Myofibrillar ATPase activity in rat heart after chronic propranolol administration RUSSELL Department Oklahoma

T. DOWELL of Physiology City, Oklahoma

and Biophysics,

University

DOWELL, RUSSELL T. MyofibriUar ATPase activity in rat heart after chronic propranolol administration. Am. J. Physiol. 237(5): C195-C199, 1979 or Am. J. Physiol.: Cell Physiol. 6(3): C195-C199, 1979.-A previous study has shown that chronic chemical sympathectomy brought about by 6-hydroxydopamine injections results in a depression in myocardial contractile function which is accompanied by reduced myofibrillar ATPase activity. To determine whether chronic p-adrenergic receptor blockade elicits similar alterations in cardiac contractile-protein ATPase activity, adult rats were given twicedaily injections of propranolol 7 days/wk for 2 wk. Effective P-adrenergic receptor blockade was verified by the lack of hemodynamic responsiveness to isoproterenol infusion. Myofibrils were prepared from left ventricular tissue and analyzed for ATPase activity. Myofibrillar ATPase activity was 295 t 8 nmol Pi mg-l min-l in controls. Enzyme activity was not significantly different in propranolol-injected rats. The results demonstrate that chronic propranolol administration does not alter the ATPase activity of cardiac myofibrils. Therefore, it seems likely that the altered contractile-protein enzymatic properties resulting from chronic chemical sympathectomy do not occur as the result of a reduced level of cardiac /I-adrenergic receptor stimulation. l

of Oklahoma

Health

Sciences

Center,

73190

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panied by reduced myofibrillar ATPase activity. These experiments suggest that alterations in neural stimulation of the heart may alter contractile proteins in a manner analogous to skeletal muscle. However, it could not be determined from the chemical sympathectomy experiments whether alterations in heart contractile-protein enzymatic properties resulted from a) destruction of sympathetic nerves and/or nerve terminals, b) depletion of neurotransmitter from the sympathetic nerve endings, or c) a reduced level of cardiac P-adrenergic receptor stimulation. Therefore, the present studies were undertaken to a) determine whether chronic P-adrenergic receptor blockade elicits alterations in cardiac contractileprotein ATPase activity and b) further elucidate the mode of action by which heart contractile-protein enzymatic properties are mediated by sympathetic neural influences. METHODS

Animals and experimental treatment. Male SpragueDawley rats weighing 250-300 g were used in these experiments. Chronic P-adrenergic receptor blockade was contractile function; P-adrenergic receptor; left ventricle established in one group of rats. Rats in this group received an intraperitoneal injection of propranolol (20 mg/kg) twice daily, 7 days/wk for a 2-wk period. The A DIRECT RELATIONSHIP exists between skeletal muscle drug was prepared immediately prior to injection in contractile properties and the ATPase activity of con- physiologic saline. Injections were given in the early tractile proteins (2). Neural factors are known to modify morning and in the late afternoon so that propranolol skeletal muscle contractile function (4, 6, 14) via altera- was administered at 12- to 14-h intervals throughout the tions in contractile-protein ATPase activity (6, 14). Dra- 2-wk period. Control rats were given sham injections of matic demonstration of the neural control of skeletal physiologic saline according to the propranolol injection muscle contractile-protein properties is provided by schedule. cross-innervation experiments. When a fast-twitch musHemodynamic measurements and responses to isocle is denervated and subsequently reinnervated with proterenol infusion. Approximately 12-14 h after the final nerves from slow-twitch muscle, the twitch properties injection, rats were weighed, anesthetized with sodium and ATPase activity of the muscle assume the charac- pentobarbital(50 mg/kg ip), and placed on positive-presteristics of slow-twitch muscle (5, 23, 24). Conversely, sure ventilation (Harvard rodent respirator) with room slow-twitch muscle assumesfaster twitch properties and air via a tracheostomy. A jugular vein cannula was posiexhibits increased ATPase activity when reinnervated by tioned to allow intravenous infusion. A cannula was nerves from fast-twitch muscle (5, 16, 23, 24). inserted at the bifurcation of the abdominal aorta to Evidence is accumulating suggesting that the relationmonitor systemic blood pressure. The heart was exposed ship between cardiac muscle contractile properties and by midline sternotomy and left ventricular pressure was the ATPase activity of heart contractile proteins is sim- measured by puncturing the ventricle with a 20-gauge ilar to that seen in skeletal muscle. A previous study (9) needle attached directly to a Statham P37 miniature has shown that chronic chemical sympathectomy pressure transducer. Heart rate was determined continbrought about by 6-hydroxydopamine injections results uously with a cardiotachometer triggered by the left in a depression in myocardial contractile function accom- ventricular pressure pulse. The maximum rate of left 0363-6143/79/0000-0000$01.25

