Local cardiac responses--alternative methods of control.
Much attention has been paid to the influence of the beta-adrenoceptor system on cardiac function in heart failure. Full agonists and partial agonists acting on cardiac beta 1 receptors have been widely investigated, as has the density of these receptors in the failing heart. However, other cardiac control mechanisms may play important roles in the normal heart as well as in heart failure. The Frank-Starling mechanism of enhanced cardiac contraction produced by mechanical stretching of the ventricular myofibrils is well known. When treating patients with heart failure with diuretics, vasodilators and other drugs that influence preload, it is important to consider their overall effects in relation to the Starling curves. Atrial stretching also produces compensatory responses which are currently being intensively studied. Reflex release of atrial natriuretic factor after stimulation of atrial receptors has important physiologic effects in heart failure. The atria, but not the ventricles, are innervated by the vagus; the influence of the parasympathetic nervous system on the heart and circulation is often overlooked. The initial increase in heart rate during exercise is primarily due to withdrawal of vagal influence. Besides acetylcholine, the parasympathetic transmitter, many other local hormones may affect cardiac function; these include prostaglandins, 5-hydroxytryptamine and histamine. Although the activity of the sympathetic nervous system is mediated primarily through beta 1 adrenoceptors, both beta 2 and alpha receptors are also found in the heart. Myocardial alpha 1 receptors, which mediate a positive inotropic effect, have been identified, and prejunctional alpha 2 receptors may mediate inhibition of norepinephrine release from sympathetic nerves.(ABSTRACT TRUNCATED AT 250 WORDS)
Phillipps-University Marburg, Department of Internal Medicine and Cardiology, Federal Republic of Germany.
B
B
Maisch
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000502:physiology; D006333:Heart Failure / Q000503:physiopathology*; D006632:Histamine / Q000502:physiology; D006801:Humans; D009200:Myocardial Contraction; D011453:Prostaglandins / Q000502:physiology; D011983:Receptors, Purinergic / Q000502:physiology; D012701:Serotonin / Q000502:physiology; D014630:Vagus Nerve / Q000503:physiopathology
D000316:Adrenergic alpha-Agonists; D011453:Prostaglandins; D011983:Receptors, Purinergic; D012701:Serotonin; D006632:Histamine; D009320:Atrial Natriuretic Factor