Localization of preproenkephalin mRNA in rat heart:  selective gene expression in left ventricular myocardium

Weil, Joachim; Eschenhagen, Thomas; Fleige, Gerrit; Mittmann, Clemens; Orthey, Ellen

doi:10.1152/ajpheart.1998.275.2.h378

Cited by 20 publications

(18 citation statements)

References 30 publications

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“…Potentially relevant to the concept of a CVE control system with its sensor role for the EE are any differences between right and left ventricular myocardium and EE (141,268,484,577,620). As previously discussed, prostacyclin (PGI 2 ) release is much greater from left than from right ventricular EE under conditions of increased transmural pressure (418).…”

Section: The Endothelial System: Conjectural Role Of Cardiac Endotmentioning

confidence: 99%

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Brutsaert

2003

Physiological Reviews

612

544

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Experimental work during the past 15 years has demonstrated that endothelial cells in the heart play an obligatory role in regulating and maintaining cardiac function, in particular, at the endocardium and in the myocardial capillaries where endothelial cells directly interact with adjacent cardiomyocytes. The emerging field of targeted gene manipulation has led to the contention that cardiac endothelial-cardiomyocytal interaction is a prerequisite for normal cardiac development and growth. Some of the molecular mechanisms and cellular signals governing this interaction, such as neuregulin, vascular endothelial growth factor, and angiopoietin, continue to maintain phenotype and survival of cardiomyocytes in the adult heart. Cardiac endothelial cells, like vascular endothelial cells, also express and release a variety of auto- and paracrine agents, such as nitric oxide, endothelin, prostaglandin I2, and angiotensin II, which directly influence cardiac metabolism, growth, contractile performance, and rhythmicity of the adult heart. The synthesis, secretion, and, most importantly, the activities of these endothelium-derived substances in the heart are closely linked, interrelated, and interactive. It may therefore be simplistic to try and define their properties independently from one another. Moreover, in relation specifically to the endocardial endothelium, an active transendothelial physicochemical gradient for various ions, or blood-heart barrier, has been demonstrated. Linkage of this blood-heart barrier to the various other endothelium-mediated signaling pathways or to the putative vascular endothelium-derived hyperpolarizing factors remains to be determined. At the early stages of cardiac failure, all major cardiovascular risk factors may cause cardiac endothelial activation as an adaptive response often followed by cardiac endothelial dysfunction. Because of the interdependency of all endothelial signaling pathways, activation or disturbance of any will necessarily affect the others leading to a disturbance of their normal balance, leading to further progression of cardiac failure.

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Section: The Endothelial System: Conjectural Role Of Cardiac Endotmentioning

confidence: 99%

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Brutsaert

2003

Physiological Reviews

612

544

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“…Recent studies have provided several lines of evidence suggesting that opioid peptides play crucial roles in the regulation of cardiac sympathetic afferent nerve activity during myocardial ischemia. First, opioids and their precursors (proproenkephalin, prodynorphin, and propiomelanocortin) are synthesized, stored, and released by cardiac myocytes, sympathetic nerves, and both polymorphonuclear and mononuclear leukocytes, including monocytes/ macrophages and lymphocytes (38,41,44,67). Leukocytes accumulate in the coronary arterial plaques and release large concentrations of opioids when they are activated during plaque disruption, resulting in myocardial ischemia and infarction (12,23,36,46).…”

Section: Discussionmentioning

confidence: 99%

“…Several sources of evidence suggest that peripheral opioids may be crucial in the regulation of cardiac spinal afferent nerve activity during myocardial ischemia. For instance, cardiac myocytes, sympathetic nerves, and leukocytes can synthesize and store opioid peptides as well as their precursors (38,41,44,67). Leukocytes that accumulate in the area of coronary arterial plaques release large quantities of opioids when they are activated during plaque disruption (36,38,46).…”

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confidence: 99%

Functional role of peripheral opioid receptors in the regulation of cardiac spinal afferent nerve activity during myocardial ischemia

