AJP: Heart and Circulatory Physiology This is an RSS file. You can use it to subscribe to this data in your favourite RSS reader or to display this data on your own website or blog.

Development of dilated cardiomyopathy and impaired calcium homeostasis with cardiac-specific deletion of ESRR{beta}
Mechanisms underlying the development of idiopathic dilated cardiomyopathy (DCM) remain poorly understood. Using transcription factor expression profiling, we identified estrogen-related receptor-β (ESRRβ), a member of the nuclear receptor family of transcription factors, as highly expressed in murine hearts and other highly oxidative striated muscle beds. Mice bearing cardiac-specific deletion of ESRRβ (MHC-ERRB KO) develop DCM and sudden death at ~10 mo of age. Isolated adult cardiomyocytes from the MHC-ERRB KO mice showed an increase in calcium sensitivity and impaired cardiomyocyte contractility, which p...
Source: AJP: Heart and Circulatory Physiology - April 1, 2017 Category: Cardiology Authors: Rowe, G. C., Asimaki, A., Graham, E. L., Martin, K. D., Margulies, K. B., Das, S., Saffitz, J., Arany, Z. Tags: RESEARCH ARTICLE Source Type: research

Silica nanoparticles induce cardiotoxicity interfering with energetic status and Ca2+ handling in adult rat cardiomyocytes
This study provides the first exploration of SiO2-induced toxicity in cultured cardiomyocytes exposed to 7- or 670-nm SiO2 particles. We evaluated the mechanism of cell death in isolated adult cardiomyocytes exposed to 24-h incubation. The SiO2 cell membrane association and internalization were analyzed. SiO2 showed a dose-dependent cytotoxic effect with a half-maximal inhibitory concentration for the 7 nm (99.5 ± 12.4 µg/ml) and 670 nm (>1,500 µg/ml) particles, which indicates size-dependent toxicity. We evaluated cardiomyocyte shortening and intracellular Ca2+ handling, which showed impaired contrac...
Source: AJP: Heart and Circulatory Physiology - April 1, 2017 Category: Cardiology Authors: Guerrero-Beltran, C. E., Bernal-Ramirez, J., Lozano, O., Oropeza-Almazan, Y., Castillo, E. C., Garza, J. R., Garcia, N., Vela, J., Garcia-Garcia, A., Ortega, E., Torre-Amione, G., Ornelas-Soto, N., Garcia-Rivas, G. Tags: RESEARCH ARTICLE Source Type: research

Errata for vol. 312, p.
(Source: AJP: Heart and Circulatory Physiology)
Source: AJP: Heart and Circulatory Physiology - March 12, 2017 Category: Cardiology Tags: CORRIGENDA Source Type: research

Blood flow patterns underlie developmental heart defects
Although cardiac malformations at birth are typically associated with genetic anomalies, blood flow dynamics also play a crucial role in heart formation. However, the relationship between blood flow patterns in the early embryo and later cardiovascular malformation has not been determined. We used the chicken embryo model to quantify the extent to which anomalous blood flow patterns predict cardiac defects that resemble those in humans and found that restricting either the inflow to the heart or the outflow led to reproducible abnormalities with a dose-response type relationship between blood flow stimuli and the expressio...
Source: AJP: Heart and Circulatory Physiology - March 12, 2017 Category: Cardiology Authors: Midgett, M., Thornburg, K., Rugonyi, S. Tags: RESEARCH ARTICLE Source Type: research

Genetic determination of the vascular reactions in humans in response to the diving reflex
This study observed that humans with gene polymorphisms of the renin-angiotensin and kinin-bradykinin systems demonstrate various expressions of protective vascular reactions in response to the diving reflex. The obtained results might be used in estimation of resistance to hypoxia of any origin in human beings or in a medical practice. NEW & NOTEWORTHY Our study demonstrates that the vascular reactions in response to the diving reflex are genetically determined and depend on gene polymorphisms of the kinin-bradykinin and the renin-angiotensin systems. (Source: AJP: Heart and Circulatory Physiology)
Source: AJP: Heart and Circulatory Physiology - March 12, 2017 Category: Cardiology Authors: Baranova, T. I., Berlov, D. N., Glotov, O. S., Korf, E. A., Minigalin, A. D., Mitrofanova, A. V., Ahmetov, I. I., Glotov, A. S. Tags: RESEARCH ARTICLE Source Type: research

