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1 Laboratory for Physiology, Institute for Cardiovascular Research, Vrije Universiteit University Medical Center, Amsterdam 1081 BT, The Netherlands; and 2 Department of Physiology and Medicine, University of Antwerp, Antwerp 2020, Belgium
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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An increase in coronary perfusion, transversal stretch of the myocardium, increases developed force (Fdev) (Gregg effect) through activation of stretch-activated ion channels (SACs). Lengthening of the muscle, longitudinal stretch of the myocardium, causes an immediate increase in Fdev followed by a slow Fdev increase (Anrep effect). In isometrically contracting perfused papillary muscles of Wistar rats, we investigated whether both effects were based on similar stretch-induced mechanisms by measuring Fdev and intracellular Ca2+ concentration ([Ca2+]i) after a muscle length increase from 85% to 95% Lmax (length at which maximal isometric force develops) at low and high coronary perfusion before and after inhibition of SACs with gadolinium (10 µmol/l Gd3+). The increase of Fdev and peak [Ca2+]i by the Gregg effect was of similar magnitude as the Anrep effect (from 3.5 ± 0.8 to 3.9 ± 1.2 mN/mm2 and from 3.0 ± 0.7% to 3.8 ± 0.9% normalized [Ca2+]i, means ± SE). SAC blockade completely blunted the increase of Fdev and peak [Ca2+]i by the Gregg effect; however, it did not affect the Anrep effect. The slow force response, but not the calcium response, was augmented by an increase in coronary perfusion. Therefore, increased coronary perfusion, transversal stretch of the myocardium, and muscle lengthening, longitudinal stretch of the myocardium, increase myocardial contraction in the rat through different stretch-triggered mechanisms.
myocardial stretch; papillary muscles; gadolinium; streptomycin; stretch-activated ion channels
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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INCREASED CORONARY PERFUSION induces a slow increase of myocardial contraction, which is known as the Gregg effect (1, 7, 14, 15, 17, 19, 22, 39). Recently, we showed in perfused rat papillary muscle that the increase in coronary perfusion, which is accompanied by an increase in muscle diameter, was initiated by activation of Gd3+-sensitive stretch-activated ion channels (SACs) (31), suggesting that transversal stretch (deformation) of the myocardium is fundamental for the Gregg effect.
Increased diastolic filling of the heart results via the Frank-Starling mechanism in an immediate increase in myocardial contraction to elevate cardiac output and eventually match venous return (38). Subsequently, myocardial contraction increases slowly, which is known as the Anrep effect (44). In vitro, this biphasic response to longitudinal stretch of the myocardium was first shown by Parmley and Chuck (34). The first, rapid increase in force is related to an increase of responsiveness of the myofilaments for internal calcium (2). The second, slower force response has been attributed to a slow rise of intracellular Ca2+ concentration ([Ca2+]i) (3). In rat and cat papillary muscles, the Anrep effect was triggered by stretch-sensitive but endothelium-independent angiotensin II-induced endothelin-1 release, which results in a subsequent rise of [Ca2+]i and cardiac contraction (4, 13, 35). In contrast, it was shown in ferret papillary muscles (12) that angiotensin II was not a prerequisite for the slow force response, whereas the endocardial endothelium played a pivotal role in the Anrep effect. Recently, in isolated rat cardiomyocytes, it has been suggested that endogenous nitric oxide mediates the stretch-induced Ca2+ increase (36). It is unclear how longitudinal stretch by increase of muscle length is sensed by the multicellular myocardium; SACs, cytoskeleton effects, or other mechanisms have been suggested (4, 25).
