Chapter 5 of 5 - Physiology Course
Kidneys filter plasma, reclaim what you need, and excrete the rest. Hormones and nerves tune salt and water to keep extracellular fluid stable.
Renal questions blend filtration (what enters Bowman space), reabsorption (what returns to blood), and secretion (what moves from peritubular capillary into tubular fluid). Diuretics, acid-base disorders, and endocrine axes are easier once you can walk the nephron in order and place each transporter class on the diagrams below.
The glomerulus filters a protein-poor ultrafiltrate. The proximal tubule reabsorbs the bulk of Na+, HCO3-, glucose, and amino acids. The loop of Henle establishes a corticomedullary osmotic gradient. Distal nephron segments fine-tune Na+, K+, acid-base, and water under hormonal control.
Filtration fraction (GFR divided by renal plasma flow) rises if efferent arteriolar constriction increases filtration relative to flow through the peritubular capillary - one way angiotensin II supports GFR in some settings while still promoting proximal reabsorption. Tubular transport maxima explain glucosuria when filtered glucose exceeds the capacity of SGLT carriers, a classic link between physiology and diabetes mellitus presentations.
Each segment modifies tubular fluid composition; the collecting duct determines final urine osmolality under ADH.
Glomerular filtration
Ultrafiltrate formed; size and charge barrier exclude most protein.
Proximal tubule
Bulk reabsorption of Na+, water, HCO3−, glucose, amino acids.
Loop of Henle
Countercurrent multiplication; medullary osmotic gradient.
Distal convoluted tubule
Continued NaCl handling; calcium regulation features.
Collecting duct
Aldosterone, ADH, and flow rate tune Na+, K+, and water excretion.

Segment-specific transporters explain where diuretics act and why metabolic acidosis or potassium disorders arise.
Urea is a major nitrogenous waste product; handling in the medulla contributes to corticomedullary osmotic gradients and urine concentration physiology.
Formula
CH4N2O
Mol. Weight
60.06 g/mol
RAAS defends perfusion pressure via renin, angiotensin II, and aldosterone (Na+ retention, K+ and H+ handling consequences). ANP opposes volume expansion. Osmoreceptors and baroreceptors modulate ADH release from the posterior pituitary.
| Signal | Typical renal response |
|---|---|
| Effective circulating volume low | Increased Na+ reabsorption; ADH if osmolality/volume cues align |
| Plasma osmolality high | ADH increases; thirst center stimulated |
Sympathetic nerves and circulating hormones converge on afferent/efferent arteriolar tone, proximal reabsorption, and collecting-duct sodium channels. Understanding where aldosterone (distal nephron/collecting duct ENaC upregulation) and ADH (aquaporin insertion) act clarifies why disorders of mineralocorticoid excess produce hypertension and hypokalemia while diabetes insipidus produces dilute polyuria.
Angiotensin II is both a vasoconstrictor and a stimulus for aldosterone; ADH may rise from overlapping volume/osmolar signals.
Reduced renal perfusion / low NaCl at macula densa
Juxtaglomerular cells release renin.
Renin cleaves angiotensinogen
Angiotensin I converted to angiotensin II (ACE, lungs and elsewhere).
Angiotensin II effects
Vasoconstriction; proximal Na+ retention; aldosterone release.
Aldosterone on collecting duct
ENaC/RomK activity increases Na+ reabsorption and K+ secretion.
Net effect
Expand ECF volume; defend blood pressure; trade-offs in K+ and acid-base.
Quick Check
Which nephron region is the primary site of bulk isosmotic reabsorption of filtered glucose, amino acids, and bicarbonate?
Fill in the Blank
Aldosterone from the adrenal cortex increases epithelial sodium channel activity principally in the________, promoting Na+ reabsorption and K+ secretion.
Kidneys regenerate HCO3- and excrete net acid as titratable acid and NH4+. Integrate this with respiratory CO2 control from the respiratory physiology chapter for mixed disorders.
Proximal HCO3- reclamation and distal hydrogen ion secretion determine whether plasma bicarbonate rises or falls in chronic respiratory acidosis or alkalosis. Potassium shifts accompany acid-base disturbances because transporters exchange K+ for H+ across membranes - another reason renal physiology, respiratory physiology, and electrolyte questions travel together on exams.
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