A Role for the Renin‐Angiotensin System in the Evolution of Cardiac Memory

Ricard, Philippe; Dantlo, Peter; Cohen, Ira S.; Burkhofe, Daniel; Rosen, Michael R.

doi:10.1111/j.1540-8167.1999.tb00711.x

Cited by 59 publications

(43 citation statements)

References 14 publications

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“…Although we had previously shown that ACE inhibition or angiotensin II receptor blockade suppresses short-term CM induced by Ϸ2 hours of pacing, 7 we have now found that ACE inhibition (trandolapril) and AT 1 receptor blockade (candesartan) do not suppress long-term CM. These results suggest that modulation of calcium handling may be important in initiating and sustaining CM and that angiotensin II is involved in initiation but not sustenance.…”

Section: Discussionmentioning

confidence: 88%

“…6 However, the elevated plateau and prolonged action potential duration (APD) of epicardial and endocardial myocytes in CM are not readily explained by I to changes alone. Moreover, angiotensin II, the synthesis of which in heart cells accompanies the altered stress/strain patterns imposed by ventricular pacing, seems to be involved in initiating CM, 7 perhaps by suppressing I to . 8 The cellular responses to repeated ventricular stimulation that characterize CM have a parallel in neurons.…”

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confidence: 99%

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Role of L-Type Calcium Channels in Pacing-Induced Short-Term and Long-Term Cardiac Memory in Canine Heart

Plotnikov

Geller

et al. 2003

Circulation

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Background-We tested the hypothesis that I Ca,L is important to the development of cardiac memory. Methods and Results-The effects of L-type Ca 2ϩ channel blockade and ␤-blockade were tested on acutely anesthetized and on chronically instrumented, conscious dogs. Short-term memory (STM) was induced by 2 hours of ventricular pacing and long-term memory (LTM) by ventricular pacing for 21 days. STM dogs received placebo, nifedipine, or propranolol, and LTM dogs received placebo, atenolol, or amlodipine. AT 1 receptor blockade (candesartan) and ACE inhibition (trandolapril) were also tested in LTM. Microelectrodes were used to record transmembrane potentials from isolated epicardial and endocardial slabs using a protocol simulating STM in intact animals. Left ventricular epicardial myocytes from LTM or sham control dogs were dissociated, and I Ca,L was recorded (whole-cell patch-clamp technique). Evolution of STM and LTM was attenuated by I Ca,L blockers but not ␤-blockers. Neither AT 1 receptor blockade nor ACE inhibition suppressed LTM. In microelectrode experiments, pacing induced an epicardial-endocardial gradient change mimicking STM that was suppressed by nifedipine. In patch-clamp experiments, peak I Ca,L density in LTM and control were equivalent, but activation was more positive and time constants of inactivation longer in LTM (PϽ0.05). Conclusions-I Ca,L blockade but not ␤-adrenergic blockade suppresses cardiac memory. LTM evolution is unaffected by angiotensin II blockade and is associated with altered I

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Section: Discussionmentioning

confidence: 88%

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confidence: 99%

Role of L-Type Calcium Channels in Pacing-Induced Short-Term and Long-Term Cardiac Memory in Canine Heart

Plotnikov

Geller

et al. 2003

Circulation

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“…In the ventricle, the changed stress-strain relationships induced by altered pathways of activation induce memory that is prevented by interfering with angiotensin II synthesis or binding. 21 Sadoshima et al 22 demonstrated that cardiac cell cultures exposed to altered stress/strain synthesize increased angiotensin II. Given these results, we propose that when the site of atrial impulse initiation is altered, the changed stress-strain relationships would initiate a similar signal transduction pathway.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Memory in Canine Atrium