Because myocardial stretch seems to be at the basis of both the Anrep and Gregg effects, it was investigated whether both effects were based on similar stretch-induced mechanisms. Therefore, isometric twitches and [Ca2+]i were measured after a muscle length increase from 85% to 95% Lmax (length at which maximal isometric force develops) at low and high coronary perfusion of perfused rat papillary muscles before and after SAC blockade with Gd3+.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Preparation. All animals were treated according to the guidelines of the Animal Experimental Committee of Vrije Universiteit of Amsterdam, The Netherlands. Under ether anesthesia, the hearts of 21 male Wistar rats (weighing 300-400 g) were rapidly removed and perfused via the aorta with a crystalloid solution (see below for solution composition). To prevent contraction of the heart, the Ca2+ concentration was kept at 0.5 mmol/l, and 25 mmol/l 2,3-butanedione monoxime was added. A papillary muscle with part of the septum and septal artery was removed from the right ventricle and superfused in the experimental bath. The septum was clamped on a Perspex plate, and the muscle tendon was attached to a force transducer (type KG4, Scientific Instruments; Heidelberg, Germany), which was attached to a micrometer (type 350-521-30, Mitutoyo; Veenendaal, Holland) for length adjustments. The septal artery was cannulated using a glass cannula and connected to a pressurized reservoir through a pressure difference meter (type SCX01DN, Sensym) for flow measurements (39).
The bath (superfusion) and pressurized reservoir (perfusion) were filled with an identical crystalloid solution, which contained (in mmol/l) 120 NaCl, 4.9 KCl, 1.2 MgSO4, 1.8 NaH2PO4, 1 CaCl2, 10 glucose, 5 HEPES, 20 NaHCO3, 15 choline chloride, and 0.01 adenosine. The temperature was set at 27°C, and the solution was gassed with 95% O2-5% CO2 (pH 7.45). Muscles were stimulated via a pair of platinum electrodes at 0.2 Hz to obtain muscle isometric contractions. The passive force (Fpas; the force imposed on the resting muscle) and developed force (Fdev; difference between the total force produced during contraction and Fpas) of the isometric contractions were measured at 85% Lmax or as otherwise indicated.Experimental protocol. After being mounted, the contracting muscles were stabilized for 30 min, Lmax was determined, and perfusion of the muscle was verified (1, 39). A group of muscles (n = 8) was loaded simultaneously via bath (superfusion) and perfusion for 60 min with the cell-permeant AM form of the fluorescent intracellular Ca2+ indicator fura 2 (Molecular Probes F1221, final concentration 10 µmol/l) to measure [Ca2+]i transients. During fura 2 loading, superfusion was stopped, the electric stimulation was turned off, and the bath was bubbled with 95% O2-5% CO2. After 30 min of dye washout, during which electrical stimulation and superfusion were resumed, the experimental protocol was started. At first, the effect of a 10% increase in muscle length from 85% to 95% Lmax on force development was investigated at low perfusion pressure (Pperf; 10 cmH2O) (Anrep at low perfusion). After 10 min, muscle length was then returned to 85% Lmax and, when force was stable again, the effect of a change from low (10 cmH2O) to high (80 cmH2O) Pperf on force development was studied (Gregg effect at 85% Lmax). Finally, when force at high Pperf reached a stable value, muscle length was increased again from 85% to 95% Lmax (Anrep at high perfusion). Subsequently, the muscles were incubated for 30 min with 10 µmol/l gadolinium (III) chloride hexahydrate (Gd3+), a SAC blocker, and the entire protocol (Anrep at low perfusion, Gregg at 85% Lmax, and Anrep at high perfusion) was repeated in the presence of the SAC blocker. Because of technical reasons, the entire experimental protocol, as mentioned above, was not applied to all eight muscles, explaining the lower numbers of animals referred to in the data sets.
