Quiz 13

Angiotensin II

A powerful vasoconstrictor activated Renin

Why should you love your kidney and treat it right?

Because it controls blood pressure; it determines blood viscosity; it prevents anemia - The kidney detects low blood oxygen levels and blood pressure. When blood oxygen is too low (anemia), it releases erythropoietin (EPO), a hormone that increases red blood cell production. The more red blood cells produced, the greater the blood viscosity. When blood pressure is too high, the kidney can correct the problem by producing more urine. Urine is really just filtered blood and so with increased urine production, there is less blood volume and therefore less blood pressure. What is very amazing about this pressure/urine volume relationship is that it can work independently of hormones as a simple pressure filter. The higher the pressure, the more urine produced; the more urine made, the lower the blood volume will drop and therefore further reduce blood pressure. This is a life long mechanism for regulating blood pressure. Of course this can work in reverse such that if blood pressure is too low, less urine is made and blood volume with rise (coupled with some fluid intake as well).

During heavy exercise, cardiac output increases dramatically, although pressure may only increase modestly. How is this possible?

Because resistance increases at some vessels and decreases at others - During exercise, autoregulation to active skeletal muscles causes arterioles serving the muscle capillary beds to dilate and precapillary sphincters to open. Now that blood can find more vessels to fill as arterioles and sphincters open, decreasing resistance and increasing flow to tissues, pressure in the aorta may fall (more active muscle mass would increase number of dilating arterioles and magnitude of pressure drop). Such a drop in pressure would trigger baroreceptor reflexes that would lead to sympathetic activation. Sympathetic activation would trigger vasoconstriction in the systemic vessels except for those serving tissues that are working hard; in such tissues, autoregulation overcomes the sympathetic vasoconstriction and the vessels remain open. The vessels that do constrict (those serving gut tissue), act to increase pressure and shunt blood to other tissues that have decreased resistance. At the same time, the heart works harder (increases HR and contractility due to the sympathetic stimulation) and increases CO. It should seem that the increased CO should increase pressure radically and yet, the balance of the increased CO, vasoconstriction from sympathetic signals and vasodilation from autoregulation results in a high CO, some systemic pressure increase, but little change in the systemic peripheral resistance. In fact, peripheral resistance may even drop overall. Imagine if you needed to increase CO to deliver more blood, but you did not alter resistance (vessels could not change diameter). Pressure would increase dramatically and tear vessels. By altering resistance, we can have huge gains in CO with only a modest pressure increase.

As you move down the bronchial tree (from the trachea toward the alveoli), what changes do you observe.

Cartilage decreases

You have been gardening in a squatting position for 20 minutes. You stand up quickly to answer the phone and feel light headed. After about 10 seconds more you feel fine again. What was the cause and correction of your faint feeling?

Cause: low blood pressure due to too low cardiac output Correction: sympathetic nervous system activation from a baroreceptor signal - Squatting for a while reduces venous return from the lower limb because the veins are compressed and cannot refill with blood or send blood toward the heart (try this and look at your feet after 20 minutes of squatting). Reduced venous return will cause reduced cardiac output (Frank-Starling law) and reduced blood pressure (flow = pressure change/R). The cause of your faint feeling was reduced blood flow to the brain due to reduced blood pressure. This reduction in blood pressure associated with posture changes (orthostatic changes) is detected by baroreceptors in the carotid arteries. The correction mechanism to fix the too low blood pressure is vasoconstriction of some peripheral arteries and increased cardiac output, both due to increased sympathetic activation. The information from baroreceptors in the aorta and carotid arteries is relayed to the medulla oblongata cardiovascular centers. When too low pressure is detected, these centers direct increased sympathetic activity to blood vessels and the heart. Increased sympathetic activity increases cardiac output, thus increasing flow in the system and increasing blood pressure overall. The increased sympathetic activation to blood vessels causes increased vasoconstriction of some systemic vessels that leads to an increase in pressure overall (blood vessels to brain escape this vasoconstriction to some degree). These corrective mechanisms can increase systemic blood pressure within 5-10 seconds. Angiotensin II and ANP are chemicals that adjust blood pressure but they do so in a matter of minutes or hours. Angiotensin II production is triggered when blood flow to the kidney is reduced. Angiotensin II causes widespread vasoconstriction and increases in blood volume through decreased urine production (using the hormones aldosterone & ADH). ANP is atrial natriuretic peptide - a hormone released from the heart when pressure is too high. ANP causes increased urine formation - the more urine made, the lower the blood volume will become. Reducing blood volume will reduce blood pressure. The kidney can control blood pressure by adjusting blood volume as a pressure filter. In this manner, the kidney takes hours to days to correct blood pressure, not seconds as indicated here.

Sympathetic activation

Corrects a sudden drop in blood pressure within seconds

Kidney

Maintains blood pressure by regulating blood volume

In normal, healthy individuals, the diaphragm moves superiorly during exhalation.

True - When the diaphragm contracts, it moves inferiorly, increasing the size of the thoracic cavity to allow air to flow into the lungs. During quiet exhalation, the diaphragm relaxes and passively moves superiorly to decrease the size of the thoracic cavity and force air out of the lungs.

Myogenic autoregulation

Vasodilation in response to decreased local blood pressure