AJP Heart and Circulatory Physiology (Am J Physiol Heart Circ Physiol)

Publisher: American Physiological Society (1887- ), American Physiological Society

Journal description

The American Journal of Physiology: Heart and Circulatory Physiology publishes original investigations on the physiology of the heart, blood vessels, and lymphatics, including experimental and theoretical studies of cardiovascular function at all levels of organization ranging from the intact animal to the cellular, subcellular, and molecular levels. It embraces new descriptions of these functions and of their control systems, as well as their bases in biochemistry, biophysics, genetics, and cell biology. Preference is given to research that provides significant new insights into the mechanisms that determine the performance of the normal and abnormal heart and circulation.

Current impact factor: 3.84

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 3.838
2013 Impact Factor 4.012
2012 Impact Factor 3.629
2011 Impact Factor 3.708
2010 Impact Factor 3.88
2009 Impact Factor 3.712
2008 Impact Factor 3.643
2007 Impact Factor 3.973
2006 Impact Factor 3.724
2005 Impact Factor 3.56
2004 Impact Factor 3.539
2003 Impact Factor 3.658
2002 Impact Factor 3.369
2001 Impact Factor 3.232
2000 Impact Factor 3.243
1999 Impact Factor 2.747

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.88
Cited half-life 9.10
Immediacy index 0.77
Eigenfactor 0.04
Article influence 1.19
Website American Journal of Physiology - Heart and Circulatory Physiology website
Other titles American journal of physiology., Heart and circulatory physiology, Heart and circulatory physiology, AJP: Heart and circulatory physiology, AJP:heart, AJP:heart online
ISSN 1522-1539
OCLC 40069627
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

American Physiological Society

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • Author's Pre-print on pre-print servers
    • NIH, Wellcome Trust, HHMI, MRC and BBSRC authors will on their behalf have the Publisher's version/PDF deposited in PubMed Central for release 12 months after publication
    • Publisher's version/PDF cannot be used
    • May link to publisher version with DOI
    • Publisher last reviewed on 03/06/2015
  • Classification
    yellow