The 10% increase in muscle length from 85% to 95% Lmax was used because it reflects the physiological range in which cardiomyocytes contract in the heart and it is commonly used by others (4, 12, 26, 35) to investigate the Anrep effect. The minimal Pperf of 10 cmH2O was used because at lower Pperf the vasculature would collapse, resulting in endothelial damage, and thus affecting contractile state. Schouten et al. (39) showed that no hypoxic core is formed at these low flow conditions. The maximal Pperf of 80 cmH2O (~65 mmHg) was used because this reflects normal Pperf in the septal artery and it is the Pperf at which the increase in Fdev is maximal (18). Furthermore, at this Pperf, the Gregg effect was of comparable magnitude as the Anrep effect for a muscle length increase from 85 to 95% Lmax. Force, coronary flow, and muscle length were monitored continuously throughout the experiment. The fura 2 fluorescence signal was monitored at limited intervals of
5, 0, 5, 10, 45, 150, 250, 350, and 425 s after the start of the intervention to minimize photobleaching. The
ratio of fura 2 fluorescence at 520 nm after excitation at wavelengths
of 340 and 380 nm (acquisition rate of 66 Hz) was collected with a
photomultiplier (MPS20/21, Zeiss). In all experiments, the fura 2 signal was at least five times above the background level
(autofluorescence). Muscle diameter was measured in the central segment
of the muscle through a video analysis system by measuring the length
of a virtual marker, which was placed on the image of the muscle and
not at a fixed position on the muscle. Therefore, the measured muscle diameter changes during perfusion-induced changes reflect changes in
cross-sectional area (CSA; muscle volume), whereas muscle diameter changes during an increase in muscle length are not representative for
overall CSA.
To support that the Gd3+ effects were related to SACs, we
tested the experimental protocol in two additional groups of muscles. The first group (n = 7) was incubated for 30 min with
streptomycin (40 and 100 µmol/l), an antibiotic known to inhibit SACs
(20), and the second group was incubated for 30 min with a
L-type Ca2+ channel inhibitor, verapamil (0.1 µmol/l). In
both of these last groups, we did no fura 2-AM loading, which excluded
[Ca2+]i measurements.
Data analysis. Force (in mN/mm2) was normalized by dividing measured values by the muscle CSA (in mm2). For each muscle, the peak 340-to-380-nm ratio at the basal contraction (85% Lmax, low Pperf) was set to 1.00, and all other Ca2+ transients were normalized with respect to this value (normalized 340-to-380-nm ratio). The fluorescence signal was not converted to [Ca2+]i values with an in vivo calibration procedure because accurate reproducible calibration procedures without compartmentalization problems are difficult (41) and our primary interest was in the relative changes of [Ca2+]i at different muscle lengths and Pperf.
Statistical differences within each group of muscles were tested with a one- or two-way repeated-measures ANOVA followed by a Bonferroni or Dunnett's post hoc test. P < 0.05 was considered significant. All data are expressed as means ± SE.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Basal contractile properties.
Muscle length and mean CSAs at Lmax and low
Pperf were, respectively, 3.6 ± 0.4 mm and 0.32 ± 0.06 mm2 (means ± SE, n = 8). The
basal contractile properties at 85% Lmax and
low Pperf were not significantly affected by 10 µmol/l Gd3+ [Fdev: from 42.6 ± 6.8 to 38.4 ± 8.8 mN/mm2; Fpas: from 2.9 ± 0.9 to
2.6 ± 1.1 mN/mm2; maximal force rate of development
(+dF/dt): from 646 ± 109 to 540 ± 97 mN · mm
2 · s1; time from
stimulus to one-half relaxation (tHR): from
378 ± 27 to 382 ± 18 ms, respectively (n = 6)].
Anrep and Gregg effects.
The experimental conditions for Gregg and Anrep effects in the present
study were chosen to result in increases of Fdev of similar
magnitude. In Fig. 1,
the Gregg effect for an increase of coronary Pperf from 10 to 80 mmH2O and the Anrep effect for a muscle length
increase from 85% to 95% Lmax are compared for a representative muscle. Transversal myocardial stretch, induced by an
increase in coronary perfusion from 10 to 80 cmH2O at 85% Lmax (Gregg effect, Fig. 1A),
resulted in an increase in force, which was accompanied by an increase
in muscle diameter of 10.8 ± 2.0% (P < 0.05).
Longitudinal myocardial stretch, induced by increasing muscle length
from 85% to 95% Lmax at low perfusion, caused
a biphasic increase in force (Fig. 1B). The instantaneous fast force response was followed by a slow rise of force lasting several minutes (slow force response, Anrep effect), which, in the
present experimental conditions, was of similar magnitude as the Gregg
effect.
