Any sudden alteration in the mean arterial blood pressure tends to produce compensatory reflex changes in heart rate, contractility, and vascular tone, which will oppose the initial pressure change and restore the homeostatic balance. The primary sensory mechanisms that detect changes in the mean arterial blood pressure are stretch receptors (baroreceptors) in the carotid sinus and aortic arch.
The injection of a vasoconstrictor, which causes an increase in mean arterial blood pressure, results in activation of the baroreceptors and increased neural input to the cardiovascular centers in the medulla oblongata. The reflex compensation for the drug-induced hypertension includes an increase in parasympathetic nerve activity and a decrease in sympathetic nerve activity. This combined alteration in neural firing reduces cardiac rate and force and the tone of vascular smooth muscle. As a consequence of the altered neural control of both the heart and the blood vessels, the rise in blood pressure induced by the drug is opposed and blunted.
Injection of a drug that causes a fall in the mean arterial blood pressure triggers diametrically opposite reflex changes. There is decreased impulse traffic from the cardiac inhibitory center, stimulation of the cardiac accelerator center, and augmented vasomotor center activity. These changes in cardiac and vasomotor center activity accelerate the heart and increase sympathetic transmission to the vasculature; thus, the drug-induced fall in blood pressure is opposed and blunted.
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