Modulation by intracellular ATP and cyclic AMP of the slow inward current in isolated single ventricular cells of the guinea‐pig.

Irisawa, Hiroshi; Kokubun, Shinichiro

doi:10.1113/jphysiol.1983.sp014675

Cited by 160 publications

(67 citation statements)

References 33 publications

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“…The loss of high energy phosphate groups from intracellular proteins and a rise in internal levels of Ca2+ are both thought to play an important role in the time-dependent loss of Ca2+ channel function in single neuronal and cardiac cells recorded with patch pipettes (Doroshenko et al, 1982;Irisawa et al, 1983;Lee & Tsein, 1984;Chad & Eckert, 1986;Belles et al, 1988). The internal application of ATP (0.3-10mM), EGTA (0.1-10mM), but not cyclic AMP (<300pUM), increased the amplitude and slowed the rundown of Ca2 + channel currents in the rabbit small intestine and portal vein (Ohya et al, 1987;, guinea-pig mesenteric artery and bladder (Klockner & Isenberg, 1985;Ohya & Sperelakis, 1989) and dog colon (Langton et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Effects of okadaic acid and ATPγS on cell length and Ca²⁺‐channel currents recorded in single smooth muscle cells of the guinea‐pig taenia caeci

Lang¹,

Ozolins²,

Rutgeerts³

1991

British J Pharmacology

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1The effects of inhibiting phosphatase activity on Ca2+-channel currents and cell shortening in single cells of the guinea-pig taenia caeci were investigated by whole-cell voltage clamp and video recording techniques. 2 Ca2+-channel currents were isolated by use of pipette solutions containing Cs, tetraethylammonium and adenosine triphosphate (ATP) (3mM). Ca2+ or Ba2 + (7.5nmM) in the bathing solution acted as the charge carrier during inward current flow.3 Ca2+-channel currents in 7.5mm Ba2+ (,B.) were recorded at potentials positive to -40mV, were maximal near OmV and reversed near +60nmV. Both the inward and outward flow of current was blocked by 100pM Cd2+. 4 Addition of the ATP analogue, adenosine 5'-0(3-thiotriphosphate) (ATPyS) (1 mM) to the pipette solution (containing 3 mM ATP) caused cell shortening to 23 + 2% (n = 5) of their initial length within 5 min. Control cells (containing 4 mM ATP) did not contract during recording periods up to 60 min in duration. 5Ba. recorded 1-2 min after membrane rupture, was 134 + 19 (n = 13) pA, compared with 209 + 25 (n = 5) pA in control cells, otherwise there were no significant time-dependent effects of ATPyS. In particular, ATPyS did not prevent the decrease in amplitude, nor the acceleration of inactivation when Ca2+ (7.5 mM) replaced Ba2 + as the permeating ion.6 Okadaic acid (OA) (50pM), a chemical inhibitor of phosphatase activity, produced similar effects when applied intracellularly. When OA (25,UM) was applied extracellularly the rate of rundown of 'Ba was slowed.7 Isoprenaline (1 pM) alone had no effect on 'Ba, but induced a small increase in IBa in the presence of OA (25 uM). 8 Thus, our results indicate that (1) the contractions in ATPyS and OA may well arise from the activation of a kinase which phosphorylates myosin at low concentrations of Ca2 +, and (2) changes in the state of phosphorylation of Ca2+ channels, or associated proteins, in the taenia caeci modulate their function, but probably not via mechanisms involving cyclic AMP-dependent protein kinases.

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Section: Discussionmentioning

confidence: 99%

Effects of okadaic acid and ATPγS on cell length and Ca²⁺‐channel currents recorded in single smooth muscle cells of the guinea‐pig taenia caeci

Lang¹,

Ozolins²,

Rutgeerts³

1991

British J Pharmacology

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“…This probably represents activation of a Ca e+ current. The size of this current was variable and it tended to wane with time, presumably owing to the loss of some internal constituent necessary for Ca channel function, caused by internal dialysis with the pipette solution (Irisawa and Kokubun, 1983).…”

Section: Identification Of Immentioning

confidence: 99%

Characterization of the inward-rectifying potassium current in cat ventricular myocytes.

Harvey

Eick

1988

The Journal of General Physiology

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Whole-cell membrane currents were measured in isolated cat ventricular myocytes using a suction-electrode voltage-clamp technique. An inward-rectifying current was identified that exhibited a time-dependent activation. The peak current appeared to have a linear voltage dependence at membrane potentials negative to the reversal potential. Inward current was sensitive to K channel blockers. In addition, varying the extracellular K § concentration caused changes in the reversal potential and slope conductance expected for a K § current. The voltage dependence of the chord conductance exhibited a sigmoidal relationship, increasing at more negative membrane potentials. Increasing the extraceUular K § concentration increased the maximal level of conductance and caused a shift in the relationship that was directly proportional to the change in reversal potential. Activation of the current followed a monoexponential time course, and the time constant of activation exhibited a monoexponential dependence on membrane potential. Increasing the extracellular K + concentration caused a shift of this relationship that was directly proportional to the change in reversal potential. Inactivation of inward current became evident at more negative potentials, resulting in a negative slope region of the steady state current-voltage relationship between --140 and --180 mV. Steady state inactivation exhibited a sigmoidal voltage dependence, and recovery from inactivation followed a monoexponential time course. Removing extracellular Na + caused a decrease in the slope of the steady state current-voltage relationship at potentials negative to --140 mV, as well as a decrease of the conductance of inward current. It was concluded that this current was IK~, the inward-rectifying K + current found in multicellular cardiac preparations. The K + and voltage sensitivity of IK1 activation resembled that found for the inward-rectifying K + currents in frog skeletal muscle and various egg cell preparations. Inactivation