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Anrep effect at high coronary perfusion. The average increase of Fdev and peak [Ca2+]i during the Anrep effect at high Pperf is shown in Fig. 2C before and after the addition of Gd3+. In the steady state, the amplitude of the slow force response at high Pperf was significantly increased compared with the slow force response at low Pperf (9.2 ± 1.2 vs. 3.9 ± 1.2 mN/mm2, n = 6, P < 0.05, respectively). The time course of the force increase at high and low Pperf was similar, with time constants of 255 ± 108 and 178 ± 83 s, respectively (P > 0.05, n = 6). After SAC blockade with Gd3+, the slow force response at high Pperf returned to values found at low Pperf, i.e., 3.8 ± 0.6 vs. 3.9 ± 1.2 mN/mm2, respectively (P > 0.05, n = 6). The increase in the peak [Ca2+]i signal for an increase of muscle length was not dependent on perfusion and was not affected by Gd3+.
Fast force response.
The instantaneous fast force response after myocardial stretch is seen
as an immediate increase of Fpas and Fdev (Fig.
1A). Averaged data of the absolute increase of
Fdev and peak [Ca2+]i during the
fast force response at low and high Pperf are shown in Fig.
3 before and after the addition of
Gd3+. The fast force response was not accompanied by a
change in peak [Ca2+]i and neither
Fdev nor peak [Ca2+]i are
affected by Gd3+ or by an increase of coronary
Pperf.
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Gregg effect at different muscle lengths.
Figure 4 shows the increase of
Fdev after an increase from low to high Pperf
at 85% and 95% Lmax. The time course of the
monophasic increase of Fdev at 85%
Lmax was significantly slower than at 95%
Lmax. In the latter group, increased perfusion
resulted in a rapid increase of Fdev, which after
20-25 s declined to a steady-state value after 125 s. At the
higher muscle length, the maximal increase in Fdev was
larger than at the lower muscle length (8.7 ± 2.3 and 1.3 ± 0.6 mN/mm2, respectively, P < 0.05),
whereas steady-state effects were similar (5.4 ± 2.4 and 3.6 ± 0.7 mN/mm2, respectively, P > 0.05).
The addition of Gd3+ completely blunted the Gregg effect at
both muscle lengths (data not shown).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The experimental conditions in the present study were chosen to obtain Gregg and Anrep effects on myocardial contraction of similar magnitude. Although both effects were accompanied by a similar increase of peak [Ca2+]i, the time course with which Fdev and peak [Ca2+]i increased was different. The slow increase of Fdev during the Gregg effect was accompanied by a rapid but transient increase of peak [Ca2+]i. The slow increase of Fdev during the Anrep effect was accompanied by a slow increase of peak [Ca2+]i with a similar time course. Furthermore, whereas the increase of Fdev and peak [Ca2+]i during the Gregg effect were blunted completely by Gd3+, the inhibitor of SACs was ineffective during the Anrep effect. Therefore, our study suggests that increased coronary perfusion, transversal stretch of the myocardium (Gregg effect), and muscle lengthening, longitudinal stretch of the myocardium (Anrep effect), both induce an increase in myocardial contraction but through different stretch-triggered mechanisms.
Gregg effect. The increase of Fdev, which results from a change from low to high Pperf (Gregg effect), has been reported several times in literature (1, 14, 15, 17, 18, 39). Recently, we showed in perfused rat papillary muscle that the Gregg effect, which is accompanied by an increase in muscle diameter (transversal stretch), was initiated by activation of Gd3+-sensitive SACs (31). The [Ca2+]i measurements of this study reveal new information on the mechanism behind the Gregg effect. An increase in Pperf results in an immediate and transient increase in peak [Ca2+]i, which is inhibited by SAC blockade without affecting diastolic [Ca2+]i. The perfusion-induced increase in peak [Ca2+]i returns to basal values after ~2 min, probably due to adaptation of the SACs (8, 21, 37). The immediate, yet transient, perfusion-induced increase in peak [Ca2+]i implies an important role for the influx of Ca2+ as a potential trigger for the Gregg effect and also indicates that after the increase in [Ca2+]i, another Gd3+- and Ca2+-sensitive positive inotropic mechanism is active.
