An acute increase in mean arterial pressure would cause an increase in the stretch of the
baroreceptor, causing an increase in the frequency of action potentials sent to the
medulla. The medulla responds to that stimulus in the short term in a manner that rapidly decreases mean arterial pressure. That response includes both limbs of the autonomic nervous system: parasympathetic activity increases as sympathetic activity decreases. This causes a decrease in heart rate. At the same time, the reduction in sympathetic activity decreases stroke volume (ventricular contractility decreases), reduces venomotor tone (as veins relax as they become more compliant), and decreases total peripheral resistance (arterioles dilate). Arteriole dilation will also result from a decrease in angiotensin II and vasopressin levels within the blood. The reduction in angiotensin II occurs as a consequence of a decrease in the release of renin from the kidneys, which is required for the eventual conversion of angiotensinogen to angiotensin I and thereafter
angiotensin II. Any changes in the release of vasopressin usually results from changes in the stimulation of the
hypothalamus, which determines the release of vasopressin from the posterior pituitary. However, any changes in angiotensin II and vasopressin also have more long-term consequences. Angiotensin II stimulates the release of aldosterone from the adrenal cortex.
Aldosterone and
vasopressin stimulate the expansion of blood volume by decreasing urine output. Thus, a decrease in these hormones will decrease blood volume by increasing urine output (diuresis).