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“…18 Figure 2 shows that Ang II (10 Ϫ8 mmol/L) increased I Ca generated by a test pulse from Ϫ40 to 0 mV in ventricular myocytes by 35.4Ϯ2.8% (nϭ24; PϽ0.05). Significance was estimated by comparing I Ca values before and after Ang II administration.…”

Section: Intracellular Ang II Effect On I Camentioning

confidence: 99%

Intracellular and Extracellular Angiotensin II Enhance the L-Type Calcium Current in the Failing Heart

Mello

Monterrubio

2004

Hypertension

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Abstract-The influence of intracellular and extracellular angiotensin II (Ang II) on the L-type calcium current of cardiomyocytes isolated from cardiomyopathic hamsters was investigated. The results indicated that Ang II (10 Ϫ8 mmol/L), added to the bath, increased the peak inward calcium current (I Ca ) density by 37Ϯ3.4% (PϽ0.05), an effect that depends on the activation of protein kinase C. Intracellular administration of the same dose of Ang II (10 Ϫ8 mmol/L) also elicited an increase of peak I Ca density but enhanced the rate of I Ca inactivation, an effect not seen with extracellular Ang II. Moreover, in control animals, no change in the rate of I Ca inactivation was seen with intracellular Ang II. Thapsigargin (1 mol/L), a potent inhibitor of sarcoplasmic reticulum (SR) ATPase, which depletes the SR, decreased the rate of I Ca inactivation elicited by intracellular Ang II, although the cytoplasmic calcium concentration was highly buffered with 10 mmol/L EGTA. These findings might indicate that intracellular Ang II releases calcium from the SR and inactivates I Ca . The effect of intracellular Ang II on peak I Ca was not altered by extracellular losartan (10 Ϫ7 mmol/L), supporting the notion that the peptide acted intracellularly. Other studies showed that intracellular Ang I administration (10 Ϫ8 mmol/L) enhanced the peak I Ca density and the rate of I Ca inactivation, an effect that was reduced by intracellular enalaprilat (10 Ϫ8 mmol/L). Moreover, intracellular enalaprilat by itself reduced the peak I Ca density. These observations might indicate that endogenous Ang II is contributing to I Ca modulation in the failing heart. Key Words: angiotensin Ⅲ heart failure Ⅲ calcium current T he concept of a cardiac renin-angiotensin system 1 gained support with the demonstration that: (1) angiotensin I (Ang I) is converted to Ang II in the isolated and perfused heart; 2 (2) the angiotensin-converting enzyme (ACE) has been found around the nucleus of heart cells in culture 3 ; and (3) ACE inhibitors prevent cardiac remodeling, an effect independent of the change in blood pressure. 4 However, in normal heart, renin mRNA levels 5 and renin content are negligible in nephrectomized rats. 6 Moreover, no renin is released from the isolated and perfused rat heart, 7 which suggests that cardiac renin is attributable to its uptake from plasma. However, under some conditions, such as stretch, renin gene expression is enhanced, 8 and overexpression of angiotensinogen gene in normal mice leads to hypertrophy of the right and left ventricles and to an increase of Ang II levels in both ventricles without any change in arterial blood pressure. 9,10 Furthermore, a second renin gene transcript that may code for intracellular renin because it lacks the coding zone of the secretory signal peptide is upregulated in the left ventricle after myocardial infarction. 11 Moreover, cardiac angiotensinogen is upregulated after myocardial infarction. 12 These observations support the notion that renin and Ang II can be formed inside the hear...

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Modulation by intracellular ATP and cyclic AMP of the slow inward current in isolated single ventricular cells of the guinea‐pig.

Cited by 160 publications

References 33 publications

Effects of okadaic acid and ATPγS on cell length and Ca²⁺‐channel currents recorded in single smooth muscle cells of the guinea‐pig taenia caeci

Effects of okadaic acid and ATPγS on cell length and Ca²⁺‐channel currents recorded in single smooth muscle cells of the guinea‐pig taenia caeci

Characterization of the inward-rectifying potassium current in cat ventricular myocytes.

Intracellular and Extracellular Angiotensin II Enhance the L-Type Calcium Current in the Failing Heart

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Modulation by intracellular ATP and cyclic AMP of the slow inward current in isolated single ventricular cells of the guinea‐pig.

Cited by 160 publications

References 33 publications

Effects of okadaic acid and ATPγS on cell length and Ca2+‐channel currents recorded in single smooth muscle cells of the guinea‐pig taenia caeci

Effects of okadaic acid and ATPγS on cell length and Ca2+‐channel currents recorded in single smooth muscle cells of the guinea‐pig taenia caeci

Characterization of the inward-rectifying potassium current in cat ventricular myocytes.

Intracellular and Extracellular Angiotensin II Enhance the L-Type Calcium Current in the Failing Heart

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Effects of okadaic acid and ATPγS on cell length and Ca²⁺‐channel currents recorded in single smooth muscle cells of the guinea‐pig taenia caeci

Effects of okadaic acid and ATPγS on cell length and Ca²⁺‐channel currents recorded in single smooth muscle cells of the guinea‐pig taenia caeci