Isolation of High Quality Murine Atrial and Ventricular Myocytes for Simultaneous Measurements of Ca2+ Transients and L-Type Calcium Current

10.3791/61964 ◽  
2020 ◽  
Author(s):  
Philipp Tomsits ◽  
Dominik Schüttler ◽  
Stefan Kääb ◽  
Sebastian Clauss ◽  
Niels Voigt
Keyword(s):  
Calcium Current ◽  
Ventricular Myocytes ◽  
High Quality ◽  
Simultaneous Measurements

scholarly journals Simultaneous measurements of intracellular cAMP and L‐type Ca 2+ current in single frog ventricular myocytes

2001 ◽  
Vol 530 (1) ◽  
pp. 79-91 ◽  
Author(s):  
Jean‐Marc Goaillard ◽  
Pierre Vincent ◽  
Rodolphe Fischmeister
Keyword(s):  
Ventricular Myocytes ◽  
Intracellular Camp ◽  
Simultaneous Measurements

scholarly journals Impaired beta-adrenergic response and decreased L-type calcium current of hypertrophied left ventricular myocytes in postinfarction heart failure

2003 ◽  
Vol 36 (5) ◽  
pp. 635-648 ◽  
Author(s):  
R.M. Saraiva ◽  
N.G.B. Chedid ◽  
C.C. Quintero H. ◽  
L.E. Díaz G. ◽  
M.O. Masuda
Keyword(s):  
Heart Failure ◽  
Calcium Current ◽  
Ventricular Myocytes ◽  
Left Ventricular ◽  
Beta Adrenergic ◽  
Adrenergic Response

Influence of long-chain acylcarnitines on voltage-dependent calcium current in adult ventricular myocytes

1992 ◽  
Vol 263 (2) ◽  
pp. H410-H417 ◽  
Author(s):  
J. Wu ◽  
P. B. Corr
Keyword(s):  
Calcium Current ◽  
Ventricular Myocytes ◽  
Indirect Evidence ◽  
Cell Voltage ◽  
Time Dependent ◽  
Similar Degree ◽  
Tetraacetic Acid ◽  
Voltage Dependent ◽  
Long Chain

Long-chain acylcarnitines (LCAC) increase 3.5-fold within 2 min in ischemic myocardium in vivo, and previous studies have suggested, through indirect evidence, that LCAC can stimulate the voltage-dependent L-type Ca2+ current [ICa(L)] in both cardiac and smooth muscle cells. In the present study, whole cell voltage-clamp procedures were performed in isolated adult guinea pig ventricular myocytes to assess the direct effect of LCAC on ICa(L). The intracellular solution contained (in mM) 80 CsCl, 40 K-aspartic acid, and 5 ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). Maximal current density of ICa(L) at 0 mV was 10.1 +/- 0.5 pA/pF (n = 22) at extracellular Ca2+ concentration ([Ca2+]o) = 2.7 mM. LCAC induced a concentration (1-25 microM, n = 23)- and time-dependent, reversible decrease in ICa(L). When delivered extracellularly for 10 min, LCAC (5 microM) inhibited the maximal current of ICa(L) by 48.1 +/- 1.3% (n = 9, P less than 0.01) and shifted the half-maximal voltage of steady-state activation and inactivation from -13.1 +/- 0.5 to -6.8 +/- 0.4 mV (n = 4; P less than 0.05) and from -21.8 +/- 0.2 to -16.5 +/- 0.6 mV (n = 4; P less than 0.01), respectively. Intracellular delivery of LCAC (5 microM) also suppressed ICa(L) to a similar degree (47.5 +/- 1.5%, n = 4; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Do β2-adrenergic receptors modulate Ca2+ in adult rat ventricular myocytes?

1998 ◽  
Vol 274 (4) ◽  
pp. H1308-H1314 ◽  
Author(s):  
Michael A. Laflamme ◽  
Peter L. Becker
Keyword(s):  
Pertussis Toxin ◽  
Calcium Homeostasis ◽  
Adrenergic Receptors ◽  
Calcium Current ◽  
Ventricular Myocytes ◽  
Camp Accumulation ◽  
Camp Production ◽  
Rat Ventricular Myocytes ◽  
Adult Rat