et al. 2001

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Background-Memory is a diverse biological phenomenon whose importance in the ventricle has been demonstrated. We hypothesized its occurrence in the atrium, contributing to the modulation of cardiac rhythm. Methods and Results-We analyzed P and Ta waves in conscious chronically instrumented dogs with complete heart block. Animals were atrioventricularly sequentially paced at 5% greater than the sinus rate from the lateral right atrium (RA) during control, followed by 2 periods of 1-hour test pacing at 50% greater than the sinus rate, or by equivalent test pacing from the left atrial appendage (LAA) at 5% or 50% greater than the sinus rate. Recovery RA pacing periods of 20-and 30-minute duration, respectively, succeeded each test pacing period. RA test pacing at either rate did not affect the variables measured, but changing the pacing site from RA to LAA altered the P and Ta waves. Displacement of the spatial atrial gradient vector occurred during recovery from LAA pacing, was more marked at rapid pacing rates, and manifested accumulation and resolution consistent with cardiac memory. Concurrently, the right effective refractory period decreased. Conclusions-Memory is demonstrable in canine atrium, showing rapid onset, accumulation during successive pacing periods, and resolution on cessation of pacing. Given its association with a reduced effective refractory period, it may contribute to the substrate for atrial arrhythmias.

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“…Our work in progress 22,23 and the published literature 3,19,24 suggest that altered stress-strain relationships induced by ventricular pacing activate the endogenous cardiac renin-angiotensin II system; this protein kinase C-linked signaling cascade both alters channel phosphorylation (perhaps explaining the changes in I to in short-term memory) and induces the immediate early gene program, which alters new protein (channel) synthesis. Although we hypothesize that new gene expression and protein synthesis are involved in long-term memory, we do not know which genes are expressed and which new proteins are synthesized.…”

Section: Kinetics Of I Tomentioning

confidence: 99%

Transient Outward Current, I _to1 , Is Altered in Cardiac Memory

et al. 1999

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Background-Cardiac memory refers to an altered T-wave morphology induced by ventricular pacing or arrhythmias that persist for variable intervals after resumption of sinus rhythm. Methods and Results-We induced long-term cardiac memory (LTM) in conscious dogs by pacing the ventricles at 120 bpm for 3 weeks. ECGs were recorded daily for 1 hour, during which time pacing was discontinued. At terminal study, the heart was removed and the electrophysiology of left ventricular epicardial myocytes was investigated. Control (C) and LTM ECG did not differ, except for T-wave amplitude, which decreased from 0.12Ϯ0.18 to Ϫ0.34Ϯ0.21 mV (ϮSEM, PϽ0.05), and T-wave vector, which shifted from Ϫ37Ϯ12°to Ϫ143Ϯ4°(PϽ0.05). Epicardial action potentials revealed loss of the notch and lengthening of duration at 20 days (both PϽ0.05). Calcium-insensitive transient outward current (I to ) was investigated by whole-cell patch clamp. No difference in capacitance was seen in C and LTM myocytes. I to activated on membrane depolarization to Ϫ25Ϯ1 mV in C and Ϫ7Ϯ1 mV (PϽ0.05) in LTM myocytes, indicating a positive voltage shift of activation. I to density was reduced in LTM myocytes, and a decreased mRNA level for Kv4.3 was observed. Recovery of I to from inactivation was significantly prolonged: it was 531Ϯ80 ms (nϭ10) in LTM and 27Ϯ6 ms (nϭ9) in C (PϽ0.05) at Ϫ65 mV. Conclusions-I to changes are associated with and can provide at least a partial explanation for action-potential and T-wave changes occurring with LTM. (Circulation. 1999;99:1898-1905.)

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A Role for the Renin‐Angiotensin System in the Evolution of Cardiac Memory

Cited by 59 publications

References 14 publications

Role of L-Type Calcium Channels in Pacing-Induced Short-Term and Long-Term Cardiac Memory in Canine Heart

Role of L-Type Calcium Channels in Pacing-Induced Short-Term and Long-Term Cardiac Memory in Canine Heart

Cardiac Memory in Canine Atrium

Transient Outward Current, I _to1 , Is Altered in Cardiac Memory

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A Role for the Renin‐Angiotensin System in the Evolution of Cardiac Memory

Cited by 59 publications

References 14 publications

Role of L-Type Calcium Channels in Pacing-Induced Short-Term and Long-Term Cardiac Memory in Canine Heart

Role of L-Type Calcium Channels in Pacing-Induced Short-Term and Long-Term Cardiac Memory in Canine Heart

Cardiac Memory in Canine Atrium

Transient Outward Current, I to1 , Is Altered in Cardiac Memory

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Transient Outward Current, I _to1 , Is Altered in Cardiac Memory