Cardiac inotropic responses to calcium and forskolin are not altered by prolonged isoproterenol infusion

Bowling, Nancy; Wyss, V; Gengo, Peter J.; Utterback, Barbara G.; Kauffman, Raymond F.; Hayes, J S

doi:10.1016/0014-2999(90)90002-n

Cited by 8 publications

(4 citation statements)

References 27 publications

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“…These findings suggest homologous desensitization of adenylate cyclase activity following chronic h-AR activation. This notion is consistent with results showing neither a reduction in the inotropic and adenylate cyclasestimulating effects of forskolin (Bowling et al, 1990;Giannuzzi et al, 1995), nor with inhibition of adenylate cyclase responses to sodium fluoride (Iaccarino et al, 1999) following chronic adrenergic activation. Nevertheless, previous studies have reported a decrease in the stimulatory effects of forskolin accompanying a reduction in isoproterenol-induced myocardial adenylate cyclase activation in ISO-treated rats (Hakamata et al 1997).…”

Section: Discussionsupporting

confidence: 89%

Mechanisms of preserved baseline cardiac systolic function in rats with adrenergic inotropic downregulation

et al. 2005

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Section: Discussionsupporting

confidence: 89%

Mechanisms of preserved baseline cardiac systolic function in rats with adrenergic inotropic downregulation

et al. 2005

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“…Authors who used DP max or dP/dt max as indices of contractile capacity in the same model 13,14,16,17 concluded that the contractile state of the ISO‐induced cardiac hypertrophy was enhanced because DP max or dP/dt max was higher in these hearts than in control. Nevertheless, most studies in which force was evaluated from muscle strips 8–12 have shown that force generation is impaired in this model, indicating that the contractile state is depressed. There is only one report 18 of contraction improvement among the studies in which muscle strips were used.…”

Section: Discussionmentioning

confidence: 88%

“…According to authors 4–7 who have studied heart pumping ability, depression of the ejection function occurs in ISO‐induced hypertrophy. An equivalent opinion regarding depressed contractile ability was reported by those 8–12 who evaluated the capacity of isolated muscle to develop force. In contrast, others who evaluated systolic function in isolated heart preparations consider ISO hypertrophy to be accompanied by contractile function enhancement.…”

Section: Introductionmentioning

confidence: 93%

Isoproterenol‐Induced Hypertrophy May Result In Distinct Left Ventricular Changes

Murad

Tucci

2000

Clin Exp Pharma Physio

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1. The aim of the present study was to analyse the possible lack of uniformity in isoproterenol (ISO)-induced myocardial hypertrophy. 2. Data obtained for isovolumic hearts isolated from 20 rats treated with ISO (0.3 mg/kg over 8 days) were divided into two groups (H1, n = 10; H2, n = 10) according to the volume (mean+/-SD) needed to change left ventricle diastolic pressure from 0 to 40 mmHg (H1, 184+/-30 microL; H2, 108+/-14 microL). Eight control rats (C; 165+/-37 microL) were used for comparison. 3. In addition to ventricular distensibility differences, the groups differed in terms of myocardial mass (mean+/-SEM: H1, 181+/-3 mg > H2, 166+/-3 mg > C, 136+/-3 mg; P < 0.001), of relaxation constant (H2, 43+/-4 msec > H1, 28+/-2 msec; P = 0.0012) and of maximum developed circumferential stress (C, 145+/-9 kdyn/cm2 = H1, 137+/-6 kdyn/cm2 > H2, 110+/-4 kdyn/cm2; P = 0.002). 4. Our results show that ISO-induced myocardial hypertrophy is not homogeneous. Data obtained for H2, taken as a whole and compared with H1 (smaller myocardial mass and impairment of relaxation, elastic stiffness and force generation), suggest that, in some animals, myocardial necrosis and reparative fibrosis may prevail over the stimulus for myocyte growth. The lack of uniformity of ISO-induced myocardial hypertrophy has not been previously reported and may have contributed to the divergence observed in the literature regarding the functional characteristics of the present model.

