Fisiología Renal - ADH (Hormona antidiurética) y Sed (IG:@doctor.paiva)

Introduction to Renal Physiology

Overview of Topics

• The class will cover generalities about ADH (antidiuretic hormone), its release stimuli, the thirst center, and drinking thresholds.

• Discussion includes the relationship between ADH, thirst, body hydration status, and osmolarity.

• Emphasis on how increased water leads to lower osmolarity and vice versa; implications for urine concentration.

Mechanisms of Osmolarity Regulation

• A person with low water intake experiences increased plasma osmolarity, stimulating hypothalamic receptors that enhance ADH production.

• Conversely, excess water intake results in diluted urine due to decreased ADH activity.

ADH Release Mechanism

Hypothalamic Structures Involved

• The hypothalamus contains magnocellular neurons in the supraoptic and paraventricular nuclei that are crucial for ADH synthesis.

• These nuclei respond to changes in plasma osmolarity through specialized receptors lacking a typical blood-brain barrier.

Response to Osmolarity Changes

• Increased plasma osmolarity activates these receptors leading to enhanced ADH production and release from the posterior pituitary gland.

• Magnocellular neurons also receive input from various cardiovascular receptors detecting volume and pressure changes.

Stimuli for ADH Release

Factors Influencing Secretion

• Key stimuli for ADH release include elevated plasma osmolarity, reduced blood pressure, and decreased blood volume detected by cardiac atrial receptors.

• The transport of synthesized ADH occurs via neurophysin proteins from the hypothalamus to the posterior pituitary where it is stored until needed.

Mechanism of Action

• When activated by high osmolarity or low blood pressure/volume, calcium channels facilitate exocytosis of stored ADH into circulation.

Mechanisms of Renin-Angiotensin System and Antidiuretic Hormone (ADH)

Role of Carotid and Aortic Receptors

• Various receptors located in the carotid sinus and aortic arch respond to decreases in blood volume and pressure, leading to renal hypoperfusion. This triggers the release of renin, which subsequently activates angiotensin II.

Osmolarity's Influence on ADH Release

• The secretion of ADH is primarily stimulated by changes in plasma osmolarity. An increase in osmolarity causes dehydration of osmoreceptors, promoting the production and release of ADH.

Effects of Osmolarity Changes

• Conversely, a decrease in osmolarity leads to edema in osmoreceptors, inhibiting both ADH production and thirst. The main stimulus for ADH release remains elevated plasma osmolarity due to sodium concentration or reduced blood volume/pressure.

Sensitivity to Volume Changes

• Increased plasma osmolarity is more sensitive than decreased blood volume or pressure; it can trigger ADH secretion with just a 1% change, while significant drops (5-10%) are needed for volume-related stimulation.

Receptor Types and Functions

• Different types of vasopressin receptors exist: V1 receptors cause vasoconstriction; V2 receptors promote water reabsorption in kidneys; V3 receptors are involved in neuromodulation within the central nervous system.

Mechanism of Action at Kidney Level

• In distal tubules and collecting ducts, aquaporins facilitate water reabsorption. When ADH binds to V2 receptors, it activates adenylate cyclase via G-proteins, increasing cAMP levels that enhance aquaporin insertion into membranes.

Summary of Key Points on ADH

Understanding the Role of ADH and Thirst Mechanisms

The Impact of Antidiuretic Hormone (ADH) on Water Absorption

• Inhibiting ADH leads to reduced water absorption, resulting in increased urination and significant dehydration, which can cause severe hangovers.

• The thirst mechanism is linked to the release of ADH, primarily regulated by osmotic receptors that stimulate thirst when plasma osmolarity increases.

• Key stimuli for thirst include elevated plasma osmolarity, decreased blood volume, low blood pressure, and increased angiotensin levels.

Digestive Influences on Thirst

• Dryness in the mouth stimulates thirst while gastric distension inhibits it; drinking water hydrates the mouth and esophagus, reducing the sensation of thirst.

• It takes 30 to 60 minutes for plasma osmolarity to normalize after hydration; immediate relief from thirst does not equate to instant regulation of osmolarity.

Age-related Changes in Thirst Sensitivity

• Older adults exhibit decreased sensitivity in their thirst response due to a less responsive center for regulating fluid balance.

• A sodium concentration increase beyond normal levels activates a threshold mechanism for drinking behavior.

Interplay Between Sodium Intake and ADH Regulation

• High sodium intake causes minor changes in plasma sodium concentration but significantly affects ADH and thirst mechanisms when feedback systems are disrupted.

• Proper functioning of ADH helps reabsorb water at the kidney level, normalizing plasma osmolarity relative to sodium concentration.

Feedback Mechanisms Affecting Thirst and Fluid Balance

• Increased osmolarity stimulates both the thirst center and vasopressin production; this process involves complex feedback loops involving renal function.

• Decreased blood volume triggers renin release from kidneys, further stimulating both thirst and hormone production related to fluid retention.

Comparative Analysis of Stimuli for Thirst vs. ADH Release

• Small changes in osmolarity strongly influence thirst while larger fluctuations in volume or pressure have a more potent effect on ADH secretion.