Longhurst

2013

American Journal of Physiology-Heart and Circulatory Physiology

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Fu LW, Longhurst JC. Functional role of peripheral opioid receptors in the regulation of cardiac spinal afferent nerve activity during myocardial ischemia. Am J Physiol Heart Circ Physiol 305: H76-H85, 2013. First published May 3, 2013 doi:10.1152/ajpheart.00091.2013.-Thinly myelinated A␦-fiber and unmyelinated C-fiber cardiac sympathetic (spinal) sensory nerve fibers are activated during myocardial ischemia to transmit the sensation of angina pectoris. Although recent observations showed that myocardial ischemia increases the concentrations of opioid peptides and that the stimulation of peripheral opioid receptors inhibits chemically induced visceral and somatic nociception, the role of opioids in cardiac spinal afferent signaling during myocardial ischemia has not been studied. The present study tested the hypothesis that peripheral opioid receptors modulate cardiac spinal afferent nerve activity during myocardial ischemia by suppressing the responses of cardiac afferent nerve to ischemic mediators like bradykinin and extracellular ATP. The nerve activity of single unit cardiac afferents was recorded from the left sympathetic chain (T2-T5) in anesthetized cats. Forty-three ischemically sensitive afferent nerves (conduction velocity: 0.32-3.90 m/s) with receptive fields in the left and right ventricles were identified. The responses of these afferent nerves to repeat ischemia or ischemic mediators were further studied in the following protocols. First, epicardial administration of naloxone (8 mol), a nonselective opioid receptor antagonist, enhanced the responses of eight cardiac afferent nerves to recurrent myocardial ischemia by 62%, whereas epicardial application of vehicle (PBS) did not alter the responses of seven other cardiac afferent nerves to ischemia. Second, naloxone applied to the epicardial surface facilitated the responses of seven cardiac afferent nerves to epicardial ATP by 76%. Third, administration of naloxone enhanced the responses of seven other afferent nerves to bradykinin by 85%. In contrast, in the absence of naloxone, cardiac afferent nerves consistently responded to repeated application of ATP (n ϭ 7) or bradykinin (n ϭ 7). These data suggest that peripheral opioid peptides suppress the responses of cardiac sympathetic afferent nerves to myocardial ischemia and ischemic mediators like ATP and bradykinin. sympathetic afferent nerves; opioid receptors; myocardial ischemia; naloxone ACTIVATION of thinly myelinated A␦-fiber and unmyelinated C-fiber cardiac sympathetic (spinal) afferent nerves during myocardial ischemia is responsible for the transmission of information from the heart to the brain that ultimately elicits the perception of cardiac pain and evokes excitatory cardiaccardiovascular reflex responses (19,22,39). For many years, attention has been focused on characterizing the excitatory effects elicited by a number of ischemic mediators on cardiac spinal afferent nerve activity during myocardial ischemia. In contrast, inhibitory influences of ischemic mediators on cardiac spinal...

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“…Opioid peptides are not limited to neuronal tissue but can also be localized in nonneuronal tissue. Enkephalins and their precursors have been found in the heart (13,28,33) as well as other tissues that include the spleen, vas deferens, stomach, lung, pancreas, and liver (2,30). These enkephalins appear to be localized in such a way as to be able to modulate cardiovascular activity.…”

Section: Discussionmentioning

confidence: 99%

“…We believe for the data presented that it is the endogenous opioids that then contribute to downstream signaling through the ␦-opioid receptor to manifest delayed cardioprotection possibly through stimulation of mitochondrial ATP-dependent K channels (mitoKATP), as has been proposed in numerous models. endocrine or autocrine function (32,33). It seems likely that these opioid precursors may be the common mediator that is induced by various stimuli including whole body hyperthermia.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of heat shock-induced cardioprotection by treatment with the opiate receptor antagonist naloxone

Patel

Hsu

Gross

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Attenuation of heat shock-induced cardioprotection by treatment with the opiate receptor antagonist naloxone. Am J Physiol Heart Circ Physiol 282: H2011-H2017, 2002. First published January 17, 2002 10.1152/ajpheart.00828.2001.-Whole body hyperthermia induces heat shock proteins (HSPs), which confer cardioprotection. Several opioid receptor subtypes are expressed in the heart and are linked to cardioprotection; however, no one has attempted to link the protection elicited by heat stress (HS) to opioids. Therefore, we investigated the effect of an opiate receptor antagonist, naloxone, on HS-induced cardioprotection. Anesthetized Sprague-Dawley rats were subjected to HS (42°C for 20 min) with and without naloxone pretreatment and were allowed to recover for 48 h. They then underwent 30 min of ischemia followed by 2 h of reperfusion. An acute HS group was given an intravenous bolus of naloxone (3 mg/kg) 10 min before index ischemia. Infarct size (IS), expressed as a percentage of the area at risk (IS/AAR), was determined. The right heart was excised for analysis of HSP content by Western blot. Heat-shocked rats showed significant reductions in IS/AAR versus control (16 Ϯ 3 vs. 58 Ϯ 4%, P Ͻ 0.001). Pretreatment with naloxone before HS attenuated the protective effects in a dose-dependent fashion, with significant attenuation of protection occurring at 15 mg/kg naloxone versus heat shock (42 Ϯ 6 vs. 16 Ϯ 3%, P Ͻ 0.001). Acute treatment with naloxone (3 mg/kg) 48 h after recovery from HS also significantly attenuated the delayed protective effect (47 Ϯ 4 vs. 16 Ϯ 3%, P Ͻ 0.001). No difference was seen in the level of HSP70 induced in the different groups. We conclude that heat shock-induced cardioprotection can be attenuated by naloxone, an opiate receptor antagonist, without reducing the levels of certain HSPs. These results suggest there may be a link between the endogenous release of opioids and HS that mediates cardioprotection.heat shock proteins; whole body hyperthermia

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Localization of preproenkephalin mRNA in rat heart: selective gene expression in left ventricular myocardium

Cited by 20 publications

References 30 publications

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Functional role of peripheral opioid receptors in the regulation of cardiac spinal afferent nerve activity during myocardial ischemia

Attenuation of heat shock-induced cardioprotection by treatment with the opiate receptor antagonist naloxone

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