Changes in Hemodynamics and Bradykinin Concentration in Coronary Sinus Blood in Experimental Coronary Artery Occlusion

Hashimoto, Keiichi; Hirose, Masaru; Furukawa, Shinya; Hayakawa, Hirokazu; Kimura, Eiichi

doi:10.1536/ihj.18.679

Cited by 65 publications

(19 citation statements)

References 17 publications

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“…Inhaled ammonia in animals has been shown to activate vagal pulmonary A-delta and C afferents or receptors (Kohl and Koller 1980;Matsumoto 1989;Wang et al 1996) as well as upper thoracic spinal neurons (Hummel et al 1997;Qin et al 2007). Intrapericardial bradykinin was used as a noxious cardiac stimulus for activating vagal and sympathetic cardiac receptors because it can be released during myocardial ischemia (Hashimoto et al 1977;Kimura et al 1973). Stimulation of these receptors can elicit angina pectoris and autonomic responses (Gaspardone et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Characterization of thoracic spinal neurons with noxious convergent inputs from heart and lower airways in rats

2007

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Respiratory symptoms experienced in some patients with cardiac diseases may be due to convergence of noxious cardiac and pulmonary inputs onto neurons of the central nervous system. For example, convergence of cardiac and respiratory inputs onto single solitary tract neurons may be in part responsible for integration of regulatory and defensive reflex control. However, it is unknown whether inputs from the lungs and heart converge onto single neurons of the spinal cord. The present aim was to characterize upper thoracic spinal neurons responding to both noxious stimuli of the heart and lungs in rats. Extracellular potentials of single thoracic (T3) spinal neurons were recorded in pentobarbital anesthetized, paralyzed, and ventilated male rats. A catheter was placed in the pericardial sac to administer bradykinin (BK, 10 μg/ml, 0.2 ml, 1 min) as a noxious cardiac stimulus. The lung irritant, ammonia, obtained as vapor over a 30% solution of NH 4 OH was injected into the inspiratory line of the ventilator (0.5-1.0 ml over 20 sec). Intrapericardial bradykinin (IB) altered activity of 58/65 (89%) spinal neurons the responded to inhaled ammonia (IA). Among those cardiopulmonary convergent neurons, 81% (47/58) were excited by both IA and IB, and the remainder had complex response patterns. Bilateral cervical vagotomy revealed that vagal afferents modulated but did not eliminate responses of individual spinal neurons to IB and IA. The convergence of pulmonary and cardiac nociceptive signaling in the spinal cord may be relevant to situations where a disease process in one organ influences the behavior of the other.

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Section: Discussionmentioning

confidence: 99%

Characterization of thoracic spinal neurons with noxious convergent inputs from heart and lower airways in rats

2007

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“…After myocardial infarction (MI), increased plasma levels of KLK, kininogen and BK were found (24)(25)(26)(27)(28), and the increase in plasma KLK levels was positively correlated with the early survival rate of post-MI patients (29). It has been shown that kinins are released directly from the myocardium during MI (27,28) and contribute to the impact of ischemic damage (29).…”

Section: Regulation Of B1r and B2r After Induction Of Myocardial Infamentioning

confidence: 99%

Regulation of the kinin receptors after induction of myocardial infarction: a mini-review

Tschöpe

Heringer-Walther

Walther

2000

Braz J Med Biol Res

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It is well known that the responses to vasoactive kinin peptides are mediated through the activation of two receptors termed bradykinin receptor B1 (B1R) and B2 (B2R). The physiologically prominent B2R subtype has certainly been the subject of more intensive efforts in structure-function studies and physiological investigations. However, the B1R activated by a class of kinin metabolites has emerged as an important subject of investigation within the study of the kallikreinkinin system (KKS). Its inducible character under stress and tissue injury is therefore a field of major interest. Although the KKS has been associated with cardiovascular regulation since its discovery at the beginning of the last century, less is known about the B1R and B2R regulation in cardiovascular diseases like hypertension, myocardial infarction (MI) and their complications. This mini-review will summarize our findings on B1R and B2R regulation after induction of MI using a rat model. We will develop the hypothesis that differences in the expression of these receptors may be associated with a dual pathway of the KKS in the complex mechanisms of myocardial remodeling. Key wordsThe kallikrein-kinin system Kinins are biologically active peptides which exert a broad spectrum of physiological effects, including vasodilation, smooth muscle contraction and pain induction. Several kinin peptides have been identified in mammalian species: the nonapeptide bradykinin (BK) and the decapeptide Lys-bradykinin (kallidin) belong to the best investigated members of the kinin family. Kinins are formed by cleavage from precursor kininogens by kallikreins (KLK). They are rapidly degraded by several kininases, including kininase II which is identical to angiotensinconverting enzyme. Kinins exert their effect after stimulation of their cell surface receptors: BK B1 receptor (B1R) and B2 receptor (B2R). Whereas the B2R is responsive to the intact kinins, BK and kallidin, the B1R has a higher affinity for the carboxypeptidase metabolites of kinins, des-Arg 9 -BK and des-

