Hormonal feedback loop, blood pressure

Blood pressure is also regulated via the hormonal feedback loop shown in Figure II-1-3. The system is affected only by decreases in mean blood pressure (hypotension), which result in decreased renal blood flow. Decreased renal pressure causes the release of renin, which promotes formation of the angiotensins. Angiotensin II increases aldosterone release from the adrenal cortex, which, via its mineralocorticoid actions to retain sodium and water, increases blood volume. Increased venous return results in an increase in cardiac output. Angiotensin II also causes vasoconstriction, resulting in an increase in TPR. 

Blood pressure is also regulated via the hormonal feedback loop shown in Figure-II-1-3. 

Baroreceptors increase their firing rate with increased blood pressure. Therefore, a decrease in baroreceptor sensitivity would decrease input to the vasomotor center, which would be interpreted by the vasomotor center as a decrease in blood pressure. This would lead to an increase in sympathetic outflow. The answer is (E). (If you chose a different answer, review the components of the autonomic and hormonal feedback loops for the maintenance of blood pressure Figure 6-4.)... 

Autonomic and hormonal control of cardiovascular function. Note that two feedback loops are present the autonomic nervous system loop and the hormonal loop. The sympathetic nervous system directly influences four major variables peripheral vascular resistance, heart rate, force, and venous tone. It also directly modulates renin production (not shown). The parasympathetic nervous system directly influences heart rate. In addition to its role in stimulating aldosterone secretion, angiotensin II directly increases peripheral vascular resistance and facilitates sympathetic effects (not shown). The net feedback effect of each loop is to compensate for changes in arterial blood pressure. Thus, decreased blood pressure due to blood loss would evoke increased sympathetic outflow and renin release. Conversely, elevated pressure due to the administration of a vasoconstrictor drug would cause reduced sympathetic outflow, reduced renin release, and increased parasympathetic (vagal) outflow. 

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