Copyright

0 1979 the American

Physiological

Society

Cl95

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Cl96 ventricular pressure development (dP/dt,,,) was derived with an analog differentiator. This measurement was used as an index of myocardial contractility. The frequency response characteristics of the pressure measurement system and functional stability and responsiveness of the preparation have been described previously (10). All hemodynamic measurements were recorded simultaneously on a Beckman Dynograph recorder. After initial hemodynamic measurements had been completed, the responsiveness of the cardiovascular system to isoproterenol was evaluated. Isoproterenol was prepared fresh in physiologic saline containing sodium metabisulfite, 50 pg/ml. Physiologic saline containing sodium metabisulfite was first infused via the jugular vein cannula at a rate of 0.15 ml/min for 3 min. The responses to 1 and 3 min of saline infusion were taken as control values. Isoproterenol (0.03 pg/min) then was given in an identical manner and hemodynamic responses were recorded at 1 and 3 min of infusion. After the preparation had returned to control levels (approx 5 min), the heart was excised and placed into a beaker in crushed ice. Tissue and myofibril preparation. Right and left atria were dissected from the heart, pooled into a single sample, and weighed. Extraneous tissue and the remaining great vessels were then removed from the base of the heart. The right ventricular free wall was dissected from the heart and weighed. The remaining left ventricle, including the interventricular septum, was weighed and frozen. Subsequently, purified myofibrils were prepared from left ventricular tissue using minor modifications of the method described by Zak et al. (26). Tissue was minced with scissors and homogenized in soZution I (250 mM sucrose, 5 mM EGTA, 5 mM MgC12, 75 mM KCl, pH 6.8) with a ground glass homogenizer. Following centrifugation, the precipitate was washed with soZution II (175 mM KCl, 5 mM EGTA, 5 mM MgClz, 0.1% Triton X-100, pH 6.8) using a Dounce homogenizer to solubilize and remove contaminating membranes. The detergent was removed from the pelleted myofibrils by further washes with soZution III (150 mM KCl, 5 mM EDTA, pH 7.0). Purified myofibrils were resuspended in 50 mM Tris buffer, pH 7.4, which contained 150 mM KCl. Protein concentration was measured by the biuret reaction (13) and subsequently adjusted to 6 mg/ml with TrisKC1 buffer. MyofibrilIar ATPase activity was measured in a reaction mixture containing (mM): 1 MgS04, 0.1 CaC12, 1 NazATP, 20 Tris, pH 7.4, and 1.2 mg myofibrillar protein in a final volume of 4.0 ml. Sodium azide (2 mM final concentration) was routinely added to inhibit possible contaminating mitochondrial ATPase activity. The reaction was initiated by substrate (ATP) addition. After 2 min incubation at 30°C the reaction was stopped with 1 ml 10% (wt/vol) trichloroacetic acid. Precipitated protein was removed by centrifugation and the supernatant was assayed for inorganic phosphate (Pi) by the method of Rockstein and Herron (19). Enzyme activity is expressed as nanomole Pi per milligram myofibrillar protein per minute. Because structurally different forms of contractile proteins exhibit differences in their enzymatic sensitivity to

