8.3 Renal_Urine formation_Regulation of Glomerular filtrationn

REGULATION OF GLOMERULAR FILTRATION RATE (GFR)

Complex: GFR is regulated mainly by controlling glomerular capillary blood pressure (GCP), since capsular hydrostatic pressure (CP) and plasma colloid osmotic pressure (COP) remain relatively constant, like adjusting a faucet rather than changing the drain.
Simple: The kidneys mostly change blood pressure in the glomerulus to control filtration.

KEY DETERMINANTS OF GFR

Complex: GFR depends on GCP, capillary surface area, and membrane permeability, summarized by GFR = Kf(GCP − CP − COP), where Kf reflects surface area and permeability like the size and porosity of a filter.
Simple: Pressure and filter size determine how much is filtered.

PRIMARY CONTROL SITE: AFFERENT & EFFERENT ARTERIOLES

Complex: Changes in afferent and efferent arteriole diameter are the main way to regulate GCP and thus GFR, similar to tightening or loosening hose clamps.
Simple: Narrow or widen blood vessels to control filtration.

AUTOREGULATION (LOCAL CONTROL)

Complex: Autoregulation maintains nearly constant GFR when mean arterial pressure is between 80–180 mmHg via afferent arteriole adjustments, like cruise control in a car.
Simple: The kidney self-adjusts to keep filtration steady.

MYOGENIC MECHANISM

Complex: Increased blood pressure stretches afferent arteriole smooth muscle, causing Ca²⁺-mediated contraction to stabilize GCP at ~55 mmHg, like a pressure-sensitive valve.
Simple: High pressure makes the vessel tighten automatically.

TUBULOGLOMERULAR FEEDBACK (JGA)

Complex: Macula densa cells detect Na⁺/Cl⁻ and flow changes and signal the afferent arteriole via nitric oxide to adjust GFR, like a sensor correcting conveyor belt speed.
Simple: Tubules sense flow and tell vessels to adjust.

SYMPATHETIC NERVOUS SYSTEM CONTROL

Complex: Intense sympathetic stimulation causes afferent vasoconstriction, increased Na⁺ reabsorption, and renin release, prioritizing blood pressure over GFR during stress, like diverting power in an emergency.
Simple: In stress, kidneys conserve fluid and reduce filtration.

RENIN–ANGIOTENSIN–ALDOSTERONE SYSTEM (RAAS)

Complex: Decreased blood volume, pressure, or Na⁺ triggers renin release, producing ANG II, which raises blood pressure and conserves fluid via vasoconstriction and aldosterone, like a backup pressure system.
Simple: RAAS saves salt, water, and raises blood pressure.

ANGIOTENSIN II EFFECTS ON GFR

Complex: Low ANG II preferentially constricts efferent arterioles to maintain GFR, while high ANG II constricts both arterioles and decreases GFR, like tightening both ends of a hose.
Simple: A little ANG II helps filtration, too much reduces it.

ALDOSTERONE (Na⁺ REGULATION)

Complex: Aldosterone increases Na⁺ reabsorption in the distal tubule and collecting duct, expanding extracellular fluid volume and blood pressure, like retaining more water in a reservoir.
Simple: Aldosterone keeps sodium and water in the body.

ATRIAL NATRIURETIC PEPTIDE (ANP)

Complex: ANP is released with increased blood volume and promotes Na⁺ and water excretion while increasing glomerular surface area, acting as a pressure-release valve.
Simple: ANP lowers blood volume and pressure.

PROSTAGLANDINS (RENAL PROTECTION)

Complex: Prostaglandin E₂ preserves renal blood flow during stress by dilating afferent arterioles, and NSAIDs block this protection, like disabling a safety buffer.
Simple: Prostaglandins protect kidneys under stress.