Effects of Angiotensin II on Adenylcyclase Activity, Phosphodiesterase Activity and on the Level of Cyclic AMP in Rat Uterus

1973 ◽  
Vol 45 (s1) ◽  
pp. 247s-250s
Author(s):  
G. Anglès D'Auriac ◽  
P. Meyer
Keyword(s):  
Angiotensin Ii ◽  
Cyclic Amp ◽  
Enzyme Activities ◽  
Phosphodiesterase Activity ◽  
Rat Uterus ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Cyclic Phosphate ◽  
Intracellular Concentrations

1. Intracellular concentrations of adenosine 3′: 5′-cyclic phosphate (cyclic AMP) and activities of adenylcyclase and phosphodiesterase were determined in oestrogen-pretreated rat uteri during exposure to different concentrations of angiotensin II. 2. No significant variations in cyclic AMP or in the enzyme activities were observed at concentrations of angiotensin inducing significant contractions. 3. It is concluded that in rat uterus, the process of excitation-contraction coupling triggered by angiotensin is not mediated by variations in intracellular levels of cyclic AMP.

Accumulation of Adenosine 3′,5′-Monophosphate and Relaxation in the Rat Uterus In Vitro

1971 ◽  
Vol 49 (11) ◽  
pp. 999-1004 ◽  
Author(s):  
Ivo Polacek ◽  
Jean Bolan ◽  
Edwin E. Daniel
Keyword(s):  
Cyclic Amp ◽  
Contractile Activity ◽  
Phosphodiesterase Activity ◽  
Dibutyryl Camp ◽  
Rat Uterus ◽  
Low Concentrations ◽  
Uterine Contractile ◽  
Camp Levels

Theophylline, diazoxide, and papaverine in low concentrations relaxed the uterus with minimal or no elevation of cyclic AMP (cAMP) levels. In higher concentrations, theophylline relaxed the uterus and increased its cAMP levels, but imidazole reversed the increase in cAMP without causing recontraction. Imidazole and NaF caused uterine contractures but did not detectably decrease cAMP levels until several minutes after the onset of contractures. The uterine relaxations produced by theophylline and/or dibutyryl cAMP in amounts which increased uterine cAMP were not reversed by propranolol. These results eliminate the possibility that propranolol interfered with a relaxant action of cAMP. Along with previous data, these results also show that uterine contractile activity was not determined primarily by the general levels of cAMP and that phosphodiesterase activity in the uterus was insufficient to rapidly affect these cAMP levels. Also, substances like theophylline, diazoxide, and papaverine, postulated to inhibit phosphodiesterase activity, did not bring about their relaxant effects by this mechanism.

Overexpression of type 1 angiotensin II receptors impairs excitation-contraction coupling in the mouse heart

2011 ◽  
Vol 301 (5) ◽  
pp. H2018-H2027 ◽  
Author(s):  
Katy Rivard ◽  
Scott A. Grandy ◽  
Annie Douillette ◽  
Pierre Paradis ◽  
Mona Nemer ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Cardiac Contractility ◽  
Mouse Heart ◽  
Angiotensin Ii Receptor ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Cell Shortening ◽  
Fractional Shortening

Transgenic mice that overexpress human type 1 angiotensin II receptor (AT1R) in the heart develop cardiac hypertrophy. Previously, we have shown that in 6-mo AT1R mice, which exhibit significant cardiac remodeling, fractional shortening is decreased. However, it is not clear whether altered contractility is attributable to AT1R overexpression or is secondary to cardiac hypertrophy/remodeling. Thus the present study characterized the effects of AT1R overexpression on ventricular L-type Ca2+ currents ( ICaL), cell shortening, and Ca2+ handling in 50-day and 6-mo-old male AT1R mice. Echocardiography showed there was no evidence of cardiac hypertrophy in 50-day AT1R mice but that fractional shortening was decreased. Cellular experiments showed that cell shortening, ICaL, and Cav1.2 mRNA expression were significantly reduced in 50-day and 6-mo-old AT1R mice compared with controls. In addition, Ca2+ transients and caffeine-induced Ca2+ transients were reduced whereas the time to 90% Ca2+ transient decay was prolonged in both age groups of AT1R mice. Western blot analysis revealed that sarcoplasmic reticulum Ca2+-ATPase and Na+/Ca2+ exchanger protein expression was significantly decreased in 50-day and 6-mo AT1R mice. Overall, the data show that cardiac contractility and the mechanisms that underlie excitation-contraction coupling are altered in AT1R mice. Furthermore, since the alterations in contractility occur before the development of cardiac hypertrophy, it is likely that these changes are attributable to the increased activity of the renin-angiotensin system brought about by AT1R overexpression. Thus it is possible that AT1R blockade may help maintain cardiac contractility in individuals with heart disease.

scholarly journals Cyclic AMP-mediated regulation of excitation-contraction coupling in canine gastric smooth muscle.

1992 ◽  
Vol 447 (1) ◽  
pp. 351-372 ◽  
Author(s):  
H Ozaki ◽  
D P Blondfield ◽  
M Hori ◽  
K M Sanders ◽  
N G Publicover
Keyword(s):  
Smooth Muscle ◽  
Cyclic Amp ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Gastric Smooth Muscle

scholarly journals Angiotensin II–Mediated Adaptive and Maladaptive Remodeling of Cardiomyocyte Excitation–Contraction Coupling

2009 ◽  
Vol 105 (1) ◽  
pp. 42-50 ◽  
Author(s):  
Konstantin Gusev ◽  
Andrea A. Domenighetti ◽  
Lea M.D. Delbridge ◽  
Thierry Pedrazzini ◽  
Ernst Niggli ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling
Sign in / Sign up

Export Citation Format

Share Document