Describe the short-term and long-term mechanisms regulating arterial blood pressure. Add a note on the renin–angiotensin system.

Definitions and Normal Values

Classification of Regulatory Mechanisms

Rapid — Nervous Mechanisms

A. Baroreceptor reflex (marey reflex)

• Receptors — carotid sinus and aortic arch; stretch receptors
• Afferent — carotid sinus via Hering nerve → glossopharyngeal (IX); aortic via vagus (X)
• Centre — nucleus tractus solitarius in the medulla

↑ BP → Baroreceptors stretched → ↑ Afferent firing → Inhibits vasomotor centre; stimulates vagal centre → ↓ Sympathetic, ↑ parasympathetic → ↓ HR, ↓ contractility, vasodilatation → BP falls

• Most sensitive between 60–180 mmHg
• Resets in 1–2 days to a new level → therefore useless for long-term regulation
• Chief function — buffering sudden changes, especially on standing

B. Chemoreceptor reflex

• Carotid and aortic bodies; stimulated by ↓ PO2, ↑ PCO2, ↑ H+
• Operates only when BP falls below 80 mmHg → vasoconstriction

C. CNS ischaemic response

• The most powerful of all sympathetic activators
• Operates when BP falls below 60 mmHg; maximal at 15–20 mmHg
• Cushing reflex — raised intracranial pressure → medullary ischaemia → ↑ BP + bradycardia + irregular respiration
• A "last-ditch" mechanism to preserve cerebral perfusion

Intermediate Mechanisms

• Renin–angiotensin system — onset in minutes; see below
• Capillary fluid shift — ↓ BP → ↓ capillary hydrostatic pressure → fluid drawn from interstitium into blood
• Stress relaxation of vessels — vessels gradually accommodate a changed volume
• Vasopressin (ADH) — vasoconstriction at high concentration

Long-term — Renal Body Fluid Mechanism

↑ BP → Pressure diuresis and natriuresis → ↑ Renal excretion of salt and water → ↓ ECF volume → ↓ Venous return → ↓ cardiac output → BP returns TO normal

• This system has infinite gain — it continues to act until BP is exactly restored
• Therefore the kidney is the ultimate long-term regulator of blood pressure

Renin–angiotensin–aldosterone system

↓ Renal perfusion / ↓ Na+ / sympathetic stimulation → renin from juxtaglomerular cells → Angiotensinogen → Angiotensin I → ACE (chiefly in lung) → angiotensin II → Vasoconstriction + aldosterone + ADH + thirst → BP rises

Peripheral Resistance and Poiseuille’s Law

• Halving the radius increases resistance 16-fold
• Arterioles are the chief resistance vessels — the "stopcocks" of the circulation; they account for about 50% of total peripheral resistance
• Viscosity also matters — ↑ in polycythaemia, ↓ in anaemia
• Laminar flow is silent; turbulent flow produces sound, which is the basis of Korotkoff sounds and murmurs
• Reynolds number > 2000 predicts turbulence

Applied Aspects

• Carotid sinus syncope — a tight collar or neck massage stimulates the sinus → bradycardia and hypotension → fainting
• Postural hypotension — failure of the baroreceptor reflex, as in autonomic neuropathy of diabetes
• Antihypertensives act on these mechanisms — ACE inhibitors and ARBs on the RAAS, diuretics on the renal mechanism, β-blockers on cardiac output
• Essential hypertension — the renal pressure–natriuresis curve is reset to the right, so a higher pressure is needed to excrete the same sodium load
• Cushing reflex — a rising BP with bradycardia in a head-injured patient is an ominous sign of raised intracranial pressure
• Renal artery stenosis → persistent renin release → secondary hypertension, correctable by angioplasty