β<sub>3</sub>‐Adrenoceptors modulate left ventricular relaxation in the rat heart via the NO‐cGMP‐PKG pathway

Angelone, Tommaso; Filice, E.; Quintieri, A.M.; Imbrogno, Sandra; Recchia, Anna Grazia; Pulerà, E.; Mannarino, C.; Pellegrino, Daniela; Cerra, Maria Carmela

doi:10.1111/j.1748-1716.2008.01838.x

Cited by 52 publications

(47 citation statements)

References 35 publications

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“…In the trout Oncorhynchus mykiss, b3-ARs are richly expressed in the heart and are homologous to their mammalian counterparts (Nickerson et al, 2003). In mammals, b3 activation elicits negative inotropism [for references, see Gauthier et al (Gauthier et al, 2000)] and negative lusitropism (Angelone et al, 2008a), both involving NO-cGMP signaling. Similarly, in Anguilla anguilla, b3-ARs activation decreases cardiac mechanical performance through a pertussis toxin (PTx)-sensitive G i protein mechanism, consistent with a major b3-ARs myocardial localization, and requires the NO-cGMP-cGMP-activated protein kinase (PKG) cascade .…”

Section: Adrenergic Neuroendocrine Patternsmentioning

confidence: 99%

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

Tota

Cerra

Gattuso

2010

Journal of Experimental Biology

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Summary In the past 50 years, extensive evidence has shown the ability of vertebrate cardiac non-neuronal cells to synthesize and release catecholamines (CA). This formed the mindset behind the search for the intrinsic endocrine heart properties, culminating in 1981 with the discovery of the natriuretic peptides (NP). CA and NP, co-existing in the endocrine secretion granules and acting as major cardiovascular regulators in health and disease, have become of great biomedical relevance for their potent diagnostic and therapeutic use. The concept of the endocrine heart was later enriched by the identification of a growing number of cardiac hormonal substances involved in organ modulation under normal and stress-induced conditions. Recently, chromogranin A (CgA), a major constituent of the secretory granules, and its derived cardio-suppressive and antiadrenergic peptides, vasostatin-1 and catestatin, were shown as new players in this framework, functioning as cardiac counter-regulators in ‘zero steady-state error’ homeostasis, particularly under intense excitatory stimuli, e.g. CA-induced myocardial stress. Here, we present evidence for the hypothesis that is gaining support, particularly among human cardiologists. The actions of CA, NP and CgA, we argue, may be viewed as a hallmark of the cardiac capacity to organize ‘whip-brake’ connection-integration processes in spatio-temporal networks. The involvement of the nitric oxide synthase (NOS)/nitric oxide (NO) system in this configuration is discussed. The use of fish and amphibian paradigms will illustrate the ways that incipient endocrine-humoral agents have evolved as components of cardiac molecular loops and important intermediates during evolutionary transitions, or in a distinct phylogenetic lineage, or under stress challenges. This may help to grasp the old evolutionary roots of these intracardiac endocrine/paracrine networks and how they have evolved from relatively less complicated designs. The latter can also be used as an intellectual tool to disentangle the experimental complexity of the mammalian and human endocrine hearts, suggesting future investigational avenues.

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Section: Adrenergic Neuroendocrine Patternsmentioning

confidence: 99%

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

Tota

Cerra

Gattuso

2010

Journal of Experimental Biology

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“…First, B 3 -adrenoreceptors exist in the fish heart (Nikinmaa, 2003;Nickerson et al, 2003;Imbrogno et al, 2006) and may play a 'protective role' in some fish hearts (including the cod) by preventing excessive  1 / 2 -stimulation of the myocardium (Gauthier et al, 2007;Angelone et al, 2008). Second, catecholamine-induced sarcolemma Ca 2+ influx varies between species, and may be somewhat independent of sarcolemma Ca 2+ channel density.…”

Section: Cardiac Function and Adrenergic Stimulationmentioning

confidence: 99%

Atlantic cod (Gadus morhua L.) in situ cardiac performance at cold temperatures: long-term acclimation, acute thermal challenge and the role of adrenaline

Lurman

Petersen

Gamperl

2012

Journal of Experimental Biology

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SUMMARYThe resting and maximum in situ cardiac performance of Newfoundland Atlantic cod (Gadus morhua) acclimated to 10, 4 and 0°C were measured at their respective acclimation temperatures, and when acutely exposed to temperature changes: i.e. hearts from 10°C fish cooled to 4°C, and hearts from 4°C fish measured at 10 and 0°C. Intrinsic heart rate (f H ) decreased from 41beatsmin -1 at 10°C to 33beatsmin -1 at 4°C and 25beatsmin -1 at 0°C. However, this degree of thermal dependency was not reflected in maximal cardiac output (Q max values were ~44, ~37 and ~34mlmin -1 kg -1 at 10, 4 and 0°C, respectively). Further, cardiac scope showed a slight positive compensation between 4 and 0°C (Q 10 1.7), and full, if not a slight over compensation between 10 and 4°C (Q 10 0.9). The maximal performance of hearts exposed to an acute decrease in temperature (i.e. from 10 to 4°C and 4 to 0°C) was comparable to that measured for hearts from 4°C-and 0°C-acclimated fish, respectively. In contrast, 4°C-acclimated hearts significantly out-performed 10°C-acclimated hearts when tested at a common temperature of 10°C (in terms of both Q max and power output). Only minimal differences in cardiac function were seen between hearts stimulated with basal (5nmoll ) levels of adrenaline, the effects of which were not temperature dependent. These results: (1) show that maximum performance of the isolated cod heart is not compromised by exposure to cold temperatures; and (2) support data from other studies, which show that, in contrast to salmonids, cod cardiac performance/myocardial contractility is not dependent upon humoral adrenergic stimulation.