Publications in this journal

  • Yujia Wang · Zenghui Wu · Eric Thorin · Johanne Tremblay · Julie L Lavoie · Hongyu Luo · Junzheng Peng · Shijie Qi · Tao Wu · Fei Chen · Jianzhong Shen · Shenjiang Hu · Jiangping Wu
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    ABSTRACT: EPH kinases and their ligands, ephrins (EFNs), have vital and diverse biological functions, although their function in blood pressure (BP) control has not been studied in detail. In the present study, we report that Efnb3 gene knockout (KO) led to hypertension in female but not male mice. Vascular smooth muscle cells (VSMCs) were target cells for EFNB3 function in BP regulation. The deletion of EFNB3 augmented contractility of mesenteric arteries and VSMCs from female but not male KO mice, compared to their WT counterparts. Estrogen augmented VSMC contractility while testosterone reduced it in the absence of EFNB3, although these sex hormones had no effect on the contractility of VSMCs from WT mice. The effect of estrogen on KO VSMC contractility was via a non-genomic pathway involving GPR30, while that of testosterone was likely via a genomic pathway, according to VSMC contractility assays and GPR30 knockdown assays. The sex hormone-dependent contraction phenotypes in KO VSMCs were reflected in BP in vivo. Ovariectomy rendered female KO mice normotensive, while castration, male KO mice hypertensive. At the molecular level, EFNB3 KO in VSMCs resulted in reduced MLC kinase phosphorylation, an event enhancing sensitivity to Ca++ flux in VSMCs. Our investigation has revealed previously unknown EFNB3 functions in BP regulation and shown that EFNB3 is a hypertension risk gene in certain individuals.
    No preview · Article · Feb 2016 · AJP Heart and Circulatory Physiology
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    ABSTRACT: Background: Clinical Doppler-based studies at rest suggest left ventricular (LV) diastolic function rapidly improves from the neonate to infant. Whether this translates to its response to hemodynamic challenges is uncertain. We sought to explore the impact of early LV maturation on its ability to tolerate atrial tachycardia. As tachycardia reduces filling time, we hypothesized that the neonatal LV would be less tolerant of atrial tachycardia. Methods and results: Landrace cross piglets of two age groups (1-3days, NP; 14-17days, YP; n=7/group) were instrumented for an atrial pacing protocol (from 200 to 300bpm) and assessed by invasive monitoring and echocardiography. At all rates, NP maintained their LV output and blood pressure, whereas YP did not. Negative dP/dt in NP at baseline was lower than that of YP (-1599±83 vs -2470±226mmHg/s, respectively, p=0.007). Negative dP/dt of NP increased with pacing (p=0.002), whereas that of YP tended to decrease (p=0.056). Except for fractional shortening which was reduced in YP at 260bpm, all invasive and noninvasive measures of contractility did not differ between groups. Twist studies demonstrated a similar increase in peak LV twist and untwisting rate in response to tachycardia (combined data: baseline -259±22; at 260bpm -498±59 deg/s, p=0.003); however, NP tended to increase apical positive rotation and YP increased basal negative rotation (p=0.009) to augment LV twist. Conclusions: The LV of the newborn piglet appears more tolerant of atrial tachycardia than that of the piglet at 2 weeks which could relate to better diastolic performance and differences in twist mechanics.
    No preview · Article · Dec 2015 · AJP Heart and Circulatory Physiology
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    ABSTRACT: Cancer cachexia is a multifactorial syndrome characterized by a progressive loss of skeletal muscle mass associated with significant functional impairment. In addition to a loss of skeletal muscle mass and function, many patients with cancer cachexia also experience cardiac atrophy, remodeling and dysfunction, which in the field of cancer cachexia is described as 'cardiac cachexia'. The cardiac alterations may be due to underlying heart disease, the cancer itself or problems initiated by the cancer treatment and unfortunately, remains largely underappreciated by clinicians and basic scientists. Despite recent major advances in the treatment of cancer, little progress has been made in the treatment of cardiac cachexia in cancer and much of this is due to lack of information regarding the mechanisms. This review focuses on the cardiac atrophy associated with cancer cachexia, describing some of the known mechanisms and discussing the current and future therapeutic strategies to treat this condition. Above all else, improved awareness of the condition and an increased focus on identification of mechanisms and therapeutic targets will facilitate the eventual development of an effective treatment for cardiac atrophy in cancer cachexia.
    No preview · Article · Dec 2015 · AJP Heart and Circulatory Physiology
