Decreased inotropic response to beta-adrenergic stimulation and normal sarcoplasmic reticulum calcium stores in the spontaneously hypertensive rat heart

1995 ◽  
Vol 27 (10) ◽  
pp. 2101-2109 ◽  
Author(s):  
Christine Schomisch Moravec ◽  
Eva Keller ◽  
Meredith Bond
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Rat Heart ◽  
Spontaneously Hypertensive Rat ◽  
Calcium Stores ◽  
Inotropic Response ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Sarcoplasmic Reticulum Calcium

Geometrical models of left ventricular contraction from MRI of the normal and spontaneously hypertensive rat heart

1999 ◽  
Vol 44 (10) ◽  
pp. 2657-2676 ◽  
Author(s):  
Richard G Wise ◽  
Christopher L-H Huang ◽  
Ahmed I M Al-Shafei ◽  
T Adrian Carpenter ◽  
Laurance D Hall
Keyword(s):  
Rat Heart ◽  
Spontaneously Hypertensive Rat ◽  
Left Ventricular ◽  
Ventricular Contraction ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat

scholarly journals Effects of Chronic Administration of Carteolol on β-Adrenoceptors in Spontaneously Hypertensive Rat Heart

1991 ◽  
Vol 56 (4) ◽  
pp. 505-512
Author(s):  
Koichi Ebii ◽  
Reiko Fukunaga ◽  
Takashi Taniguchi ◽  
Motohatsu Fujiwara ◽  
Sunao Nakayama ◽  
...  
Keyword(s):  
Rat Heart ◽  
Spontaneously Hypertensive Rat ◽  
Chronic Administration ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat

scholarly journals Effects of chronic treatment of beta antagonists on beta adrenoceptors in spontaneously hypertensive rat heart

1990 ◽  
Vol 52 ◽  
pp. 367
Author(s):  
Koichi Ebii ◽  
Reiko Fukunaga ◽  
Takashi Taniguchi ◽  
Hidefumi Nishikawa ◽  
Motohatsu Fujiwara ◽  
...  
Keyword(s):  
Rat Heart ◽  
Chronic Treatment ◽  
Spontaneously Hypertensive Rat ◽  
Spontaneously Hypertensive ◽  
Beta Adrenoceptors ◽  
Hypertensive Rat

Troponin I phosphorylation in spontaneously hypertensive rat heart: effect of beta-adrenergic stimulation

1997 ◽  
Vol 273 (3) ◽  
pp. H1440-H1451 ◽  
Author(s):  
B. K. McConnell ◽  
C. S. Moravec ◽  
I. Morano ◽  
M. Bond
Keyword(s):  
Troponin I ◽  
Ventricular Myocytes ◽  
Spontaneously Hypertensive Rat ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Spontaneously Hypertensive ◽  
Myosin Light Chain 2 ◽  
Wistar Kyoto ◽  
Phospholamban Phosphorylation

We compared baseline and protein kinase A (PKA)-dependent troponin I (TnI) phosphorylation in 32Pi-labeled left ventricular myocytes from hearts of 26-wk spontaneously hypertensive rats (SHR) and Wistar-Kyoto controls (WKY). TnI phosphorylation was normalized to myosin light chain 2 phosphorylation, which was invariant. There was no difference in baseline TnI phosphorylation in SHR and WKY, but stimulation with isoproterenol, norepinephrine plus prazosin, forskolin, chloroadenosine 3',5'-cyclic monophosphate, or 3-isobutyl-1-methylxanthine caused a greater increase in TnI phosphorylation in the SHR than in the WKY. This was observed both in the presence and absence of the phosphatase inhibitor calyculin A; thus the differences in TnI phosphorylation between SHR and WKY are not due to decreased phosphatase activity in the SHR. After stimulation of the beta-adrenergic pathway, phospholamban phosphorylation was not different in SHR and WKY, indicating that the observed differences may be specific for PKA phosphorylation of TnI. The increased PKA-dependent TnI phosphorylation in the SHR resulted in decreased Ca2+ sensitivity of actomyosin adenosinetriphosphatase activity as compared with the WKY. We conclude that increased PKA-dependent TnI phosphorylation in the SHR may contribute to the impaired response to sympathetic stimulation.

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