Publications
464 results found
Tweedie D, Harding SE, MacLeod KT, 2000, Sarcoplasmic reticulum Ca content, sarcolemmal Ca influx and the genesis of arrhythmias in isolated guinea-pig cardiomyocytes, JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, Vol: 32, Pages: 261-272, ISSN: 0022-2828
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- Citations: 41
Ranu HK, Mak JCW, Barnes PJ, et al., 2000, G(i)-dependent suppression of β<inf>1</inf>-adrenoceptor effects in ventricular myocytes from NE-treated guinea pigs, American Journal of Physiology - Heart and Circulatory Physiology, Vol: 278, ISSN: 0363-6135
It has been suggested that there is a preferential coupling in heart muscle between the inhibitory G protein (G(i)) and the β2-subtype of the β-adrenergic receptor (β-AR), since pertussis toxin (which inactivates G(i)) reveals latent β2-ARs in rat and mouse myocytes. We have previously shown that guinea pigs treated with norepinephrine (NE) for 7 days have myocytes that are desensitized to β-AR-agonist stimulation, and that pertussis toxin restores these responses. The purpose of the present investigation was to determine whether pertussis toxin specifically upregulated β2-ARs in myocytes from NE-treated guinea pigs. The sole β-AR subtype in control guinea pig myocytes was confirmed as β1-AR by radioligand binding, single-cell autoradiography, and concentration-response curves to isoproterenol in contracting myocytes. In contrast, a minor pool of β2-ARs was observed in rat myocytes by use of the same methods. NE treatment decreased the maximum isoproterenol response (relative to high Ca2+) from 0.89 ± 0.06 to 0.58 ± 0.08 (n = 7, P < 0.01) and the pD2 (- log EC50) from 8.8 ± 0.2 to 7.5 ± 0.2 (n = 7, P < 0.01). Pertussis toxin treatment increased the isoproterenol-to-Ca2+ ratio to 0.88 ± 0.04 (n = 6, P < 0.05) and the pD2 to 8.6 ± 0.3 (P < 0.01). This was not mediated by increases in either number or function of β2-ARs. G(i) is therefore able to modulate β1-AR responses in guinea pig myocytes.
Terracciano CMN, Bernobich E, Davia K, et al., 2000, Adenovirus-mediated Na/Ca exchanger overexpression reduces sarcoplasmic reticulum (SR) Ca content in adult rabbit cardiomyocytes, BIOPHYSICAL JOURNAL, Vol: 78, Pages: 373A-373A, ISSN: 0006-3495
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- Citations: 3
Bernobich E, Davia K, Ranu HK, et al., 2000, Adenovirus-mediated Na/Ca exchanger overexpression depresses contractile function in adult rabbit cardiomyocytes, BIOPHYSICAL JOURNAL, Vol: 78, Pages: 373A-373A, ISSN: 0006-3495
del Monte F, Harding SE, Schmidt U, et al., 1999, Restoration of contractile function in isolated cardiomyocytes from failing human hearts by gene transfer of SERCA2a, CIRCULATION, Vol: 100, Pages: 2308-2311, ISSN: 0009-7322
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- Citations: 372
Davia K, Hajjar RJ, Terracciano CMN, et al., 1999, Functional alterations in adult rat myocytes after overexpression of phospholamban with use of adenovirus, Physiological Genomics, Vol: 1999, Pages: 41-50, ISSN: 1531-2267
An increased phospholamban (PLB)-to-sarco(endo)plasmic reticulum Ca2+-ATPaSe (SERCA) ratio has been suggested to contribute to the slowing of relaxation in failing human ventricle. We have used an adenoviral vector carrying the sequence for PLB to increase this ratio in isolated adult rat ventricular myocytes, and we have examined the functional consequences. With use of adenoviral vectors, the PLB content of adult rat myocytes was increased 2.73-fold, with SERCA2a levels unchanged. Maximum contraction amplitude of PLB-overexpressing myocytes was decreased to 6.9 ± 0.3% shortening compared with 11.2 ± 0.8% for 24-h controls (Con; P < 0.001, 5 preparations, 103 myocytes). Maximum rates of shortening and relengthening were also significantly decreased. Ca2+ transient amplitudes were slightly depressed, and time to 50% decay of the transients was significantly increased: 237 ± 18 (n = 14 myocytes) and 432 ± 32 ms in Con and PLB (n = 15) myocytes, respectively (P < 0.001). The amount of Ca2+ in the sarcoplasmic reticulum stores was reduced by 21% (P < 0.05). Relaxation was significantly slower in PLB than in Con myocytes when the Na+/Ca2+ exchanger was blocked but not when sarcoplasmic reticulum Ca2+ uptake was inhibited. Adenovirus infection with Ad.RSV.PLB was therefore able to produce functional changes in adult cardiac myocytes within 24 h, consistent with overexpression of PLB and similar to those seen in failing human heart.