R. T. DOWELL

salt (25), ATPase activity was determined in myofibrils from control and propranolol-treated hearts as outlined above with the exception that increased concentrations of KC1 were present in the assay mixture. Enzyme activity was measured at 7.5 (control), 50, 100, and 200 mM final KC1 concentrations. The relative decrease in ATPase activity was plotted versus KC1 concentration to evaluate possible structural alterations in myocardial contractile proteins resulting from chronic propranolol administration. StatisticaL methods. All experimental results were compared with appropriate control values by Student’s t analyses. Since each animal served as its own control infusion, these hemofor the responses to isoproterenol dynamic data were statistically evaluated using the Student paired t test. All other experimental results were camp-ared with appropriate control values by Student’s unpaired t test. A P value of 0.05 or less was considered statistically significant. RESULTS

Effects of experimental treatments on overall growth and heart weight. The body weights and heart weights of rats at the time they were killed are shown in Table 1. Chronic propranolol administration had no significant effect on normal overall growth pattern as indicated by nearly identical body weights in the sham-injected and propranolol-injected rats. Atrial, right ventricular, and left ventricular weights were not significantly different in the two groups of animals and uniform left ventricularto-body weight ratios were observed. The above results indicate that the experimental procedures used in the present study did not create disproportionate growth or atrophy in any of the several portions of the heart that were examined. Initial hemodynamic measurements and response- to isoproterenol infusion. Marked reductions in heart rate and dP/dt,,, were observed following chronic propran0101 administration (Table 2). In contrast, chronic p1. Weight measurements in sham-injected and propranolol-injected rats TABLE

Body

Sham (6) Propranolol

Wt, g

354tll 351t9

Atria,

mg

71t4 83~6

RV, mg

W

219t7 212t,8

708t25 673t35

LV/Body W mg/g

mg

2.OOt,O.O7 1.92t0.06

(7) Values are mean t SE. Number of rats in each group parentheses. RV, right ventricle; LV, left ventricle.

is given

in

2. Initial hemodynamic measurements from sham-injected and propranoloknjected rats TABLE

MAP, I-nI-nHg

Heart Rate, beats/min

117t7

llOt7

123t6

112t7

476-+6 424t5*

LVP, mn-miz

Sham (6) Propranolol

dWdcn,x, [email protected]/s

7,870+330 5,610+450*

(6) Values are mean it SE. Number of rats in each group is given in parentheses. LVP, left ventricular pressure; MAP, mean arterial pressure. * P < 0.01 compared to sham.

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HEART

ATPASE

AFTER

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adrenergic receptor blockade had no significant effect on either peak left ventricular pressure or mean arterial blood pressure (Table 2). The above hemodynamic results are consistent with the known pharmacological effects of propranolol. The hemodynamic measurements of responses to isoproterenol infusion are shown in Fig. 1. The infusion of drug vehicle at a rate comparable to that used for isoproterenol infusion served as a control for the drug responses. Saline infusion produced negligible hemodynamic effects when compared to initial hemodynamic measurements. In response to isoproterenol infusion, sham-injected rats exhibited appropriate and significant reductions in mean arterial blood pressure after 1 and 3 min of drug administration. Significant heart rate and dP/dtmaX increases after isoproterenol infusion illustrate the appropriate chronotropic and inotropic responsiveness of the sham-injected rats. Infusing 0.03 pg/min of isoproterenol for 3 min elicited near maximal hemodynamic responses in sham-injected rats. In contrast to the sham-injected rats, animals that had received propran0101 injections exhibited no significant alteration in mean arterial blood pressure after 1 and 3 min of isoproterenol infusion. Isoproterenol infusion was equally ineffective in influencing either heart rate or dP/dt,,, in propranololinjected rats. Taken together, the initial hemodynamic and isoproterenol infusion response results seen in propranolol-inISOPROTERENOL 130 r

MAP,

CONTROL

3 M+lN.

1 MIN.

*

mmHg

500 480 440 420 400 0

MAX

dP/dt,

mmHgig

F

CONTROL

3 MIN.

1 MIN.

ISOPROTERENOL 0

n

SHAM (6) PROPRANOLOL

Myofibrillar Protein, mg/g

Sham (6) Propranolol Values are means in parentheses.