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“…Actually, CST is known to counteract exaggerated β-adrenergic activity, which is relevant part of the neuroendocrine scenario of heart failure [1][2][3][4], and to dilate human vessels in vivo [16], thus exerting positive effects on cardiac afterload. In line with these evidences and since β-blockade is largely used as post-ischaemic treatment, the present work suggests that exogenous CST may provide new tool for pharmacological postconditioning.…”

Section: Clinical Considerationsmentioning

confidence: 99%

“…The methods were similar to those previously described [1,33,35,36,[39][40][41]. In brief, after anaesthesia chest was opened and heart excised.…”

Section: Isolated Heart Perfusionmentioning

confidence: 99%

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Catestatin reduces myocardial ischaemia/reperfusion injury: involvement of PI3K/Akt, PKCs, mitochondrial KATP channels and ROS signalling

Perrelli

Tullio

Angotti

et al. 2013

Pflugers Arch - Eur J Physiol

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Aims: Catestatin (CST) limits myocardial ischaemia/reperfusion (I/R) injury with unknown mechanisms. Clearly phosphoinositide-3-kinase (PI3K), protein-kinase-C (PKC) isoforms, including intra-mitochondrial PKCε, mitochondrial-K ATP (mitoK ATP ) channels and subsequent reactiveoxygen-species (ROS)-signalling play important roles in postconditioning cardioprotection, preventing mitochondrial permeability transition pore (mPTP) opening. Therefore, we studied the role of these extra-and intra-mitochondrial factors in CST-induced protection. Methods and Results: Isolated rat hearts and H9c2 cells underwent I/R and oxidative stress, respectively. In isolated hearts CST (75nM, CST-Post) given in early-reperfusion significantly reduced infarct-size, limited post-ischaemic contracture, and improved recovery of developed left ventricular pressure.PI3K inhibitor, LY-294002 (LY), large spectrum PKC inhibitor, Chelerythrine (CHE), specific PKCε inhibitor (εV1-2), mitoK ATP channel blocker, 5-Hydroxydecanoate (5HD) or ROS scavenger, 2-mercaptopropionylglycine (MPG) abolished the infarct-sparing effect of CST. Notably the CSTinduced contracture limitation was maintained during co-infusion of 5HD, MPG or εV1-2, but it was lost during co-infusion of LY or CHE. In H9c2 cells challenged with H 2 O 2 , mitochondrialdepolarization (an index of mPTP-opening studied with JC1-probe) was drastically limited by CST (75nM). Conclusions: Our results suggest that the protective signalling pathway activated by CST includes mitoK ATP channels, ROS-signalling and prevention of mPTP opening, with a central role for upstream PI3K/Akt and PKCs. In fact, all inhibitors completely abolished CST-infarct-sparing effect. Since CST-anti-contracture effect cannot be explained by intra-mitochondrial mechanisms (PKCε activation and mitoK ATP channel opening) or ROS-signalling, it is proposed that these downstream signals are part of a reverberant loop which re-activates upstream PKCs, which therefore play a pivotal role in CST-induced protection.

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β₃‐Adrenoceptors modulate left ventricular relaxation in the rat heart via the NO‐cGMP‐PKG pathway

Cited by 52 publications

References 35 publications

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

Atlantic cod (Gadus morhua L.) in situ cardiac performance at cold temperatures: long-term acclimation, acute thermal challenge and the role of adrenaline

Catestatin reduces myocardial ischaemia/reperfusion injury: involvement of PI3K/Akt, PKCs, mitochondrial KATP channels and ROS signalling

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β3‐Adrenoceptors modulate left ventricular relaxation in the rat heart via the NO‐cGMP‐PKG pathway

Cited by 52 publications

References 35 publications

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

Atlantic cod (Gadus morhua L.) in situ cardiac performance at cold temperatures: long-term acclimation, acute thermal challenge and the role of adrenaline

Catestatin reduces myocardial ischaemia/reperfusion injury: involvement of PI3K/Akt, PKCs, mitochondrial KATP channels and ROS signalling

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Product

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β₃‐Adrenoceptors modulate left ventricular relaxation in the rat heart via the NO‐cGMP‐PKG pathway