Adamson DL, O'Brookes CI, Kemp M, et al., 1999, Neurohormonal activation correlates with cellular and clinical markers of left ventricular dysfunction in patients with chronic mitral regurgitation, CIRCULATION, Vol: 100, Pages: 461-461, ISSN: 0009-7322
Adamson DL, Davies CH, Moat N, et al., 1999, Isolated ventricular myocytes from patients with chronic mitral regurgitation have significant abnormalities of relaxation, CIRCULATION, Vol: 100, Pages: 94-95, ISSN: 0009-7322
Song GJ, Harding SE, Duchen M, et al., 1999, Altered cardiomyocyte dynamics in annexin VI knockout mice, CIRCULATION, Vol: 100, Pages: 762-763, ISSN: 0009-7322
Davia K, Hajjar RJ, Terracciano CMN, et al., 1999, Functional alterations in adult rat myocytes after overexpression of phospholamban with use of adenovirus, PHYSIOLOGICAL GENOMICS, Vol: 1, Pages: 41-50, ISSN: 1094-8341
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- Citations: 42
Adamson DL, Harding SE, 1999, The ups and downs of the beta-adrenoceptor: Editorial, British Journal of Cardiology, Vol: 6, Pages: 377-378, ISSN: 0969-6113
Owen VJ, Burton PBJ, Michel MC, et al., 1999, Myocardial dysfunction in donor hearts -: A possible etiology, CIRCULATION, Vol: 99, Pages: 2565-2570, ISSN: 0009-7322
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- Citations: 36
Heubach JF, Trebess I, Wettwer E, et al., 1999, L-type calcium current and contractility in ventricular myocytes from mice overexpressing the cardiac β<sub>2</sub>-adrenoceptor, CARDIOVASCULAR RESEARCH, Vol: 42, Pages: 173-182, ISSN: 0008-6363
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- Citations: 40
Kent NS, Davia K, Harding SE, 1999, Characterisation of the function of adult guinea-pig ventricular myocytes following co-culture with neonatal rat myocytes, BASIC RESEARCH IN CARDIOLOGY, Vol: 94, Pages: 9-14, ISSN: 0300-8428
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- Citations: 2
Terracciano CMN, Davia K, Kent NS, et al., 1999, Overexpression of phospholamban affects sarcoplasmic reticulum (SR) Ca uptake in rat ventricular myocytes, BIOPHYSICAL JOURNAL, Vol: 76, Pages: A306-A306, ISSN: 0006-3495
Harding SE, Money-Kyrle ARW, 1998, Adrenergic Regulation, Advances in Organ Biology, Vol: 4, Pages: 81-114, ISSN: 1569-2590
Harding SE, Davies CH, Money-Kyrle AM, et al., 1998, An inhibitor of nitric oxide synthase does not increase contraction or β-adrenoceptor sensitivity of ventricular myocytes from failing human heart, CARDIOVASCULAR RESEARCH, Vol: 40, Pages: 523-529, ISSN: 0008-6363
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- Citations: 18
Harding SE, Davia K, Davies CH, et al., 1998, From overload to failure: what happens inside the myocyte, ANNALS OF MEDICINE, Vol: 30, Pages: 14-23, ISSN: 0785-3890
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- Citations: 5
Money-Kyrle ARW, Davies CH, Ranu HK, et al., 1998, The role of CAMP in the frequency-dependent changes in contraction of guinea-pig cardiomyocytes, CARDIOVASCULAR RESEARCH, Vol: 37, Pages: 532-540, ISSN: 0008-6363
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- Citations: 13
Davia K, Harding SE, 1998, Post-rest contraction amplitude in myocytes from failing human ventricle, BASIC RESEARCH IN CARDIOLOGY, Vol: 93, Pages: 33-37, ISSN: 0300-8428
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- Citations: 6
Ferrara N, Davia K, Abete P, et al., 1997, Altercations in β-adrenoceptor mechanisms in the aging heart.: Relationship with heart failure, AGING CLINICAL AND EXPERIMENTAL RESEARCH, Vol: 9, Pages: 391-403, ISSN: 1594-0667
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- Citations: 43
MoneyKyrle ARW, OGara P, Davies CH, et al., 1997, The force-frequency relationship in myocytes from failing human ventricle is not altered by either blocking or stimulating protein kinase A with membrane permeant cAMP analogues, CIRCULATION, Vol: 96, Pages: 3414-3414, ISSN: 0009-7322