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“…Several authors have reported increased endogenous levels of kallikrein (KLK), kininogen, and bradykinin (BK) and an upregulation of B 1 and B 2 receptors in response to cardiac ischemia (1,12,15,18,25,34,35). Direct application of BK in perfusion medium improves cardiac left ventricular (LV) function, coronary flow, and myocardial metabolism and reduces the infarct size of isolated working rat hearts during and after induction of myocardial ischemia via activation of the prostaglandin and nitric oxide (NO) axis (36).…”

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confidence: 99%

Cardiac kinin level in experimental diabetes mellitus: role of kininases

Koch

Wendorf²,

Dendorfer³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Diabetes mellitus impairs the cardiac kallikrein-kinin system by reducing cardiac kallikrein (KLK) and kininogen levels, a mechanism that may contribute to the deleterious outcome of cardiac ischemia in this disease. We studied left ventricular (LV) function and bradykinin (BK) coronary outflow in buffer-perfused, isolated working hearts (n ϭ 7) of controls and streptozotocin (STZ)-induced diabetic rats before and after global ischemia. With the use of selective kininase inhibitors, the activities of angiotensin I-converting enzyme, aminopeptidase P, and neutral endopeptidase were determined by analyzing the degradation kinetics of exogenously administered BK during sequential coronary passages. Basal LV function and coronary flow were impaired in STZ-induced diabetic rats. Neither basal nor postischemic coronary BK outflow differed between control and diabetic hearts. Reperfusion after 15 min of ischemia induced a peak in coronary BK outflow that was of the same extent and duration in both groups. In diabetic hearts, total cardiac kininase activity was reduced by 41.4% with an unchanged relative kininase contribution compared with controls. In conclusion, despite reduced cardiac KLK synthesis, STZ-induced diabetic hearts are able to maintain kinin liberation under basal and ischemic conditions because of a primary impairment or a secondary downregulation of kinindegrading enzymes.bradykinin; kininase; myocardial ischemia AN INCREASE IN CARDIAC KININS might be a mechanism for protecting the heart during hypertension, cardiac failure, or acute myocardial infarction (MI). Several authors have reported increased endogenous levels of kallikrein (KLK), kininogen, and bradykinin (BK) and an upregulation of B 1 and B 2 receptors in response to cardiac ischemia (1,12,15,18,25,34,35). Direct application of BK in perfusion medium improves cardiac left ventricular (LV) function, coronary flow, and myocardial metabolism and reduces the infarct size of isolated working rat hearts during and after induction of myocardial ischemia via activation of the prostaglandin and nitric oxide (NO) axis (36). Likewise, the inhibition of kinin breakdown by kininase inhibitors has been shown to exert cardioprotective effects in in vivo models of MI (11,42).Several changes of the cardiac kallikrein-kinin system (KKS) have been found under diabetic conditions that may contribute to the profoundly altered myocardial and vascular integrity during the development of diabetic cardiopathy (30,31,38). Reduced effectiveness of exogenously applied BK on vascular dilation has been reported in diabetic subjects with endothelial dysfunction (14, 39). Moreover, we and others (30, 31, 38) have described reduced endogenous cardiac kininogen and KLK levels and/or alterations in the activation of cardiac tissue KLK in diabetic animals. Thus a reduction in the BK precursor content and in the activity of the BK-forming enzyme KLK may indicate a decreased capacity for generating cardiac BK and may be among the mechanisms involved in the development of coronary...

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Changes in Hemodynamics and Bradykinin Concentration in Coronary Sinus Blood in Experimental Coronary Artery Occlusion

Cited by 65 publications

References 17 publications

Characterization of thoracic spinal neurons with noxious convergent inputs from heart and lower airways in rats

Characterization of thoracic spinal neurons with noxious convergent inputs from heart and lower airways in rats

Regulation of the kinin receptors after induction of myocardial infarction: a mini-review

Cardiac kinin level in experimental diabetes mellitus: role of kininases

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