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    ABSTRACT: Dyspnea and reduced exercise capacity, caused, in part, by respiratory muscle dysfunction, are common symptoms in patients with heart failure (HF). However, the etiology of diaphragmatic dysfunction has not been identified. To investigate the effects of HF on diaphragmatic function, models of HF were surgically induced in CD-1 mice by transverse aortic constriction (TAC) and acute myocardial infarction (AMI), respectively. Assessment of myocardial function, isolated diaphragmatic strip function, myofilament force-pCa relationship and phosphorylation status of myofilament proteins were performed at either 2 or 18 wk post-surgery. Echocardiography and invasive hemodynamics revealed development of HF by 18 wk post-surgery in both models. In vitro diaphragmatic force production was preserved in all groups while morphometric analysis revealed diaphragmatic atrophy and fibrosis in 18 wk TAC and AMI groups. Isometric force-pCa measurements of myofilament preparations revealed reduced Ca(2+) sensitivity of force generation and force generation at half-maximum and maximum Ca(2+) activation in 18 wk TAC. The rate of force redevelopment (ktr) was reduced in all HF groups at high levels of Ca(2+) activation. Finally, there were significant changes in the myofilament phosphorylation status of the 18 wk TAC group. This includes a decrease in the phosphorylation of troponin T, desmin, myosin light chain (MLC) 1, and MLC 2 as well as a shift in myosin isoforms. These results indicate that there are multiple changes in diaphragmatic myofilament function, which are specific to the type and stage of HF and occur before overt impairment of in vitro force production.
    No preview · Article · Dec 2015 · AJP Heart and Circulatory Physiology
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    ABSTRACT: To determine the impact of progressive elevations in peripheral vascular disease (PVD) risk on microvascular function, we utilized eight rat models spanning "healthy" to "high PVD risk" and used a multi-scale approach to interrogate microvascular function and outcomes. Healthy: Sprague-Dawley rats (SDR), lean Zucker rats (LZR); Mild Risk: SDR on high salt diet (HSD), SDR on high fructose diet (HFD); Moderate Risk: reduced renal mass hypertension (RRM), spontaneously hypertensive rats (SHR); High Risk: obese Zucker rats (OZR) and Dahl salt sensitive rats (DSS). Vascular reactivity and biochemical analyses demonstrated that even mild elevations in PVD risk severely attenuated nitric oxide bioavailability and caused progressive shifts in arachidonic acid metabolism increasing thromboxane A2 levels. With the introduction of hypertension, arteriolar myogenic activation and adrenergic constriction were increased. However, while functional hyperemia and fatigue resistance of in situ skeletal muscle were not impacted with mild or moderate PVD risk, blood oxygen handling suggested an increasingly heterogeneous perfusion within resting and contracting skeletal muscle. Analysis of in situ networks demonstrated an increasingly stable and heterogeneous distribution of perfusion at arteriolar bifurcations with elevated PVD risk; a phenomenon that was manifested first in the distal microcirculation, and evolved proximally with increasing risk. The increased perfusion distribution heterogeneity and loss of flexibility throughout the microvascular network, the result of the combined effects on NO bioavailability, arachidonic acid metabolism, myogenic activation, and adrenergic constriction, may represent the most accurate predictor of the skeletal muscle microvasculopathy and poor health outcomes associated with chronic elevations in PVD risk.
    No preview · Article · Dec 2015 · AJP Heart and Circulatory Physiology
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    ABSTRACT: The mammalian heart has long been considered to be a post-mitotic organ. It was thought that in the postnatal period, the heart underwent a transition from hyperplasic growth (more cells) to hypertrophic growth (larger cells) due to the conversion of cardiomyocytes from a proliferative state to one of terminal differentiation. This hypothesis was gradually disproven as data were published showing that the myocardium is a more dynamic tissue in which cardiomyocyte karyokinesis and cytokinesis produce new cells, leading to the hyperplasic regeneration of some of the muscle mass lost in various pathological processes. microRNAs have been shown to be critical regulators of cardiomyocyte differentiation and proliferation, and may offer the novel opportunity of regenerative hyperplasic therapy. Here we summarize the relevant processes and recent progress regarding the functions of specific microRNAs in cardiac development and regeneration.
    No preview · Article · Dec 2015 · AJP Heart and Circulatory Physiology
