Physiology of hypertension !
- Mechanism
- Exam priority: medium
Hypertension is sustained high blood pressure; almost always, a kidney needs more pressure to get rid of salt.
Updated 2026-11-01
See it in 3D: Kidneys · Left renal artery · Left adrenal gland · Right adrenal gland · Left ventricle · Aortic arch
What it is
In primary hypertension (90–95% of cases) genetics, high salt intake, obesity, sympathetic and renin–angiotensin–aldosterone activity, and arterial stiffness combine. All of them converge on a kidney that needs more pressure to excrete sodium. Sustained high pressure damages the target organs: heart, kidney, brain, retina and arteries.
How it works, step by step
- Salt intake exceeds what the kidney can excrete at normal pressure (genetics, nephron loss or excess angiotensin II and aldosterone).
- Volume is retained; cardiac output and pressure rise.
- Tissues get more flow than they need and their arterioles constrict (autoregulation): peripheral resistance rises.
- Pressure stays high with near-normal output and high resistance, the typical pattern of established hypertension.
- The arterial wall thickens and stiffens; systolic pressure climbs further.
- The left ventricle hypertrophies, oxygen demand rises and coronary reserve shrinks.
- In the kidney arteriolosclerosis destroys nephrons and closes a vicious circle.
Hormone axes and feedback
Renin–angiotensin–aldosterone systemLesion None (normal)
Tap a box to see the hormone, or choose a lesion to see the lab pattern.
- Stimulates (+)
- Inhibits / negative feedback (−)
- Level ↑
- Level ↓
Secondary causes: the physiological clue
| Cause | Mechanism | Clue |
|---|---|---|
| Chronic kidney disease | Fewer nephrons: salt is not excreted | High creatinine, proteinuria |
| Renal artery stenosis | Underperfused kidney releases renin | Abdominal bruit; creatinine rises on ACE inhibitors |
| Primary hyperaldosteronism | High aldosterone with low renin | Hypokalemia, metabolic alkalosis |
| Pheochromocytoma | Excess catecholamines | Spells of headache, sweating and palpitations |
| Coarctation of the aorta | Aortic obstruction and underperfused kidney | Arms with higher pressure than legs |
| Obstructive sleep apnea | Nocturnal hypoxia and sympathetic activation | Snoring, daytime sleepiness |
Clinical notes
- Hypertension is the leading modifiable risk factor for stroke and myocardial infarction in Colombia and worldwide.
- Target organ damage: LV hypertrophy, heart failure, nephrosclerosis, retinopathy, stroke and aortic dissection.
- A hypertensive emergency is defined by acute organ damage, not by the number alone.
Test yourself
Think of the answer, then tap the question to see it.
Why does established hypertension usually show normal cardiac output and high peripheral resistance, even though it starts with volume retention?
Extra volume first raises output; tissues are overperfused and autoregulation constricts their arterioles, so resistance rises and output returns to normal.
A 30-year-old with resistant hypertension has hypokalemia and low renin. Which mechanism does this suggest?
Primary hyperaldosteronism: high aldosterone retains sodium and wastes potassium in the collecting duct, and the expanded volume suppresses renin.
Why is pressure higher in the arms than the legs in aortic coarctation?
The obstruction lies beyond the arm branches; distal pressure falls and the underperfused kidney activates renin, raising proximal pressure.
Why does hypertensive LV hypertrophy cause diastolic dysfunction first?
The thick, fibrotic wall is less compliant and relaxes more slowly: the ventricle needs higher pressure to fill even though it ejects well.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- Long-term blood pressure control by the kidney
- The renin–angiotensin–aldosterone system
- Vascular compliance and capacitance
- Systolic, diastolic, mean and pulse pressure
- Heart failure physiology
Related conditions
- Arterial hypertension
- Hypertensive heart disease
- Chronic kidney disease
- Coarctation of the aorta
- Phaeochromocytoma
- Obesity
- Metabolic syndrome
In Biochemistry
In Pharmacology
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: Essential Hypertension (StatPearls (NCBI Bookshelf), 2023); Hypertensive Heart Disease (StatPearls (NCBI Bookshelf), 2025); Coarctation of the Aorta (StatPearls (NCBI Bookshelf), 2024); Pheochromocytoma (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 19). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
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Representative model, for educational purposes only.