Sympathetic modulation of electrical activation in normal and infarcted myocardium: implications for arrhythmogenesis
In conclusion, sympathoexcitation increases CV in normal myocardium and modulates activation propagation in peri-infarcted ventricular myocardium. These data demonstrate functional control of arrhythmogenic peri-infarct substrates by sympathetic nerves and in part explain the temporal nature of arrhythmogenesis. NEW & NOTEWORTHY This study demonstrates regional control of conduction velocity in normal hearts by sympathetic nerves. In infarcted hearts, however, not only is modulation of propagation heterogeneous, some regions showed paradoxical conduction slowing. Sympathoexcitation altered propagation in all infarcted ...
Source: AJP: Heart and Circulatory Physiology - March 12, 2017 Category: Cardiology Authors: Ajijola, O. A., Lux, R. L., Khahera, A., Kwon, O., Aliotta, E., Ennis, D. B., Fishbein, M. C., Ardell, J. L., Shivkumar, K. Tags: RESEARCH ARTICLE Source Type: research

Effect of anisotropy on ventricular vulnerability to unidirectional block and reentry by single premature stimulation during normal sinus rhythm in rat heart
Single high-intensity premature stimuli when applied to the ventricles during ventricular drive of an ectopic site, as in Winfree's "pinwheel experiment," usually induce reentry arrhythmias in the normal heart, while single low-intensity stimuli barely do. Yet ventricular arrhythmia vulnerability during normal sinus rhythm remains largely unexplored. With a view to define the role of anisotropy on ventricular vulnerability to unidirectional conduction block and reentry, we revisited the pinwheel experiment with reduced constraints in the in situ rat heart. New features included single premature stimulation during normal si...
Source: AJP: Heart and Circulatory Physiology - March 12, 2017 Category: Cardiology Authors: Rossi, S., Buccarello, A., Ershler, P. R., Lux, R. L., Callegari, S., Corradi, D., Carnevali, L., Sgoifo, A., Miragoli, M., Musso, E., Macchi, E. Tags: RESEARCH ARTICLE Source Type: research

Kv{beta}1.1 (AKR6A8) senses pyridine nucleotide changes in the mouse heart and modulates cardiac electrical activity
The present study investigates the physiological role of Kvβ1 subunit for sensing pyridine nucleotide (NADH/NAD+) changes in the heart. We used Kvβ1.1 knockout (KO) or wild-type (WT) mice and established that Kvβ1.1 preferentially binds with Kv4.2 and senses the pyridine nucleotide changes in the heart. The cellular action potential duration (APD) obtained from WT cardiomyocytes showed longer APDs with lactate perfusion, which increases intracellular NADH levels, while the APDs remained unaltered in the Kvβ1.1 KO. Ex vivo monophasic action potentials showed a similar response, in which the APDs were pro...
Source: AJP: Heart and Circulatory Physiology - March 12, 2017 Category: Cardiology Authors: Tur, J., Chapalamadugu, K. C., Katnik, C., Cuevas, J., Bhatnagar, A., Tipparaju, S. M. Tags: RESEARCH ARTICLE Source Type: research

A novel complex I inhibitor protects against hypertension-induced left ventricular hypertrophy
Since left ventricular hypertrophy (LVH) increases the susceptibility for the development of other cardiac conditions, pharmacotherapy that mitigates pathological cardiac remodeling may prove to be beneficial in patients with LVH. Previous work has shown that the activation of the energy-sensing kinase AMP-activated protein kinase (AMPK) can inhibit some of the molecular mechanisms that are involved in LVH. Of interest, metformin activates AMPK through its inhibition of mitochondrial complex I in the electron transport chain and can prevent LVH induced by pressure overload. However, metformin has additional cellular effect...
Source: AJP: Heart and Circulatory Physiology - March 12, 2017 Category: Cardiology Authors: Matsumura, N., Robertson, I. M., Hamza, S. M., Soltys, C.-L. M., Sung, M. M., Masson, G., Beker, D. L., Dyck, J. R. B. Tags: RESEARCH ARTICLE Source Type: research

