scholarly journals Metformin exaggerates phenylephrine-induced AMPK phosphorylation independent of CaMKKβ and attenuates contractile response in endothelium-denuded rat aorta

2014 ◽  
Vol 92 (2) ◽  
pp. 266-279 ◽  
Author(s):  
Rajkumar Pyla ◽  
Islam Osman ◽  
Prahalathan Pichavaram ◽  
Paul Hansen ◽  
Lakshman Segar
Pharmacology ◽  
1996 ◽  
Vol 53 (2) ◽  
pp. 98-108 ◽  
Author(s):  
M.A. Noguera ◽  
S. Chulia ◽  
M. Elorriaga ◽  
M.D. Ivorra ◽  
P. D’Ocon

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Bruno Rodrigues Silva ◽  
Laena Pernomian ◽  
Marcella Daruge Grando ◽  
Lusiane Maria Bendhack

1993 ◽  
Vol 265 (6) ◽  
pp. H2073-H2080 ◽  
Author(s):  
J. N. Stallone

In rat thoracic aorta, contractile responses to arginine vasopressin (AVP) are twofold higher in females than in males. To determine the role of the endothelium in this phenomenon, the effects of endothelium removal and inhibition of nitric oxide (NO) synthase and cyclooxygenase were examined in thoracic aortas prepared from male and female Sprague-Dawley rats and mounted for isometric tension recording. Maximal contractile response to AVP was substantially higher in female (4,232 +/- 316 mg/mg ring dry wt) than in male aortas (1,365 +/- 239; P < 0.01). Removal of the endothelium markedly potentiated maximal response to AVP in male aortas (4,100 +/- 422 mg/mg ring wt; P < 0.01); endothelium removal increased sensitivity but not maximal response in female aortas. Inhibition of NO synthase with NG-monomethyl-L-arginine (L-NMMA, 250 microM) doubled maximal contraction to AVP in male aortas (3,175 +/- 193 mg/mg ring wt; P < 0.01); L-NMMA increased sensitivity but not maximal response in female aortas. Inhibition of cyclooxygenase with indomethacin (10 microM) did not alter maximal response to AVP in male aortas but significantly attenuated responses of female aortas (2,816 +/- 306 mg/mg ring wt; P < 0.01). In contrast, maximal contractile response to phenylephrine hydrochloride (PE) was 40% higher in males than in females (P < 0.01); L-NMMA increased both the sensitivity and maximal response to PE to a greater extent in female (3,061 +/- 121 vs. 4,971 +/- 135 mg/mg ring wt; P < 0.01) than in male aortas (4,317 +/- 227 vs. 4,899 +/- 104 mg/mg ring wt; P < 0.01). (ABSTRACT TRUNCATED AT 250 WORDS)


1993 ◽  
Vol 423-423 (1-2) ◽  
pp. 161-163 ◽  
Author(s):  
O. A. Sofola ◽  
P. C. M. Obiefuna ◽  
B. J. Adegunloye

1982 ◽  
Vol 60 (12) ◽  
pp. 1737-1737
Author(s):  
Richard J. Heaslip ◽  
Ralf G. Rahwan

On page 745, left column, the first complete sentence should read "Contractions induced by U44069 in the absence of extracellular calcium (and in the absence or the presence of nifedipine, bu-MDI, or Q-bu-MDI) were expressed as a percentage of the maximum contraction induced by U44069 alone in the presence of 2.5 mM bath calcium."On page 745, the second sentence of the Results section should read "Although tissues which had been washed in calcium-free buffer containing no EGTA contracted tonically upon exposure to 100 mM KCl to 14% of the maximum attainable contraction in the presence of extracellular calcium, tissues which had been washed in calcium-free EGTA buffers were refractory."


1982 ◽  
Vol 60 (5) ◽  
pp. 743-746 ◽  
Author(s):  
Richard J. Heaslip ◽  
Ralf G. Rahwan

The aim of the present investigation was to elucidate the pharmacological mechanism by which U44069, a stable PGH2 analogue, contracts the rat aorta. The results obtained demonstrate that while the contractile effect of potassium chloride is obliterated by removal of extracellular calcium, a substantial proportion of the contractile effect of U44069 persists under these conditions. The persistent effect of U44069 under calcium-free conditions was not diminished by nifedipine (a slow calcium channel blocker) but was blocked by 2-n-butyl-3-dimethylamino-5,6-methylenedioxyindene (an intracellular calcium antagonist). These results provide experimental evidence for the proposal that U44069 contracts the aorta in the absence of extracellular calcium by mobilizing intracellular calcium.


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