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[Physiology](https://durgical.com/en/physiology/) · [Cardiovascular](https://durgical.com/en/physiology/#s-cardio)

# 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](https://durgical.com/en/anatomy/kidney/) · [Left renal artery](https://durgical.com/en/anatomy/renal-artery/) · [Left adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland/) · [Right adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland-abdomen/) · [Left ventricle](https://durgical.com/en/anatomy/left-ventricle/) · [Aortic arch](https://durgical.com/en/anatomy/aortic-arch/)

## Key points

- Definition: ≥140/90 mmHg in most guidelines; the 2017 US guideline uses ≥130/80 mmHg. It is confirmed with repeated readings.
- Primary: 90–95%. Suspect a secondary cause in the young, in resistant hypertension, with hypokalemia or with abrupt onset.
- Classic secondary causes: kidney disease, renal artery stenosis, primary hyperaldosteronism, pheochromocytoma, aortic coarctation, sleep apnea.
- The heart answers high afterload with concentric LV hypertrophy: relaxation fails first (diastolic dysfunction).
- Coarctation: higher pressure in the arms than the legs, weak and delayed femoral pulses, rib notching.

## 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 system **Lesion** None (normal)

Tap a box to see the hormone, or choose a lesion to see the lab pattern.

- Stimulates (+)
- Inhibits / negative feedback (−)
- Level ↑
- Level ↓

Tap each step of the renin–angiotensin–aldosterone axis and try the lesion patterns.

## Secondary causes: the physiological clue

| Cause | Mechanism | Clue |
| --- | --- | --- |
| [Chronic kidney disease](https://durgical.com/en/conditions/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](https://durgical.com/en/conditions/phaeochromocytoma/) | Excess catecholamines | Spells of headache, sweating and palpitations |
| [Coarctation of the aorta](https://durgical.com/en/conditions/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.

## Memory aid

"Salt goes in, pressure waits": until the kidney clears the salt at normal pressure, pressure stays up.

## 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.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/physiology-of-hypertension/)

## See it in 3D

The structures of Durgical's 3D anatomy where it happens.

- [Kidneys](https://durgical.com/en/anatomy/kidney/)
- [Left renal artery](https://durgical.com/en/anatomy/renal-artery/)
- [Left adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland/)
- [Right adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland-abdomen/)
- [Left ventricle](https://durgical.com/en/anatomy/left-ventricle/)
- [Aortic arch](https://durgical.com/en/anatomy/aortic-arch/)

## Related topics

- [Long-term blood pressure control by the kidney](https://durgical.com/en/physiology/long-term-blood-pressure-control-by-the-kidney/)
- [The renin–angiotensin–aldosterone system](https://durgical.com/en/physiology/the-renin-angiotensin-aldosterone-system/)
- [Vascular compliance and capacitance](https://durgical.com/en/physiology/vascular-compliance-and-capacitance/)
- [Systolic, diastolic, mean and pulse pressure](https://durgical.com/en/physiology/systolic-diastolic-mean-and-pulse-pressure/)
- [Heart failure physiology](https://durgical.com/en/physiology/heart-failure-physiology/)

## Related conditions

- [Arterial hypertension](https://durgical.com/en/conditions/arterial-hypertension/)
- [Hypertensive heart disease](https://durgical.com/en/conditions/hypertensive-heart-disease/)
- [Chronic kidney disease](https://durgical.com/en/conditions/chronic-kidney-disease/)
- [Coarctation of the aorta](https://durgical.com/en/conditions/coarctation-of-the-aorta/)
- [Phaeochromocytoma](https://durgical.com/en/conditions/phaeochromocytoma/)
- [Obesity](https://durgical.com/en/conditions/obesity/)
- [Metabolic syndrome](https://durgical.com/en/conditions/metabolic-syndrome/)

## In Biochemistry

- [Aldosterone](https://durgical.com/en/biochemistry/molecules/aldosterone/)
- [Angiotensin-converting enzyme (ACE)](https://durgical.com/en/biochemistry/enzymes/angiotensin-converting-enzyme/)
- [Catecholamines: synthesis and breakdown](https://durgical.com/en/biochemistry/topics/catecholamines-synthesis-and-breakdown/)

## In Pharmacology

- [ACE inhibitors](https://durgical.com/en/pharmacology/classes/ace-inhibitors/)
- [Angiotensin II receptor blockers (ARBs)](https://durgical.com/en/pharmacology/classes/angiotensin-ii-receptor-blockers/)
- [Beta blockers](https://durgical.com/en/pharmacology/classes/beta-blockers/)
- [Enalapril](https://durgical.com/en/pharmacology/enalapril/)
- [Losartan](https://durgical.com/en/pharmacology/losartan/)

[← All of physiology](https://durgical.com/en/physiology/)

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](https://www.ncbi.nlm.nih.gov/books/NBK539859/) (StatPearls (NCBI Bookshelf), 2023); [Hypertensive Heart Disease](https://www.ncbi.nlm.nih.gov/books/NBK539800/) (StatPearls (NCBI Bookshelf), 2025); [Coarctation of the Aorta](https://www.ncbi.nlm.nih.gov/books/NBK430913/) (StatPearls (NCBI Bookshelf), 2024); [Pheochromocytoma](https://www.ncbi.nlm.nih.gov/books/NBK589700/) (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.

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Source: https://durgical.com/en/physiology/physiology-of-hypertension/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/physiology-of-hypertension/