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The effects of carbachol on cAMP and protein kinase A activity in rat ventricles Zhang, Jack Zhen
Abstract
It has been shown that (CCH) antagonizes the positive inotropic response to forskolin (FSK) in rabbit ventricles without decreasing total cAMP levels elevated by FSK. Further reports proposed that only cAMP (Cyclic AMP) in the particulate fraction of myocardium determines the inotropic state and Ca2+ transients of the cell in the presence of cAMP elevating agents. In this investigation, we studied the effects of CCH on compartmental cAMP and PKA (protein kinase A) activity changed by cAMP-generating agents in rat ventricles. The elevation of particulate cAMP content was correlated with the LVP (left ventricle pressure) increased by isoproterenol (ISO) (10-7 M), and FSK (10-6 M) (r=0.90). Although PGE1 (prostaglandin E-\, 3x10-5 M) increased the total cAMP content and soluble PKA activity, it neither significantly affected the particulate cAMP content and PKA activity nor the LVP. Pre-perfusion with CCH (3x10-6 M) for 1 min, in addition to antagonizing the LVP elevated by ISO (122.8 ± 12.4 to 60.3 ± 8.4 mm Hg), decreased the total and particulate cAMP (26.8 ± 1.3 to 18.2 ± 1.6 and 16.4 ± 1.2 to 12.1 ± 0.8 pmol/mg protein respectively), lowered the soluble PKA ratio (0.60 ± 0.02 to 0.42 ± 0.03) and increased the percentage of particulate PKA (19.46 ±1.15 to 26.22 ± 0.54 %). CCH had no effect on either total and particulate cAMP levels or soluble and particulate PKA activity in the presence of FSK although the positive inotropic response to FSK was abolished by CCH (93.1 ±8.1 to 54.2 ± 8.5 mm Hg). The results support the hypothesis that particulate cAMP and PKA may determine the inotropic state of myocardium after cAMP-generating agent stimulation. However, the ability of CCH to antagonize the positive inotropic effect of FSK does not appear to be associated with a reduction in particulate cAMP or PKA activity.
Item Metadata
Title |
The effects of carbachol on cAMP and protein kinase A activity in rat ventricles
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
1994
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Description |
It has been shown that (CCH) antagonizes the positive inotropic response to
forskolin (FSK) in rabbit ventricles without decreasing total cAMP levels elevated
by FSK. Further reports proposed that only cAMP (Cyclic AMP) in the particulate
fraction of myocardium determines the inotropic state and Ca2+ transients of the
cell in the presence of cAMP elevating agents. In this investigation, we studied the
effects of CCH on compartmental cAMP and PKA (protein kinase A) activity
changed by cAMP-generating agents in rat ventricles. The elevation of particulate
cAMP content was correlated with the LVP (left ventricle pressure) increased by
isoproterenol (ISO) (10-7 M), and FSK (10-6 M) (r=0.90). Although PGE1
(prostaglandin E-\, 3x10-5 M) increased the total cAMP content and soluble PKA
activity, it neither significantly affected the particulate cAMP content and PKA
activity nor the LVP. Pre-perfusion with CCH (3x10-6 M) for 1 min, in addition to
antagonizing the LVP elevated by ISO (122.8 ± 12.4 to 60.3 ± 8.4 mm Hg),
decreased the total and particulate cAMP (26.8 ± 1.3 to 18.2 ± 1.6 and 16.4 ± 1.2 to
12.1 ± 0.8 pmol/mg protein respectively), lowered the soluble PKA ratio (0.60 ±
0.02 to 0.42 ± 0.03) and increased the percentage of particulate PKA (19.46 ±1.15
to 26.22 ± 0.54 %). CCH had no effect on either total and particulate cAMP levels
or soluble and particulate PKA activity in the presence of FSK although the positive
inotropic response to FSK was abolished by CCH (93.1 ±8.1 to 54.2 ± 8.5 mm Hg).
The results support the hypothesis that particulate cAMP and PKA may determine
the inotropic state of myocardium after cAMP-generating agent stimulation.
However, the ability of CCH to antagonize the positive inotropic effect of FSK does
not appear to be associated with a reduction in particulate cAMP or PKA activity.
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Extent |
3379060 bytes
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Genre | |
Type | |
File Format |
application/pdf
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Language |
eng
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Date Available |
2009-02-26
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0087347
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Graduation Date |
1994-05
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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Item Media
Item Citations and Data
Rights
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.