We examined the role of β2-adrenergic receptors (ARs) in modulating calcium homeostasis in rat ventricular myocytes. Zinterol (10 μM), an agonist with a 25-fold greater affinity for β2-ARs over β1-ARs, modestly enhanced L-type calcium current ( I Ca) magnitude by ∼30% and modestly accelerated the rate of Ca2+ concentration ([Ca2+]) decline (∼35%) but had little effect on the magnitude of the [Ca2+] transient (a nonsignificant 6% increase). However, 1 μM of the highly selective β1-AR antagonist CGP-20712A completely blocked the I Ca increase induced by 10 μM zinterol. Pretreatment of cells with pertussis toxin (PTX) did not alter I Ca enhancement by 10 μM zinterol, although it did abolish the ability of acetylcholine to block the forskolin-induced enhancement of I Ca. Zinterol (10 μM) approximately doubled adenosine 3′,5′-cyclic monophosphate (cAMP) accumulation, although one-half of this increase was blocked by CGP-20712A. In contrast, 1 μM of the nonselective β-agonist isoproterenol increased cAMP production 15-fold. Thus we found no evidence that activation of β2-ARs modulates calcium homeostasis in rat ventricular myocytes, even after treatment with PTX.

cGMP facilitates calcium current via cGMP-dependent protein kinase in isolated rabbit ventricular myocytes

1998 ◽  
Vol 435 (3) ◽  
pp. 388-393 ◽  
Author(s):  
J. Han ◽  
Euiyong Kim ◽  
S. H. Lee ◽  
S. Yoo ◽  
Won-Kyung Ho ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Calcium Current ◽  
Ventricular Myocytes ◽  
Dependent Protein Kinase ◽  
Cgmp Dependent Protein Kinase ◽  
Dependent Protein ◽  
Rabbit Ventricular Myocytes

scholarly journals Stimulation-dependent facilitation of the high threshold calcium current in guinea-pig ventricular myocytes.

1990 ◽  
Vol 428 (1) ◽  
pp. 653-671 ◽  
Author(s):  
A C Zygmunt ◽  
J Maylie
Keyword(s):  
Guinea Pig ◽  
Calcium Current ◽  
Ventricular Myocytes ◽  
High Threshold

scholarly journals Loss of Rad-GTPase produces a novel adaptive cardiac phenotype resistant to systolic decline with aging

2015 ◽  
Vol 309 (8) ◽  
pp. H1336-H1345 ◽  
Author(s):  
Janet R. Manning ◽  
Catherine N. Withers ◽  
Bryana Levitan ◽  
Jeffrey D. Smith ◽  
Douglas A. Andres ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Calcium Current ◽  
Ventricular Myocytes ◽  
Morphological Changes ◽  
Heart Function ◽  
Early Time ◽  
Cardiac Phenotype ◽  
Systolic And Diastolic Function

Rad-GTPase is a regulator of L-type calcium current (LTCC), with increased calcium current observed in Rad knockout models. While mouse models that result in elevated LTCC have been associated with heart failure, our laboratory and others observe a hypercontractile phenotype with enhanced calcium homeostasis in Rad−/−. It is currently unclear whether this observation represents an early time point in a decompensatory progression towards heart failure or whether Rad loss drives a novel phenotype with stable enhanced function. We test the hypothesis that Rad−/− drives a stable nonfailing hypercontractile phenotype in adult hearts, and we examine compensatory regulation of sarcoplasmic reticulum (SR) loading and protein changes. Heart function was measured in vivo with echocardiography. In vivo heart function was significantly improved in adult Rad−/− hearts compared with wild type. Heart wall dimensions were significantly increased, while heart size was decreased, and cardiac output was not changed. Cardiac function was maintained through 18 mo of age with no decompensation. SR releasable Ca2+ was increased in isolated Rad−/− ventricular myocytes. Higher Ca2+ load was accompanied by sarco/endoplasmic reticulum Ca2+ ATPase 2a (SERCA2a) protein elevation as determined by immunoblotting and a rightward shift in the thapsigargan inhibitor-response curve. Rad−/− promotes morphological changes accompanied by a stable increase in contractility with aging and preserved cardiac output. The Rad−/− phenotype is marked by enhanced systolic and diastolic function with increased SR uptake, which is consistent with a model that does not progress into heart failure.

scholarly journals The antifungal antibiotic clotrimazole potently inhibits L-type calcium current in guinea-pig ventricular myocytes

1999 ◽  
Vol 126 (7) ◽  
pp. 1531-1533 ◽  
Author(s):  
George P Thomas ◽  
Morris Karmazyn ◽  
Andrew C Zygmunt ◽  
Charles Antzelevitch ◽  
Njanoor Narayanan
Keyword(s):  
Guinea Pig ◽  
Calcium Current ◽  
Ventricular Myocytes ◽  
Antifungal Antibiotic
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