pain-producing effects of kinins; BK 2 receptors mediate most of the known cardiovascular effects of kinins. In the vasculature, BK-mediated activation of endothelial BK 2 receptors stimulates endogenous nitric oxide synthase (NOS), thus increasing NO and counteracting the effects of Ang II by inhibiting contraction and growth of smooth muscle cells. 4 Both BK 2 receptors 5 and NOS activity have been detected in cardiac myocytes, 6 and an intact kallikrein/kinin system has been found in the heart. 7 Kinins are detectable in the effluent of isolated perfused hearts and are increased by ACE inhibitors, as well as by ischemia, 8,9 which demonstrates that the cardiac kallikrein/ kinin system can be regulated.Studies in a mouse strain with targeted disruption of the BK 2 receptor gene have give...

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Section: See P 2359mentioning

confidence: 82%

Bradykinin in the Heart

Dell’Italia

Oparil

1999

Circulation

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“…A direct inhibitory effect of prostaglandin E 2 on NA release in the mouse atrium has so far not been shown. However, the fact that diclofenac (an inhibitor of prostaglandin synthesis) increases the facilitatory effect of bradykinin on atrial NA release is an indirect evidence that prostaglandins are capable of inhibiting NA release in the atrium of this species ( Chulak et al , 1998 ).…”

Section: Discussionmentioning

confidence: 99%

Lack of CB₁ receptors increases noradrenaline release in vas deferens without affecting atrial noradrenaline release or cortical acetylcholine release

Schlicker

Redmer

Werner

et al. 2003

British J Pharmacology

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1 We studied whether cannabinoid CB 1 receptor gene disruption (to yield CB 1 À/À mice) affects the electrically evoked tritium overflow from vas deferens and atrial pieces preincubated with [ 3 H]-noradrenaline (NA) ('noradrenaline release') and from cerebral cortex slices preincubated with [ 3 H]-choline ('acetylcholine release'). 2 NA release was higher by 37% in vas deferens from CB 1 À/À mice than in vas deferens from CB 1 þ / þ and CB 1 À/À mice in any preparation. 6 In conclusion, the increase in NA release associated with CB 1 receptor deficiency in the vas deferens, which cannot be ascribed to an alteration of tritium content of the preparations, suggests an endogenous tone at the CB 1 receptors of CB 1 þ / þ mice in this tissue. Furthermore, the effect of WIN 55,212-2 on NA release in the vas deferens and on cortical Ach release involves CB 1 receptors, whereas the involvement of non-CB 1 -non-CB 2 receptors can be excluded.

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“…Noradrenaline released from the nerve terminals can be estimated by the amount that diffuses into circulation, i.e., spillover. Bradykinin facilitates noradrenaline release in the dog gracilis muscle (Schwieler et al 1994) and the human, guinea pig, and mouse heart (Chulak et al 1998;Hatta et al 1999). These authors reported that this potentiating effect of bradykinin was exerted through the stimulation of B 2 receptors.…”

Section: Discussionmentioning

confidence: 99%

“…Bradykinin facilitates the release of noradrenaline in many tissues in different species through the stimulation of B 2 receptors (Chulak et al 1998;Hatta et al 1999;Schwieler et al 1994). The bradykinin B 2 receptor appears to be responsible for most of the biological actions of bradykinin, whereas the B 1 receptor is usually induced by pathological conditions such as tissue injury or stress (Burch and Kyle 1992).…”

Section: Introductionmentioning

confidence: 99%

Bradykinin facilitates noradrenaline spillover during contraction in the canine gracilis muscle

Lavoie

Béliveau²

2001

Can. J. Physiol. Pharmacol.

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Noradrenaline spillover from skeletal muscle vascular areas increases during exercise but the underlying mechanisms are not well understood. Muscle contraction itself causes changes in many factors that could affect noradrenaline spillover. For instance, it has been reported that bradykinin is synthesized in skeletal muscle areas during contraction. Because the B2 bradykinin receptor facilitates noradrenaline spillover, it may be involved in the increase associated with contraction. In this experiment, we studied the effect of bradykinin on noradrenaline spillover in the in situ canine gracilis muscle, using the specific B2 antagonist HOE 140. The drug did not modify noradrenaline spillover at rest, but did cause a significant decrease during muscle contraction, from 558 to 181 pg min(-1). As reported previously in the literature, fractional extraction of noradrenaline decreased during muscle contraction. This effect was independent of HOE 140 treatment. In light of our results, it seems that bradykinin formation during muscle contraction may play an important part in the observed increase in noradrenaline spillover but does not affect fractional extraction.

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Modulatory effect of bradykinin on noradrenaline release in isolated atria from normal and B2 knockout transgenic mice

Cited by 21 publications

References 26 publications

Bradykinin in the Heart

Bradykinin in the Heart

Lack of CB₁ receptors increases noradrenaline release in vas deferens without affecting atrial noradrenaline release or cortical acetylcholine release

Bradykinin facilitates noradrenaline spillover during contraction in the canine gracilis muscle

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Modulatory effect of bradykinin on noradrenaline release in isolated atria from normal and B2 knockout transgenic mice

Cited by 21 publications

References 26 publications

Bradykinin in the Heart

Bradykinin in the Heart

Lack of CB1 receptors increases noradrenaline release in vas deferens without affecting atrial noradrenaline release or cortical acetylcholine release

Bradykinin facilitates noradrenaline spillover during contraction in the canine gracilis muscle

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Lack of CB₁ receptors increases noradrenaline release in vas deferens without affecting atrial noradrenaline release or cortical acetylcholine release