Cardiomyocyte-specific ablation of CD36 accelerates the progression from compensated cardiac hypertrophy to heart failure
Previous studies have shown that loss of CD36 protects the heart from dysfunction induced by pressure overload in the presence of diet-induced insulin resistance and/or obesity. The beneficial effects of CD36 ablation in this context are mediated by preventing excessive cardiac fatty acid (FA) entry and reducing lipotoxic injury. However, whether or not the loss of CD36 can prevent pressure overload-induced cardiac dysfunction in the absence of chronic exposure to high circulating FAs is presently unknown. To address this, we utilized a tamoxifen-inducible cardiomyocyte-specific CD36 knockout (icCD36KO) mouse and genetical...
Source: AJP: Heart and Circulatory Physiology - March 12, 2017 Category: Cardiology Authors: Sung, M. M., Byrne, N. J., Kim, T. T., Levasseur, J., Masson, G., Boisvenue, J. J., Febbraio, M., Dyck, J. R. B. Tags: RESEARCH ARTICLE Source Type: research

Ventricular tachycardia in ischemic heart disease: the sympathetic heart and its scars
(Source: AJP: Heart and Circulatory Physiology)
Source: AJP: Heart and Circulatory Physiology - March 12, 2017 Category: Cardiology Authors: Meyer, C., Scherschel, K. Tags: EDITORIAL FOCUS Source Type: research

Myriad roles of voltage-activated potassium channel subunit Kv{beta}1.1 in the heart
(Source: AJP: Heart and Circulatory Physiology)
Source: AJP: Heart and Circulatory Physiology - March 12, 2017 Category: Cardiology Authors: Kukreja, R. C. Tags: EDITORIAL FOCUS Source Type: research

Ischemic preconditioning in pigs: a causal role for signal transducer and activator of transcription 3
Ischemic preconditioning (IPC), i.e., brief episodes of nonlethal myocardial ischemia-reperfusion (I/R) before sustained ischemia with subsequent reperfusion, reduces infarct size in all species tested so far, including humans. In rodents, the cardioprotective signal transduction causally involves an activation of Akt, ERK1/2, and STAT3. However, there are apparent species differences in the signal transduction between rodents and larger mammals such as pigs, where data on IPC's signal transduction are inconsistent for Akt and ERK1/2. The role of STAT3 has not yet been analyzed. Pigs were subjected to 60 min of left anteri...
Source: AJP: Heart and Circulatory Physiology - February 28, 2017 Category: Cardiology Authors: Gent, S., Skyschally, A., Kleinbongard, P., Heusch, G. Tags: RESEARCH ARTICLE Source Type: research

The JCR:LA-cp rat: a novel rodent model of cystic medial necrosis
In conclusion, the normal chow-fed JCR:LA-cp rat represents a novel rodent model of cystic medial necrosis, associated with multiple metabolic abnormalities, vascular smooth muscle cell apoptosis, and vessel hypoxia. NEW & NOTEWORTHY Triggers for cystic medial necrosis (CMN) have been difficult to study due to lack of animal models to recapitulate the pathologies seen in humans. Our study is the first description of CMN in the rat. Thus the JCR:LA-cp rat represents a useful model to investigate the underlying molecular changes leading to the development of CMN. (Source: AJP: Heart and Circulatory Physiology)
Source: AJP: Heart and Circulatory Physiology - February 28, 2017 Category: Cardiology Authors: Pung, Y. F., Chilian, W. M., Bennett, M. R., Figg, N., Kamarulzaman, M. H. Tags: RAPID REPORT Source Type: research

Elevated 20-HETE impairs coronary collateral growth in metabolic syndrome via endothelial dysfunction
Coronary collateral growth (CCG) is impaired in metabolic syndrome (MetS). microRNA-145 (miR-145-Adv) delivery to our rat model of MetS (JCR) completely restored and neutrophil depletion significantly improved CCG. We determined whether low endogenous levels of miR-145 in MetS allowed for elevated production of 20-hydroxyeicosatetraenoic acid (20-HETE), which, in turn, resulted in excessive neutrophil accumulation and endothelial dysfunction leading to impaired CCG. Rats underwent 0–9 days of repetitive ischemia (RI). RI-induced cardiac CYP4F (neutrophil-specific 20-HETE synthase) expression and 20-HETE levels were i...
Source: AJP: Heart and Circulatory Physiology - February 28, 2017 Category: Cardiology Authors: Joseph, G., Soler, A., Hutcheson, R., Hunter, I., Bradford, C., Hutcheson, B., Gotlinger, K. H., Jiang, H., Falck, J. R., Proctor, S., Schwartzman, M. L., Rocic, P. Tags: RESEARCH ARTICLE Source Type: research