Changes in cardiovascular adrenoceptor response in rats subsequent to myocardial infarction.
Since sympatho-adrenal activity was greatest on the second day after experimental myocardial infarction in the rat, we investigated the responsiveness of cardiovascular adrenoceptors in pithed rats at this time and also determined the number of beta-adrenoceptors in the myocardium of the rats. In addition, the sympathetic outflow was measured, as a presynaptic parameter for estimating sympathetic nervous activity. The number of beta-adrenoceptor binding sites and the frequency responses of the heart were unchanged by myocardial infarction on the second day. There was also no difference from control animals with respect to sympathetic outflow. However, the rise in diastolic blood pressure, caused by electrical stimulation of the sympathetic nervous system, was far more pronounced in animals with infarction than in controls. In contrast, rats with myocardial infarction exhibited an attenuated response of diastolic blood pressure to infused noradrenaline. The observed effects can possibly be explained by changes of alpha-adrenoceptors, or perhaps by an enhanced degradation of catecholamines in the endothelium.
Türck
D
D
Physiologisches Institut, Universität München.
Dominiak
P
P
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002319:Cardiovascular System / Q000503:physiopathology*; D003655:Decerebrate State; D004558:Electric Stimulation; D004837:Epinephrine / Q000097:blood / Q000494:pharmacology; D005280:Fenoterol / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D009203:Myocardial Infarction / Q000503:physiopathology*; D009638:Norepinephrine / Q000097:blood; D051381:Rats; D011941:Receptors, Adrenergic / Q000502:physiology*; D014403:Tubocurarine / Q000494:pharmacology; D014630:Vagus Nerve / Q000503:physiopathology
D011941:Receptors, Adrenergic; D005280:Fenoterol; D014403:Tubocurarine; D009638:Norepinephrine; D004837:Epinephrine