The Gregg effect has been suggested to be related to the "garden hose" effect, a better overlap of the actin and myosin filaments of the cardiomyocytes, resulting via the Frank-Starling mechanism in increased force development (5, 28). However, the present study shows that the initial perfusion-induced increase in force is related to a Gd3+-sensitive increase in [Ca2+]i via SACs and is not related to an initial higher sensitivity of the myofilaments for calcium. Also, previous studies at our laboratory (39) have shown that in the isolated perfused papillary muscle of the rat, a change in muscle length (the garden hose effect) does not occur with increased perfusion and thus cannot explain the Gregg effect. The exact location of SACs in papillary muscle preparations was not investigated in the present study. From the literature, it is known that SACs could be located on the sarcolemma or t-tubular system of the cardiomyocytes (45); however, SACs have also been found on the vascular (33) or endocardial (24, 27) endothelium. Dijkman et al. (16-18) showed that perfusion-induced changes in contractility were related to capillary perfusion, excluding a location on arterial endothelium. Thus the literature excludes smooth muscle cells, endocardial endothelium, and arterial endothelium, but not capillary endothelium or cardiomyocytes, as a location for SACs mediating the Gregg effect. Therefore, further studies are required to show whether the activated SACs during the Gregg effect are located on capillary endothelial cells, cardiomyocytes, or both. Gadolinium (Gd3+) is considered a nonspecific blocker of SACs due to its inhibitory effects on L-type Ca2+ channels (30). Recently, we (32) showed that nonspecific effects of Gd3+ were dependent on the experimental conditions used. Another SAC blocker, streptomycin (20), inhibited the Gregg effect also, whereas the L-type Ca2+ channel inhibitor verapamil had no effect on the Gregg effect. Therefore, it was concluded that in our experimental conditions, the effects of Gd3+ on the Gregg effect were via inhibition of SACs.Anrep effect. Parmley and Chuck (34) were the first to show that an increase of muscle length and longitudinal myocardial stretch of isolated papillary muscles resulted in biphasic force responses, i.e., a rapid increase followed by a slow increase lasting several minutes.
The first phase has been related to an increase in calcium sensitivity of the myofilaments (2) but no change of [Ca2+]i (2, 6, 26). In the present experiments, the fast force response was indeed not accompanied by increased peak [Ca2+]i. Furthermore, neither addition of Gd3+ nor an increase of Pperf affected the fast force response. The second phase, the slow force response, seems to result from a slow rise in [Ca2+]i, supporting the data reported by Allen and Kurihara (3). Stretching of isolated single cardiomyocytes led to an increase in [Ca2+]i via SACs in the guinea pig (11), chick (40), and neonatal rat (42). Because the increase of [Ca2+]i to myocardial stretch occurred during systole and not diastole, the involvement of SACs in the slow force response in muscle preparations was criticized by Kentish and Wrzosek (26) and Hongo et al. (23). Recently, it was indicated that it was unlikely that SACs mediated the stretch-dependent augmentation of Ca2+ spark frequency in isolated cardiomyocytes (36). However, stretch could lead to elevated intracellular Na+ concentration ([Na+]i) via inward Na+ current through SACs and a subsequent rise of [Ca2+]i via the Na+/Ca2+ exchanger, as suggested for cultured chick embryo heart cells and adult guinea pig myocytes (10). Recently, it has been shown that the Na+/Ca2+ exchanger was involved in the Anrep effect (35). Myocardial stretch by lengthening in cat and rat papillary muscles triggers angiotensin II-induced endothelin-1 release, activating the Na+/H+ exchanger and resulting in increased [Na+]i and a subsequent increase in [Ca2+]i. Several observations in our experiments suggest that SACs are not involved in the Anrep effect: 1) blockade of SACs with Gd3+ or streptomycin did not affect the slow force response; 2) the accompanying increase of peak [Ca2+]i was not affected by Gd3+; 3) increased force and peak [Ca2+]i were not accompanied by a change in diastolic [Ca2+]i (23); and 4) the time course of the increase of peak [Ca2+]i is too slow to be caused by activation of stretch-induced inward cation currents via SACs, which are normally activated within 10 ms in rat ventricular myocytes (9, 