scholarly journals The role of M3 receptors in regulation of electrical activity deteriorates in the rat heart during ageing

2021 ◽  
Author(s):  
Svetlana V. Tapilina ◽  
Alexandra D. Ivanova ◽  
Tatiana S. Filatova ◽  
Pavel A. Galenko-Yaroshevsky ◽  
Denis V. Abramochkin
Keyword(s):  
Electrical Activity ◽  
Rat Heart ◽  
M3 Receptors

The Role of Computer Modeling in Electrocardiography

1990 ◽  
Vol 29 (04) ◽  
pp. 282-288 ◽  
Author(s):  
A. van Oosterom
Keyword(s):  
Electrical Activity ◽  
Computer Modeling ◽  
Body Surface ◽  
Electrical Current ◽  
The Body ◽  
Volume Conductor ◽  
Current Generator ◽  
Cardiac Electrical Activity ◽  
Source Models

AbstractThis paper introduces some levels at which the computer has been incorporated in the research into the basis of electrocardiography. The emphasis lies on the modeling of the heart as an electrical current generator and of the properties of the body as a volume conductor, both playing a major role in the shaping of the electrocardiographic waveforms recorded at the body surface. It is claimed that the Forward-Problem of electrocardiography is no longer a problem. Several source models of cardiac electrical activity are considered, one of which can be directly interpreted in terms of the underlying electrophysiology (the depolarization sequence of the ventricles). The importance of using tailored rather than textbook geometry in inverse procedures is stressed.

Both M1 and M3 receptors regulate exocrine secretion by mucous acini

1996 ◽  
Vol 271 (6) ◽  
pp. C1963-C1972 ◽  
Author(s):  
D. J. Culp ◽  
W. Luo ◽  
L. A. Richardson ◽  
G. E. Watson ◽  
L. R. Latchney
Keyword(s):  
Inhibitory Effect ◽  
Exocrine Secretion ◽  
Muscarinic Agonist ◽  
High Affinity ◽  
Muscarinic Response ◽  
M1 Receptor ◽  
M3 Receptors ◽  
Pharmacological Studies ◽  
Equilibrium Dissociation

We investigated the role of M1 and M3 receptors in regulating exocrine secretion from acini isolated from rat sublingual glands. In secretion experiments, we derived affinity values (KB) from Schild regression analysis for the antagonists pirenzepine (61.0 nM) and 4-diphenylacetoxy-N-methylpiperidine (4-DAMP; 1.06 nM). The KB for 4-DAMP is similar to its affinity value [equilibrium dissociation constant from competition studies (Ki); 1.81 nM] determined from radioligand competition experiments. In contrast, the KB for pirenzepine is between its high-affinity (17.6 nM) and low-affinity (404 nM) Ki values. In separate secretion experiments, we found that the M1 receptor antagonist, M1-toxin, induces a rightward shift in the concentration-response curve to muscarinic agonist and inhibits maximal secretion by 40%. The inhibitory effect of M1-toxin appears specific for M1 receptor blockade, since the toxin abolishes acinar high-affinity pirenzepine-binding sites and does not inhibit secretion induced by nonmuscarinic agents. Additional pharmacological studies indicate muscarinic receptors do not function through putative neural elements within isolated acini. Our combined results are consistent with both M1 and M3 receptors directly regulating mucous acinar exocrine secretion and indicate M3 receptors alone are insufficient to induce a maximal muscarinic response.

scholarly journals Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH

2009 ◽  
Vol 297 (1) ◽  
pp. H153-H162 ◽  
Author(s):  
Sabrina Serpillon ◽  
Beverly C. Floyd ◽  
Rakhee S. Gupte ◽  
Shimran George ◽  
Mark Kozicky ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Rat Heart ◽  
Mitochondrial Respiratory Chain ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Posterior Wall Thickness ◽  
Patients With Diabetes ◽  
Protein Kinase C Inhibitor ◽  
Glucose 6 Phosphate Dehydrogenase

Increased oxidative stress is a known cause of cardiac dysfunction in animals and patients with diabetes, but the sources of reactive oxygen species [e.g., superoxide anion (O2−)] and the mechanisms underlying O2− production in diabetic hearts are not clearly understood. Our aim was to determine whether NADPH oxidase (Nox) is a source of O2− and whether glucose-6-phosphate dehydrogenase (G6PD)-derived NADPH plays a role in augmenting O2− generation in diabetes. We assessed cardiac function, Nox and G6PD activities, NADPH levels, and the activities of antioxidant enzymes in heart homogenates from young (9–11 wk old) Zucker lean and obese (fa/fa) rats. We found that myocardial G6PD activity was significantly higher in fa/fa than in lean rats, whereas superoxide dismutase and glutathione peroxidase activities were decreased ( P < 0.05). O2− levels were elevated (70–90%; P < 0.05) in the diabetic heart, and this elevation was blocked by the Nox inhibitor gp-91ds-tat (50 μM) or by the mitochondrial respiratory chain inhibitors antimycin (10 μM) and rotenone (50 μM). Inhibition of G6PD by 6-aminonicotinamide (5 mM) and dihydroepiandrosterone (100 μM) also reduced ( P < 0.05) O2− production. Notably, the activities of Nox and G6PD in the fa/fa rat heart were inhibited by chelerythrine, a protein kinase C inhibitor. Although we detected no changes in stroke volume, cardiac output, or ejection fraction, left ventricular diameter was slightly increased during diastole and systole, and left ventricular posterior wall thickness was decreased during systole ( P < 0.05) in Zucker fa/fa rats. Our findings suggest that in a model of severe hyperlipidema and hyperglycemia Nox-derived O2− generation in the myocardium is fueled by elevated levels of G6PD-derived NADPH. Similar mechanisms were found to activate O2− production and induce endothelial dysfunction in aorta. Thus G6PD may be a useful therapeutic target for treating the cardiovascular disease associated with type 2 diabetes, if second-generation drugs specifically reducing the activity of G6PD to near normal levels are developed.

Pressure Volume Curves in Arrested Heterotopic Rat Heart Isografts: Role of Improved Myocardial Protection

1999 ◽  
Vol 86 (1) ◽  
pp. 123-129 ◽  
Author(s):  
Joanne P. Starr ◽  
Chao-Xiang Jia ◽  
David G. Rabkin ◽  
Mehrdad M.R. Amirhamzeh ◽  
Joseph P. Hart ◽  
...  
Keyword(s):  
Rat Heart ◽  
Myocardial Protection

scholarly journals ROLE OF SDF-1α/CXCR4 AXIS TO THE CARDIOPROTECTIVE EFFECT OF ISCHEMIC POST-CONDITIONING IN ISOLATED RAT HEART

2013 ◽  
Vol 61 (10) ◽  
pp. E217
Author(s):  
Jeong-Su Kim ◽  
Ju-Hyun Park ◽  
Kook-Jin Chun ◽  
Young-Ho Jang ◽  
June-Hong Kim ◽  
...  
Keyword(s):  
Rat Heart ◽  
Isolated Rat Heart ◽  
Cardioprotective Effect ◽  
Cxcr4 Axis ◽  
Isolated Rat
Sign in / Sign up

Export Citation Format

Share Document