44 k 2 46 t 1

(7) t SE. The

ATPase, mg-’

number

l

IUIIO~ Pi* min-’

295 t 8 281 k 7

of rats in each group

-

SHAM

is given

(6)

w -0 PROPRANOLOL

(7)

\\\ I! mM

Final

[KCI]

FIG. 2. Enzymatic (ATPase) salt sensitivity of left ventricular myofibrils from sham-injected and propranolol-injected rats. Bars through data points indicate 1 standard error of the mean; the number of rats in each group given in parentheses. Enzyme activity measured under conditions was considered control (100%) optimum (7.5 mM final [KCl]) activity for each determination.

1 13’

460

HEART RATE, bPm

TABLE 3. Left ventricular myofibril yield and ATPase activity from sham-injected and propranolol-injected rats

(6)

FIG. 1. Hemodynamic measurements obtained from sham-injected and propranolol-injected rats in response to isoproterenol infusion. Bars indicate means t SE; the number of rats in each group given in parentheses. MAP, mean arterial pressure. * P < 0.05 vs. control conditions by paired t test. t P < 0.01 vs. sham-injected by unpaired t test.

jetted rats demonstrate the efficacy of both peripheral and cardiac P-adrenergic receptor blockade. Furthermore, all hemodynamic measurements in propranololinjected rats were made approximately 12-14 h after the final drug injection. The presence of effective P-adrenergic receptor blockade at the time when an additional daily injection of propranolol would have been given indicates that a chronic state of P-adrenergic receptor blockade had been achieved during the previous 2 wk of drug treatment. Myofibrillar ATPase activity. The contractile protein results are given in Table 3. Myofibrillar protein yield was not significantly different in left ventricular tissue obtained from sham-injected and propranolol-injected rats. When measured under optimum conditions in the presence of 7.5 mM KCl, nearly identical myofibrillar ATPase activity was detected in both groups of animals. Myofibrils from sham-injected rat left ventricles maintained nearly 100% of control enzymatic activity in the presence of 50 mM KCl; however, enzyme activity was reduced to approximately 80% and 15% of control activity in the presence of 100 and 200 mM KCI, respectively (Fig. 2). No significant contractile-protein structural alterations were apparent in myofibrils from propranololinjected rat left ventricles as indicated by their enzymatic salt sensitivity (Fig. 2). DISCUSSION

A previous study (9) was conducted to determine whether alterations in neural stimulation of the heart

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Cl98 bring about changes in myocardial contractile function that are paralleled by changes in contractile-protein enzymatic (ATPase) activity. Chronic chemical sympathectomy was established in adult male rats by intravenous administration of 6-hydroxydopamine. After 2 wk of sustained sympathectomy, a marked reduction of myocardial contractile function was observed and this response was accompanied by reduced myofibrillar ATPase activity. Acute (16-18 h) chemical sympathectomy depressed myocardial contractile function without altering myofibrillar ATPase activity. The above experiments demonstrated that heart contractile-protein enzymatic properties can be altered by sympathetic neural influences. In general, a positive relationship seems to exist between the enzymatic properties of cardiac contractile proteins and myocardial contractile function; however, it is clear that these properties need not be altered in parallel. Furthermore, the time-dependent nature of the contractile-protein responses presented the possibility that structurally different myocardial contractile protein(s) with altered enzymatic properties may have been synthesized. Direct neural control of contractile-protein enzymatic properties is now a well-established principle for skeletal muscle. Following denervation, skeletal muscle myofibrillar ATPase activity is reduced (14, 20). Crossinnervation experiments have shown that when fasttwitch skeletal muscle is denervated and subsequently reinnervated with nerves from slow-twitch muscle, the ATPase activity of the muscle assumes the characteristics of slow-twitch muscle (5, 23, 24). Conversely, denervated slow-twitch muscle shows increased ATPase activity when reinnervated by nerves from fast-twitch muscle (5, 16, 23, 24). That there are altered ATPase activities of denervated and cross-innervated skeletal muscles suggests that there is synthesis of contractile proteins with altered enzymatic properties. The similar contractile protein responses observed in chronically sympathectomized hearts and denervated skeletal muscles present the possibility that neural control of contractile protein enzymatic properties may be effected by similar mechanisms in both tissues. Although chronic chemical sympathectomy with 6-hydroxydopamine will produce demonstrable effects on cardiac contractile protein enzymatic activity, the action of this compound on the sympathetic nervous system requires consideration when attempting to interpret the mechanism by which this contractile protein effect is elicited. Treatment with 6-hydroxydopamine specifically destroys adrenergic nerve endings (7,21,22). Endogenous myocardial norepinephrine levels are reduced by more than 90% within 5 h of a single 6-hydroxydopamine injection and weekly drug treatment maintains a chronic low level of myocardial adrenergic transmitter (8). Therefore, depletion of norepinephrine from sympathetic nerve endings would represent one potential mechanism for altering cardiac contractile protein. This mechanism may be an indirect response mediated by changes in cardiac muscle loading conditions. Because 6-hydroxydopamine destroys adrenergic nerve endings, it seems likely that the release of trophic protein substances from the adrenergic neuron would also be compromised. It is well established that certain trophic protein substances are