45). Our results show that both SAC inhibitors, gadolinium and streptomycin, do not affect the Anrep effect, whereas they completely blunt the Gregg effect; the Gregg effect, therefore, does not contribute to the observed Anrep effect, either positively or negatively.Anrep effect at high perfusion. At high Pperf, myocardial stretch by lengthening the muscle resulted in an augmented slow force response, which returned to low Pperf force values after the addition of Gd3+. The increase of peak [Ca2+]i was, however, similar at low and high perfusion. Therefore, it is suggested that muscle lengthening at high perfusion increased Fdev via the Anrep effect on top of the Gregg effect. Because the immediate SACs-sensitive influx of Ca2+ at the onset of the Gregg effect is transient, the [Ca2+]i elevation of the Anrep effect is similar at low and high perfusion. In the steady state, the Gregg effect results in increased sensitivity of the myofilaments for calcium (Fig. 2B). Together with the Anrep-induced slow [Ca2+]i elevation, this leads to an augmented Anrep effect at high perfusion. That the Anrep and Gregg effects are additive (and not synergistic) suggests further that both effects are based on different stretch-triggered mechanisms. The addition of Gd3+ to inhibit SACs prevents the perfusion trigger, the subsequent increase of Ca2+ sensitivity, and the Gregg effect, so that the augmented Anrep effect at high perfusion returns to the normal Anrep effect at low perfusion.
That the Anrep effect after myocardial stretch is augmented at higher coronary Pperf is supported by studies in intact canine hearts (43). In these studies, an increase in left ventricular volume with constant coronary Pperf resulted in a secondary rise in developed pressure. Repeating this left ventricular volume increase with reduced coronary perfusion resulted in a smaller secondary rise of developed pressure.Gregg effect at different muscle lengths. In the present study, we did not investigate the perfusion-induced changes of Fdev at different muscle lengths in detail. When Gregg effects were compared at 85% and 95% Lmax, the time course and maximal magnitude of the Gregg effect seemed to be dependent on the initial muscle length (Fig. 4). At higher muscle lengths, the immediate increase of Fdev to increased Pperf was larger than at lower muscle lengths. The increased immediate Gregg effect at longer muscle lengths could be related to a length-dependent increase of calcium sensitivity (2) or to increased activation of SACs at longer lengths (29). In the steady state, finally, when [Ca2+]i transients are back at their basal level, the Gregg effect was independent of muscle length.
Because muscle fibers and the vasculature are aligned mostly in parallel in papillary muscles, an increase of coronary perfusion deforms the muscle perpendicularly to the alignment of the myofilaments (transversal stretch) through an increase in vasculature diameter, which is reflected in increase in muscle diameter (31); this appears to activate SACs, initially increasing Ca2+ influx, followed by increased Ca2+ sensitivity, which increases cardiac contraction. Myocardial stretch via lengthening of the muscle results mainly in fiber lengthening, which stretches the muscle longitudinally and which activates Ca2+ influx, not via SACs or L-type Ca2+channels but likely via endothelin-1 release and activation of Na+/H+ exchanger (4, 35) and/or via endogenous nitric oxide mechanisms (36). We conclude that myocardial stretch, via increased coronary Pperf (transversal myocardial stretch, Gregg effect) and via an increase of muscle length (longitudinal myocardial stretch, Anrep effect), both induce an increase in myocardial contraction but through different stretch-triggered mechanisms.| |
ACKNOWLEDGEMENTS |
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The study was supported by The Netherlands Heart Foundation Grant 96-024.
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FOOTNOTES |
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Address for reprint requests and other correspondence: R. R. Lamberts, Laboratory for Physiology, VU Univ. Medical Center, Van der Boechorststraat 7, Amsterdam 1081 BT, The Netherlands (E-mail: lamberts{at}physiol.med.vu.nl).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
May 23, 2002;10.1152/ajpheart.00113.2002
Received 12 February 2002; accepted in final form 20 May 2002.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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