[Signal transduction in regulation of myocardial contractility].
Myocardial cells are able to adapt the cardiac pump function rapidly and widely to the changing requirements of vital organs through intrinsic and extrinsic regulatory mechanisms. This regulation is achieved by alteration of [Ca2+]i mobilization, Ca2+ sensitivity of myofibrils or both. Frank-Starling's mechanism achieved by alteration of Ca2+ sensitivity and force-frequency relation, primarily due to modulation of [Ca2+]i mobilization, are important intrinsic mechanisms. As extrinsic mechanisms, catecholamines play a crucial role by activation of both beta- and alpha 1-adrenoceptors through cyclic AMP, and products of phosphoinositide hydrolysis, as messengers, respectively. Adenosine and ACh act via similar transduction processes, including Gi or Gk proteins coupled to inhibition of adenylate cyclase, or activation of K+ channels. Most of these regulations are modulated and constitute crucial pathophysiological mechanisms in chronic heart failure.
Department of Pharmacology, Yamagata University School of Medicine.
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D002118:Calcium / Q000378:metabolism / Q000502:physiology; D002395:Catecholamines / Q000502:physiology; D000242:Cyclic AMP / Q000378:metabolism; D006801:Humans; D006868:Hydrolysis; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D010716:Phosphatidylinositols / Q000378:metabolism; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D015398:Signal Transduction
D002395:Catecholamines; D010716:Phosphatidylinositols; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D000242:Cyclic AMP; D002118:Calcium