R. T. DOWELL

synthesized within the cell body of neurons and transported via the nerve axon to nerve terminals for subsequent release (3, 17, 18). Trophic substances released from nerve terminals are thought to be important for the prevention of changes generally associated with skele tal muscle denervation ( 1, 15). Moreover, the release of trophic substances may be coupled to the release of neurotransmitter such that the interaction of these two materials may mutually facilitate access to the muscle cell and, in this way, regulate contractile protein synthesis via the muscle cell genome (12). A final possibility involves the action of cardiac sympathetic neurotransmitter at the target tissue. Norepinephrine released from sympa thetic nerve endings interacts with the cardiac padrenergic receptor to produce its characteristic chronotropic and inotropic effects. Depletion of norepinephrine from adrenergic nerve endings by the action of 6hydroxydopamine would result in a chronically reduced level of cardiac P-adrenergic receptor stimulation. The present study was designed to evaluate the latter possibility, i.e., that a reduced level of cardiac P-adrenergic receptor stimulation results in altered heart contractile-protein enzymatic properties. Twice-daily propran0101 injections were effective in establishing chronic padrenergic receptor blockade in view of the marked reductions in heart rate and dP/dt,,, that were observed in propranolol-injected rats. The complete lack of hemodynamic responsiveness to isoproterenol infusion in propranolol-injected rats provides additional evidence for the successful establishment of chronic P-adrenergic receptor blockade in these animals. Despite the fact that the cardiac P-receptors were effectively blocked for a period of time (2 wk)-which has previously been shown to influence myocardial contractile proteins in 6-hydroxydopamine treated rats- no alteration was detected in the ATPase activity of cardiac myofibrils from propranolol-injected rats. In addition, the relative enzymatic sensitivity to increased concentrations of KC1 was not significantly different in myofibrils from sham-injected and propranolol-injected rats. Structurally different forms of contractile proteins exhibit differences in their enzymatic sensitivity to KC1 (25). Experiments using the salt sensitivity procedures described in the present study have shown that rat fast-twitch skeletal muscle (tibialis anterior) myofibrillar ATPase activity (approx 750 nmol mg-l min-l) remains near 100% of control values when measured in the presence of 100 mM KCl. Rat left ventricular myofibrillar ATPase activity (approx 300 nmol mg-l l rein-‘) is reduced to approximately 80% of control (Fig. 2) while dog left ventricular myofibrillar ATPase activity (approx 200 nmol mg-’ min-‘) is reduced to approximately 60% of control (11) when measured in the presence of 100 mM KCl. Mixtures containing various proportions of rat fast-twitch skeletal muscle myofibrils and rat left ventricular myofibrils indicate that a lo-15% alteration in enzymatic properties can be easily detected by the salt sensitivity response. Therefore, it seems unlikely that relatively small changes in myocardial contractile-protein enzymatic activity brought about by chronic P-adrenergic blockade would remain undetected by the procedures utilized in the present study. From the results of the present study, it can be conl

