Renal Effects on Blood Pressure

Study Notes

Kidneys regulate blood pressure by modifying extracellular fluid (ECF) volume and plasma composition.
Intrinsic Mechanisms:
- Autoregulation: Protects kidneys from fluctuations in systemic blood pressure.
- Renin-Angiotensin-Aldosterone (RAA) system: Juxtaglomerular cells sense blood pressure in afferent arterioles and release renin to restore blood pressure, reliant on the juxtaglomerular apparatus (JGA).
Extrinsic Mechanisms:
- Sympathetic nervous system reduces glomerular filtration rate (GFR) to elevate blood pressure when necessary.

Composed of:
- Juxtaglomerular (JG) cells: Specialized muscle cells releasing renin in response to low blood pressure or decreased sodium concentration.
- Macula densa cells: Located in the distal convoluted tubule, these cells recognize changes in sodium levels in the filtrate, stimulating renin release.

Monitors blood pressure in afferent arterioles; a decrease triggers renin release.
Renin initiates a cascade involving angiotensin I and II, antidiuretic hormone (ADH), and aldosterone to modulate blood pressure and fluid balance.

Produced by adrenal cortex, it enhances sodium reabsorption in distal convoluted tubules and collecting ducts.
Stimulates the synthesis of Na+/K+ transport proteins via DNA coding for mRNA.
In the absence of aldosterone, significant salt loss (up to 20g/day) occurs; with aldosterone, salt loss is minimal.

Achieved by kidneys managing urine output through Counter-Current Multiplier Mechanism (CCMM).
The anatomical structure of juxtamedullary nephrons and vasa recta enables this mechanism, with varying permeability in different segments.

Counter-current: Filtrate flows in opposite directions in the loop of Henle compared to blood in vasa recta.
Multiplier mechanism: Ion movement occurs in incremental steps, resulting in significant osmotic changes.

The loop of Henle establishes an osmotic gradient from cortex (300 mOsm/L) to medulla (1200 mOsm/L) via:
- Water and ion movement from filtrate to blood in the vasa recta.
- Variances in tubular cell permeabilities between descending and ascending limbs.

Descending limb: Permeable to water but not to Na+ and Cl-; water exits by osmosis, collected by vasa recta.
Ascending limb: Impermeable to water, permeable to Na+ and Cl-; “salt pumps” reduce filtrate osmolarity to 100 mOsm/L as salts are retained by vasa recta.

Collecting ducts are typically impermeable to water but can change permeability through ADH modulation.

Controls urine concentration based on body hydration states.
Osmoreceptors in the hypothalamus detect plasma osmolality and prompt ADH release during water deficits.
ADH increases water reabsorption in distal convoluted tubule (DCT) and collecting ducts.

Presence of ADH: In dehydration, ADH causes collecting ducts to become permeable to water, resulting in concentrated urine (~500 ml/day, <1200 mOsm/L).
Absence of ADH: Collecting ducts remain impermeable to water, leading to dilute urine (~>100 mOsm/L, larger volumes).