tailieunhanh - Introduction to the Cardiovascular System - Part 6

Làm thế nào những thay đổi áp lực động mạch và nhịp tim được hiển thị trong hình 6-8 sẽ khác nhau nếu 1-adrenoceptors đã bị chặn trước khi sự quản lý của epinephrine liều thấp? | NEUROHUMORAL CONTROL OF THE HEART AND CIRCULATION 131 PROBLEM 6-2 How would the changes in arterial pressure and heart rate shown in Figure 6-8 be different if 31-adrenoceptors were blocked before the administration of low-dose epinephrine ly-adrenoceptor activation is responsible for the tachycardia and increased cardiac output produced by epinephrine. Blocking -adrenoceptors would abolish this response. Epinephrine also binds to vascular p2-adrenoceptors to cause vasodilation therefore arterial pressure would fall during epinephrine infusion in the presence of -adrenoceptor blockade because the decrease in systemic vascular resistance would not be offset by an increase in cardiac output. epinephrine are different because epinephrine binds to a-adrenoceptors as well as to p-adrenoceptors. Increasing concentrations of epinephrine result in further cardiac stimulation along with a-adrenoceptor mediated activation of vascular smooth muscle leading to vasoconstriction. This increases arterial blood pressure pressor response owing to both an increase in cardiac output and an increase in systemic vascular resistance. Circulating norepinephrine affects the heart and systemic vasculature by binding to P1 p2 1 and a2 adrenoceptors however the affinity of norepinephrine for p2 and a2-adrenoceptors is relatively weak. Therefore the predominant affects of norepinephrine are mediated through P1 and 1-adrenocep-tors. If norepinephrine is injected intravenously it causes an increase in mean arterial blood pressure systemic vasoconstriction and pulse pressure owing to increased stroke volume and a paradoxical decrease in heart rate after an initial transient increase in heart rate Fig. 6-9 Table 6-3 . The transient in crease in heart rate is due to norepinephrine binding to p1-adrenoceptors in the sinoatrial node whereas the secondary bradycardia is due to a baroreceptor reflex vagal-mediated which is in response to the increase in arterial pressure. High levels of circulating .