Blood pressure regulation

The core idea

Mean arterial pressure (MAP) = cardiac output × systemic vascular resistance. Because diastole lasts longer than systole at rest, MAP ≈ diastolic + one-third of pulse pressure: for 120/90, MAP ≈ 100 mmHg.

• Pulse pressure (systolic minus diastolic) depends on stroke volume and arterial stiffness. It widens in aortic regurgitation, thyrotoxicosis, anaemia, fever and with stiff elderly aortas; it narrows in shock, aortic stenosis and tamponade.

Resistance and flow

• Flow = pressure difference ÷ resistance. Poiseuille: resistance is proportional to length and viscosity and inversely to the fourth power of the radius; halving the radius raises resistance 16 times.
• Arterioles are the main resistance vessels; veins hold most blood volume; capillaries have the largest cross-section and slowest flow.

Short term: the baroreceptor reflex (seconds)

• Sensors: stretch receptors in the carotid sinus (afferents in IX) and aortic arch (afferents in X).
• Centre: nucleus tractus solitarius, which drives the vasomotor centre in the medulla oblongata and lower pons (sympathetic) and the vagal nuclei. The hypothalamus influences but is not the centre.
• What makes them fire most: baroreceptors respond to both the level and the rate of change of stretch. At the same mean pressure, a pulsatile pressure rising rapidly produces more firing than a steady pressure.
• Fall in BP (standing, mild haemorrhage at 90/60): less stretch and fewer impulses, so sympathetic output rises and vagal output falls: tachycardia, stronger contraction, arteriolar and venous constriction, renin release. Rise in BP does the reverse (vagal slowing, vasodilatation).
• The reflex buffers moment-to-moment pressure but resets within 1–2 days, so it does not set long-term BP.

• CNS ischaemic response: when MAP falls below about 60 mmHg, brainstem ischaemia produces an intense sympathetic discharge, the last-ditch defence. The Cushing reflex (hypertension, bradycardia, irregular breathing) is its form in raised intracranial pressure.
• Peripheral chemoreceptors (carotid and aortic bodies) raise sympathetic outflow when PO2 falls. In obstructive sleep apnoea, repeated desaturation causes chemoreflex sympathetic activation, producing resistant hypertension with loss of the normal night-time dip.

Medium term: renin–angiotensin–aldosterone (minutes to hours)

• Furosemide raises renin directly: the macula densa senses chloride through NKCC2, the same transporter furosemide blocks, so it reads "low salt" and signals renin release, besides the effect of volume loss.
• Renin cleaves angiotensinogen (from liver) to angiotensin I; ACE converts it to angiotensin II, mainly in the pulmonary capillary endothelium as blood passes through the lungs. ACE also breaks down bradykinin.
• Angiotensin II constricts arterioles (and the efferent arteriole, preserving GFR), stimulates aldosterone, ADH and thirst, and increases proximal sodium reabsorption.
• Aldosterone acts on principal cells of the collecting duct (and late distal tubule): it increases ENaC channels and Na+/K+-ATPase. Sodium entry through ENaC makes the lumen negative, driving K+ secretion (and H+ secretion by intercalated cells). Excess aldosterone (Conn adenoma) therefore causes hypertension, hypokalaemia and metabolic alkalosis with low renin; potassium can be normal.
• Secondary hyperaldosteronism (heart failure, cirrhosis, renal artery stenosis, haemorrhage) follows reduced renal perfusion and high renin. A young hypertensive with high renin suggests renal artery stenosis.
• ADH retains water and, at high levels, constricts vessels; ANP and BNP cause natriuresis and vasodilatation.
• In severe dehydration, aldosterone and ADH both rise.

Long term: the kidney (days)

• Pressure natriuresis: a rise in arterial pressure increases sodium and water excretion until volume and pressure return to the set point. Chronic hypertension means the kidney is holding sodium at a higher pressure: renal disease, high salt intake, aldosterone excess, renal artery stenosis.
• Renal blood flow is autoregulated between a MAP of about 80 and 180 mmHg by the myogenic response and tubuloglomerular feedback.

Remember Baroreflex for seconds, hormones for hours, kidneys for life.

The heart in hypertension

• Chronic pressure overload raises wall stress (Laplace). Myocytes add sarcomeres in parallel, thickening each fibre: concentric hypertrophy with a thick wall and normal cavity, which lowers wall stress but stiffens the ventricle, causing diastolic heart failure first, more oxygen demand and an S4. Volume overload (regurgitation) adds sarcomeres in series: eccentric hypertrophy with dilatation.

Exam trap Postural hypotension without a rise in heart rate means the reflex is broken, not that the patient is dry.

Secondary hypertension clues

• Berry aneurysms, which rupture with sudden rises in pressure, lack tunica media at the defect.

How FCPS asks about this

• Postural drop with no heart rate rise in a long-standing diabetic: autonomic neuropathy.
• Postural drop with tachycardia after diarrhoea: hypovolaemia with intact baroreflex.
• Where angiotensin I becomes angiotensin II: pulmonary capillary endothelium.
• Vasomotor centre: medulla and lower pons; CNS ischaemic response below MAP 60 mmHg.
• Greatest carotid sinus firing: pulsatile pressure rising rapidly.
• How furosemide raises renin: macula densa senses less chloride when NKCC2 is blocked.
• Aldosterone hypokalaemia: Na+ entry through ENaC drives K+ secretion.