Heubach JF, Harding SE, Schroeder F, et al., 1997, Delayed inactivation kinetic of L-type I-Ca in myocytes from mice overexpressing the beta(2)-adrenoceptor, CIRCULATION, Vol: 96, Pages: 2774-2774, ISSN: 0009-7322
Harding SE, 1997, Lack of evidence for beta 3-adrenoceptor modulation of contractile function in human ventricular myocytes., CIRCULATION, Vol: 96, Pages: 284-284, ISSN: 0009-7322
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- Citations: 3
Tweedie D, OGara P, Harding SE, et al., 1997, The effect of alterations to action potential duration on beta-adrenoceptor-mediated aftercontractions in human and guinea pig ventricular myocytes, JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, Vol: 29, Pages: 1457-1467, ISSN: 0022-2828
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- Citations: 14
Wright AR, Rees SA, Harding SE, et al., 1997, Sodium-calcium exchange in guinea-pig, marmoset and human cardiac cells, BIOPHYSICAL JOURNAL, Vol: 72, Pages: MP234-MP234, ISSN: 0006-3495
Ferrara N, Bohm M, Zolk O, et al., 1997, The role of Gi-proteins and beta-adrenoceptors in the age-related decline of contraction in guinea-pig ventricular myocytes, JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, Vol: 29, Pages: 439-448, ISSN: 0022-2828
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- Citations: 24
Davia K, Davies CH, Harding SE, 1997, Effects of inhibition of sarcoplasmic reticulum calcium uptake on contraction in myocytes isolated from failing human ventricle, CARDIOVASCULAR RESEARCH, Vol: 33, Pages: 88-97, ISSN: 0008-6363
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- Citations: 35
Ravens U, Trebess I, Himmel HM, et al., 1997, Contractile function and L-type Ca2+ currents (I-Ca) in myocardium from mice overexpressing the beta 2-adrenoceptor., NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY, Vol: 355, Pages: 76-76, ISSN: 0028-1298
Lefroy DC, Crake T, Del Monte F, et al., 1996, Angiotensin II and contraction of isolated myocytes from human, guinea pig, and infarcted rat hearts, American Journal of Physiology, Vol: 270, ISSN: 0002-9513
The effects of angiotensin II on myo-cardial contractility were assessed in isolated cardiac myocyte preparations, using video microscopy with a computerized edge-detection system. Angiotensin II (1 nM-10 uM) did not affect the contraction of rat (n = 10), guinea pig (n = 11), or human ventricular myocytes (n = 8) or of human atrial myocytes (n = 12). Isoproterenol or raised extracellular calcium increased the contraction amplitude of the cardiac myocytes to a maximum of between 150 and 560% above basal, and there were corresponding increases in the velocities of contraction and relaxation. In rat and guinea pig ventricular myocytes 1 uM angiotensin II did not affect the inotropic response to isoproterenol. Seven days after left coronary artery ligation in seven rats, the basal contraction amplitude was reduced in myocytes from the infarcted region (4.0 ± 1.9%) compared with the noninfarcted region (5.0 ± 2.8%, P = 0.03) and with myocytes from six sham-operated hearts (5.0 ± 2.8%, P = 0.03). There was a switch in myosin isoform expression from the V1 to the V3 isoform in myocytes from both the infarcted and noninfarcted regions. Angiotensin II (1 nM-10 μM) had no significant effect on the contraction characteristics of myocytes from the infarcted rat hearts. In conclusion, angiotensin II had no significant inotropic effect on isolated cardiac myocyte preparations from guinea pig ventricle, normal and infarcted rat ventricle, human ventricle, and human atrium. Copyright © 1996 the American Physiological Society.
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