l

l

l

l

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HEART

ATPASE

AFTER

CHRONIC

Cl99

PROPRANOLOL

eluded that chronic P-adrenergic receptor blockade does not alter the ATPase activity of cardiac myofibrils. Therefore, it seems likely that the altered contractileprotein enzymatic properties resulting from chronic chemical sympathectomy do not occur as the result of a reduced level of cardiac P-adrenergic receptor stimulation. This does not mean that the enzymatic properties of heart contractile proteins cannot be influenced by the presence or absence *of neurotransmitter or the relative amount of norepinephrine released from neuronal endings, but rather that norepinephrine does not seem to exert its influence in this regard directly via the cardiac P-receptor. Chronic propranolol treatment would not be expected to disrupt the integrity of the sympathetic nerve or nerve terminal. Normal amounts of norepinephrine should be present in the sympathetic nerve endings and the relea se of neurotransmitter and trophic substances from the neuronal endings should not be impaired. Thus,

the absence of normal amounts of neurotransmitter, trophic substances, or both may represent the critical factor(s) responsible for the reduced cardiac myofibrillar ATPase activity associated with chronic chemical sympathectomy. Although the results of the present study do not allow any conclusions to be drawn regarding the exact mechanism by which chronic chemical sympathectomy influences myocardial contractile-protein properties, it is clear that chronic propranolol administration does not alter the enzymatic activity of cardiac myofibrils. The expert technical assistance of Judith Haithcoat is gratefully acknowledged. This research was supported, in part, by National Institutes of Health Grants HL-16352, HL-23025, and HL-23206 and a grant from the American Heart Association. Received

11 December

1978; accepted

in final

form

11 June

1979.

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denervation. Exp. NeuroZ. 36: 488-497, 1972. 15. HOFFMAN, W. W., AND S. THESLOFF. Studies on the trophic influence of nerve on skeletal muscle. Eur. J. Pharmacol. 20: 256-260, 1972. 16. JEAN, D. H., L. GUTH, AND R. W. ALBERS. Neural regulation of the structure of myosin. Exp. NeuroZ. 38: 458-471, 1973. 17. KORR, I. M., P. N. WILKINSON, AND F. W. CHORNOCK. Axonal delivery of neuroplasmic components to muscle cells. Science 153: 342-345, 1967. 18. OCHS, S. Fast transport of materials in mammalian nerve fibers. Science 176: 252-260, 1972. 19. ROCKSTEIN, M., AND P. W. HERRON. Calorimetric determination of inorganic phosphate in microgram quantities. AnaZ. Chem. 23: 1500, 1951. 20. SYROVY, I., E. GUTMANN, AND J. MELICHNA. The effect of denervation on contractile and myosin properties of fast and slow rabbit and cat muscles. PhysioZ. BohemosZov. 21: 353-359, 1972. 21. THOENEN, H., AND J. R. TRANZER. Chemical sympathectomy by selective destruction of adrenergic nerve endings with 6-hydroxydopamine. Naunyn Schmiedebergs Arch. PharmokoZ. Exp. PathoZ. 261: 271-288, 1968. 22. TRANZER, J. R., AND H. THOENEN. Electron microscopic study of selective acute degeneration of sympathetic nerve terminals after administration of 6-hydroxydopamine. Experientia 24: 155-156, 1968. 23. WEEDS, A. G., AND K. BURRIDGE. Myosin from cross-innervated cat muscles: evidence for reciprocal transformation of heavy chains. FEBS Lett. 57: 203-208, 1975. 24. WEEDS, A. G., D. R. TRENTHAM, C. J. C. KEAN, AND A. J. BULLER. Myosin from cross-innervated cat muscle. Nature London 247: 135139, 1974. 25. YAZAKI, Y., AND M. S. RABEN. Cardiac myosin adenosinetriphosphatase of rat and mouse. Distinctive enzymatic properties compared with rabbit and dog cardiac myosin. Circ. Res. 35: 15-23, 1974. 26. ZAK, R., J. ETLINGER, AND D. A. FISCHMAN. Studies on the fractionation of skeletal and heart muscle. In: Research in MuscZe Development and the MuscZe Spindle (Excerpta Medical International Congress, Series 240), edited by F. Pizybyeski, J. Van der Muellan, M. Victor, and B. Banker. New York: Elsevier, 1971, p. 163-175.

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Myofibrillar ATPase activity in rat heart after chronic propranolol administration.

Myofibrillar ATPase activity in rat heart after chronic propranolol administration RUSSELL Department Oklahoma T. DOWELL of Physiology City, Oklahoma...
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