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“…Changes in the density and function of L-type voltage-sensitive calcium channels have been reported in the myocardium of patients with end-stage heart failure and in animal models of this syndrome. There are no clear explanations for these cellular changes, but exposure of excitable systems to overactivation or decreased stimulation is now fully established to result in the compensatory processes described as desensitization (downregulation) or supersensitization (upregulation), respectively (10,28,31,32,88). The cellular signal responsible for the changes in L-type calcium channel density awaits definition; however, from the available data to date it appears that changes in these channels do not take place early in the development of cardiovascular disease.…”

Section: Discussionmentioning

confidence: 99%

Physiologic and emerging pathophysiologic role of cardiac calcium channels

Gengo

1996

Heart Failure Rev

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The link between cardiac contractile dysfunction in patients with end-stage heart failure and aberrant myocardial intracellular calcium handling is now well established. The precise intracellular protein(s) responsible for this breakdown in calcium handling is at present unclear. However, a number of distinct sarcolemmal (L-type, N-type, Ttype, P-type, Q-type) and sarcoplasmic reticular (calcium release, ryanodine) calcium channels that have been defined on a biophysical, biochemical, and molecular basis lend valuable insights into possible factors that may contribute to the abnormal calcium handling in the hearts of these patients. What is now clear is that cardiac muscle contraction is a rigorously regulated event that follows the organized cycling of calcium from the sarcoplasmic reticulum (SR) into the cytosol and back into the SR, and that this cycle follows the graded entry of trigger calcium that enters the cell through the voltage-sensitive calcium channel. Furthermore, the voltage-dependent properties of potential-dependent calcium channels provide the underpinning for the vascular selectivity of the clinically available calcium channel drugs. Moreover, it has also been reported that the efficacy of these agents is augmented in pathologic (ischemic) tissue owing to the state dependence of these channels. Recently, the basis for the critical role of the SR in calcium signaling has started to emerge. The SR calcium handling proteins (SR calcium release channel/ryanodine receptor, SR Ca 2+ ATPase, phospholamban, calsequestrin) play a critical role in maintaining intracellular free ionized calcium concentrations ([Ca2+]i), which therefore regulate systolic and diastolic function on a beat-to-beat basis within the cardiac cell. This rigorous control of [Ca2+]i is in part the result of the highly developed junctional regions of the cardiac SR. Elucidation of the calcium handling process in these regions and the potential damage resulting from cardiovascular disease has been greatly aided by the invaluable molecular tool, ryanodine. From an expanding volume of information provided by animal models of ischemia, hypertrophy, and heart failure, it now appears that changes in cardiac voltage-sensitive calcium channels are likely to be the result of a secondary process that may not be directly linked to the onset of these cardiovascular diseases. Conversely, the regulation of ryanodine receptors has been suggested to be a mechanism initiating the decline in myocardial contractility leading to heart failure. These reports have been supported by studies demonstrating SR calcium release channel/ryanodine receptor changes in pressure overload hypertrophy and myocardial ischemia. Further support for the role of SR calcium release channels in cardiovascular disease is found in reports that couple leaking SR channels with ischemia and cardiac failure. These results suggest that changes in SR calcium handling proteins may be critically linked to cardiovascular disease. A more central question stemming from these results is ...

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Cardiac inotropic responses to calcium and forskolin are not altered by prolonged isoproterenol infusion

Cited by 8 publications

References 27 publications

Mechanisms of preserved baseline cardiac systolic function in rats with adrenergic inotropic downregulation

Mechanisms of preserved baseline cardiac systolic function in rats with adrenergic inotropic downregulation

Isoproterenol‐Induced Hypertrophy May Result In Distinct Left Ventricular Changes

Physiologic and emerging pathophysiologic role of cardiac calcium channels

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