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    ABSTRACT: Pre-menopausal women exhibit endogenous cardioprotective signaling mechanisms that are thought to result from the beneficial effects of estrogen, which we have shown to increase protein S-nitrosylation in the heart. S-nitrosylation is a labile protein modification that increases with a number of different forms of cardioprotection, including ischemic preconditioning. Herein, we sought to identify a potential role for protein S-nitrosylation in sex-dependent cardioprotection. We utilized a Langendorff-perfused mouse heart model of ischemia-reperfusion injury with male and female hearts, and S-nitrosylation-resin-assisted capture with liquid chromatography tandem mass spectrometry to identify S-nitrosylated proteins and modification sites. Consistent with previous studies, female hearts exhibited resilience to injury with a significant increase in functional recovery compared to male hearts. In a separate set of hearts, we identified a total of 177 S-nitrosylated proteins in female hearts at baseline compared to 109 S-nitrosylated proteins in male hearts. Unique S-nitrosylated proteins in the female group included the F1FO-ATPase and cyclophilin D. We also utilized label-free peptide analysis to quantify levels of common S-nitrosylated identifications and noted that the S-nitrosylation of SERCA2a was nearly 70% lower in male hearts compared to female with no difference in expression. Further, we found a significant increase in endothelial nitric oxide synthase expression, phosphorylation, and total nitric oxide production in female hearts compared to males, likely accounting for the enhanced S-nitrosylation protein levels in female hearts. In conclusion, we identified a number of novel S-nitrosylated proteins in female hearts that are likely to contribute to sex-dependent cardioprotection.
    No preview · Article · Dec 2015 · AJP Heart and Circulatory Physiology
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    Preview · Article · Dec 2015 · AJP Heart and Circulatory Physiology
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    ABSTRACT: Myocardial electrical impedance is influenced by the mechanical activity of the heart. Therefore, the ischemia induced mechanical dysfunction may cause specific changes in the systolic-diastolic pattern of myocardial impedance but this is not known. This study aimed to analyze the phasic changes of myocardial resistivity in normal and ischemic conditions. Myocardial resistivity was measured continuously during the cardiac cycle using 26 different simultaneous excitation frequencies (1 kHz-1 MHz) in 7 anesthetized open chest pigs. Animals were submitted to 30 minutes regional ischemia by acute left anterior descending coronary artery occlusion. The electrocardiogram, left ventricular (LV) pressure, LV dP/dt and aortic blood flow were recorded simultaneously. Baseline myocardial resistivity depicted a phasic pattern during the cardiac cycle with higher values at the pre-ejection period (4.19±1.09% increase above the mean,p<0.001) and lower values during relaxation phase (5.01±0.85% below the mean,p<0.001). Acute coronary occlusion induced two effects on the phasic resistivity curve: 1) a prompt (5 min ischemia) holosystolic resistivity rise leading to a bell-shaped waveform and to a reduction of the area under the LV pressure-impedance curve (1427±335 Ω•cm•mmHg vs 757±266 Ω•cm•mmHg,p<0.01,41 kHz) and 2) a subsequent (5-10 min ischemia) progressive mean resistivity rise (325±23 Ω•cm vs 438±37 Ω•cm at 30 min,p<0.01,1 kHz). The structural and mechanical myocardial dysfunction induced by acute coronary occlusion can be recognized by specific changes in the systolic-diastolic myocardial resistivity curve. Therefore these changes may become a new indicator (surrogate) of evolving acute myocadial ischemia.
    No preview · Article · Nov 2015 · AJP Heart and Circulatory Physiology
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    ABSTRACT: Rationale: Studies of adults with orthostatic intolerance (OI) reveal altered neurohumoral responses to orthostasis, which provide mechanistic insight into the dysregulation of blood pressure control. Similar studies in children with OI providing a thorough neurohumoral profile are lacking. Objective: Determine the cardiovascular and neurohumoral profile in adolescent subjects presenting with OI. Methods and results: Subjects ages 10-18 years were prospectively recruited if they exhibited ≥2 traditional OI symptoms and were referred for tilt testing (HUT). Circulating catecholamines, vasopressin, aldosterone, renin and angiotensins were measured supine and after 15 minutes of 70 degree tilt. Heart rate and blood pressure were continuously measured. Of the 48 patients, 30 had an abnormal tilt. Subjects with an abnormal tilt had lower systolic, diastolic, and mean arterial blood pressures during tilt, significantly higher levels of vasopressin during HUT, and relatively higher catecholamines and angiotensin II during HUT than subjects with a normal