80 Homeostasis of blood volume, blood pressure, and body osmolarity

Body Osmolarity in Dehydration and Hemorrhage

Dehydration and hemorrhage both lead to changes in body osmolarity, but in different ways:

• Dehydration: Dehydration results from excessive loss of water relative to solute, leading to increased plasma osmolarity. As water is lost, the concentration of solutes in the blood rises, causing osmolarity to increase. This high osmolarity triggers osmoreceptors in the hypothalamus, leading to thirst and the release of antidiuretic hormone (ADH) to conserve water.
• Hemorrhage: In contrast, hemorrhage involves the loss of both blood and solutes (mainly red blood cells and plasma proteins), leading to a decrease in blood volume but not necessarily an immediate change in osmolarity. However, the subsequent fluid shifts can affect osmolarity. Initially, the body compensates by moving interstitial fluid into the vascular compartment, which can dilute blood plasma and slightly decrease osmolarity until the balance is restored.

Monitoring Blood Volume and Blood Pressure

The cardiovascular, endocrine, and urinary systems closely monitor blood volume and pressure through several mechanisms:

• Cardiovascular System: Baroreceptors located in the aortic arch and carotid sinuses sense changes in blood pressure. When blood pressure falls, these receptors send signals to the brainstem, which responds by increasing sympathetic nervous system activity and decreasing parasympathetic activity. This results in increased heart rate, contractility, and vasoconstriction, all of which help to raise blood pressure.
• Endocrine System: The endocrine system monitors blood volume and pressure via hormones. For instance, the renin-angiotensin-aldosterone system (RAAS) is activated when blood pressure drops. The kidneys release renin, which converts angiotensinogen to angiotensin I. Angiotensin-converting enzyme (ACE) then converts angiotensin I to angiotensin II, a potent vasoconstrictor that also stimulates the release of aldosterone from the adrenal cortex. Aldosterone promotes sodium and water reabsorption in the kidneys, increasing blood volume and pressure. ADH is released from the posterior pituitary in response to increased plasma osmolarity or significant drops in blood volume, promoting water reabsorption in the kidneys to increase blood volume.
• Urinary System: The kidneys play a crucial role in regulating blood volume and pressure by adjusting the volume of urine produced. When blood volume or pressure decreases, the kidneys reduce urine output through mechanisms influenced by ADH and aldosterone, thereby conserving water and increasing blood volume.

Integrated Responses to Low Blood Pressure from Dehydration

When dehydration leads to low blood pressure, the body initiates several integrated responses:

1. Cardiovascular Response: Baroreceptors detect the drop in blood pressure and activate the sympathetic nervous system, which increases heart rate and contractility, and induces vasoconstriction to elevate blood pressure.
2. Endocrine Response: The hypothalamus releases ADH to promote water reabsorption in the kidneys, reducing urine output and increasing blood volume. The RAAS is also activated, leading to aldosterone release, which enhances sodium and water reabsorption in the kidneys, further increasing blood volume and pressure.
3. Behavioral Response: The hypothalamic thirst center is activated, prompting the individual to drink water, which helps to restore blood volume and reduce plasma osmolarity.

Integrated Responses to Low Blood Pressure from Hemorrhage

In response to hemorrhage, the body activates a series of compensatory mechanisms to restore blood pressure:

1. Cardiovascular Response: Similar to dehydration, baroreceptors sense the drop in blood pressure and stimulate the sympathetic nervous system. This increases heart rate, contractility, and induces widespread vasoconstriction, which helps to maintain blood pressure despite reduced blood volume.
2. Endocrine Response: The RAAS is activated by reduced renal perfusion pressure, leading to the release of renin and subsequent production of angiotensin II and aldosterone. Angiotensin II causes vasoconstriction and aldosterone increases sodium and water reabsorption, raising blood volume and pressure. ADH is also released in response to low blood volume, promoting water reabsorption in the kidneys.
3. Fluid Shift: To compensate for the lost blood volume, interstitial fluid moves into the capillaries (capillary refill), temporarily increasing blood volume and maintaining perfusion to vital organs.

Comparison of Compensatory Mechanisms

Both dehydration and hemorrhage trigger similar compensatory mechanisms involving the cardiovascular, endocrine, and urinary systems, but there are key differences:

• Dehydration primarily triggers responses to conserve water and reduce plasma osmolarity. The focus is on increasing water intake through thirst and reducing water loss through ADH-mediated kidney actions. The RAAS is activated to a lesser extent compared to hemorrhage, as the primary issue is water deficit rather than total blood volume loss.
• Hemorrhage triggers a more robust activation of the RAAS and cardiovascular responses to rapidly restore blood volume and pressure. The focus is on replacing lost blood volume through fluid shifts, increasing heart rate and contractility, and inducing vasoconstriction to maintain perfusion to vital organs.