tilt. Distinct neurohumoral profiles were observed when OI subjects were placed into groups defined by the hemodynamic response: postural orthostatic tachycardia syndrome (POTS), orthostatic hypotension (OH), Syncope, and POTS/Syn. Key characteristics included higher HUT-induced norepinephrine in POTS and vasopressin in OH and syncope, and higher supine and HUT aldosterone in OH subjects. Conclusions: Children with OI and an abnormal response to tilt exhibit distinct neurohumoral profiles associated with the type of hemodynamic response during orthostatic challenge. Elevated AVP levels in syncope and OH groups are likely an exaggerated response to decreased blood flow not compensated by higher NE levels as observed in POTS subjects. These different compensatory mechanisms support the role of measuring neurohumoral profiles towards the goal of selecting more focused and mechanistic based treatment options for pediatric patients with OI.
    No preview · Article · Nov 2015 · AJP Heart and Circulatory Physiology
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    ABSTRACT: We previously reported that the cardiomyocyte-specific protein, Leucine-rich repeat containing 10 (LRRC10), has critical functions in the mammalian heart. Here, we tested the role of LRRC10 in the response of the heart to biomechanical stress by performing transverse aortic constriction on Lrrc10 null (Lrrc10(-/-)) mice. Mild pressure overload induces severe cardiac dysfunction and ventricular dilation in Lrrc10(-/-) mice as compared to controls. In addition to dilation and cardiomyopathy, Lrrc10(-/-) mice showed a pronounced increase in heart weight with pressure overload stimulation and a more dramatic loss of cardiac ventricular performance, collectively suggesting that the absence of LRRC10 renders the heart more disease prone with greater hypertrophy and structural remodeling, although rates of cardiac fibrosis and myocyte drop-out were not different from control. Lrrc10(-/-) cardiomyocytes also exhibit reduced contractility in response to β-adrenergic stimulation, consistent with loss of cardiac ventricular performance after pressure overload. We have previously shown that LRRC10 interacts with actin in the heart. Here, we show that histidine 150 of LRRC10 is required for interaction with actin and this interaction is reduced after pressure overload, suggesting an integral role for LRRC10 in the response of the heart to mechanical stress. Importantly, these studies demonstrate that LRRC10 is required to maintain cardiac performance in response to pressure overload and suggest that dysregulated expression or mutation of LRRC10 may greatly sensitize human patients to more severe cardiac disease in conditions such as chronic hypertension or aortic stenosis.
    No preview · Article · Nov 2015 · AJP Heart and Circulatory Physiology
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    ABSTRACT: Background: Arrhythmogenic ventricular cardiomyopathy (AVC) is a frequent underlying cause for arrhythmias and sudden cardiac death especially during intense exercise. The mechanisms involved remain largely unknown. Objective: To investigate how chronic endurance exercise contributes to desmoplakin (DSP) mutation-induced AVC pathogenesis. Methods: Transgenic mice with overexpression of desmoplakin, wild-type (Tg-DSP(WT)) or the R2834H mutant (Tg-DSP(R2834H)) along with control non-transgenic (NTg) littermates were kept sedentary or exposed to a daily running regimen for 12 weeks. Cardiac function and morphology were analyzed using echocardiography, electrocardiography, histology, immunohistochemistry, RNA and protein analysis. Results: At baseline, 4-week-old mice from all groups displayed normal cardiac function. When subjected to exercise, all mice retained normal cardiac function and left ventricular morphology; however, Tg-DSP(R2834H) mutants displayed right ventricular (RV) dilation and wall thinning, unlike NTg and Tg-DSP(WT). The Tg-DSP(R2834H) hearts demonstrated focal fat infiltrations in RV and cytoplasmic aggregations consisting of desmoplakin, plakoglobin and connexin43. These aggregates coincided with disruption of the intercalated disks, intermediate filaments and microtubules. Though Tg-DSP(R2834H) mice already displayed high levels of p-GSK3-β(Ser9) and p-AKT1(Ser473) under sedentary conditions, decrease of nuclear GSK3-β and AKT1 levels with reduced p-GSK3-β(Ser9), p-AKT1(Ser473), p-AKT1(Ser308) and loss of nuclear JUP was apparent after exercise. In contrast, Tg-DSP(WT) showed up-regulation of p-AKT1(Ser473), p-AKT1(Ser308) and p-GSK3-β(Ser9) in response to exercise. Conclusions: Our data suggest that endurance exercise accelerates AVC pathogenesis in Tg-DSP(R2834H) mice and this event is associated with perturbed AKT1 and GSK3-β signaling. Our study suggests a potential mechanism-based approach to exercise management in patients with AVC.
    No preview · Article · Nov 2015 · AJP Heart and Circulatory Physiology