Regulation of Mean Arterial Pressure (MAP)

Mean Arterial Pressure (MAP): Purposes & Big-Picture Context

• MAP ≈ aortic pressure; primary goals of regulation:

  • Keep MAP at its homeostatic set-point to guarantee adequate systemic perfusion.

  • Secondarily adjust MAP to optimize O₂ transport and blood pH (H⁺ balance).

• Core effector organs: heart, systemic blood vessels, kidneys.

Core Negative-Feedback Architecture

• All classic control loops need:

  1. Sensors – continually monitor the variable.

  2. Integrating center – compares current values with set-points.

  3. Effectors – receive commands and restore balance.

• Variable list relevant here:

  • \text{MAP}, [\text{O}2]{blood}, \text{pH}_{blood}\;(\propto\;[\text{H}^+]).

Sensors

Arterial Baroreceptors

• Location & functional niches:

  • Aortic arch – directly measures MAP ("central gauge").

  • Carotid sinuses (bulges of the common carotids) – back-up MAP gauge & guardian of cerebral perfusion.

• Afferent pathways:

  • Aortic arch → Vagus n. (CN X).

  • Carotid sinus → Glossopharyngeal n. (CN IX).

Venous Baroreceptors (Low-pressure / Volume Receptors)

• Embedded in walls of the superior & inferior venae cavae and right-atrial junction.

• Pressure is extremely low; primary information conveyed = total blood volume status rather than MAP.

Chemoreceptors (Aortic & Carotid Bodies)

• Co-located with baroreceptors.

• Detect:

  • \text{O}_2 saturation (hypoxia).

  • (\text{pH}) via [\text{H}^+] (indirect monitor of \text{CO}2 because \text{CO}2+\text{H}2\text{O} \leftrightarrow \text{H}^++\text{HCO}3^-).

• Afferents run through same cranial nerves as baroreceptors.

Integrating Center – Medulla Oblongata

• Contains gray-matter cardiovascular control centers:

  • Cardiac center

  • Cardiac Accelerator Center (CAC) – sympathetic.

  • Cardiac Inhibitory Center (CIC) – parasympathetic.

  • Vasomotor center

  • Vasoconstrictor sub-center – sympathetic.

  • Vasodilator sub-center – inhibits sympathetic outflow to allow dilation.

• Always compares incoming sensory traffic with set-points and selects autonomic output pattern.

• Additional (non-exam) inputs: proprioceptors (movement), higher brain areas (cortex, limbic, hypothalamus – emotional pressure changes).

Effector Pathways

Sympathetic (thoracolumbar) Efferents

• Cardiac accelerator nerves → SA/AV nodes & myocardium → ↑ HR & ↑ contractility.

• Sympathetic vasomotor nerves → vascular smooth muscle → vasoconstriction (raising TPR).

• Stimulus transmitter: norepinephrine (NE).

Parasympathetic (craniosacral) Efferents

• Vagus nerve (CN X) → SA/AV nodes → ↓ HR (via muscarinic ACh receptors); minimal effect on ventricular contractility.

• Virtually no direct parasympathetic innervation of systemic arterioles (hence vessel tone is mainly a function of sympathetic activity).

Fundamental Equation Reminders

• \text{MAP}=\text{CO}\times \text{TPR}.

• \text{CO}=\text{HR}\times\text{SV} (stroke volume depends on contractility, preload, afterload).

Reflexes

Baroreceptor Reflex (pressure-centric)

• ↑ MAP → ↑ baroreceptor firing → medulla:

  • ↓ CAC & vasoconstrictor activity (↓ sympathetic).

  • ↑ CIC & vasodilator activity (↑ parasympathetic to heart).

  • Net → ↓ HR, ↓ contractility, vasodilation → ↓ MAP back toward set-point.

• ↓ MAP triggers the opposite cascade.

Chemoreceptor Reflex (gas/pH-centric)

• Trigger conditions: ↓ O₂, ↓ pH (↑ H⁺, typically via ↑ CO₂).

• Goal: raise MAP to accelerate perfusion of lungs & tissues.

• Medullary output:

  • ↑ sympathetic (CAC & vasoconstrictor) → ↑ CO & ↑ TPR → ↑ MAP.

  • Often coupled with respiratory center activation → ↑ ventilation (expels (\text{CO}_2), raises O₂).

Adrenergic & Cholinergic Receptors Cheat-Sheet

Mechanistic note:

• Mixed distribution in muscle arterioles: \alpha1 causes constriction but \beta2 predominates → net dilation during generalized sympathetic discharge ("fight-or-flight" shunt of blood to muscles & heart).

Hormonal Modulators of Vascular Tone & Volume

• Catecholamines (Epi/NE) – mirror autonomic actions; released from adrenal medulla when sympathetic activity spikes.

• Vasoconstrictors (raise TPR & MAP):

  • Antidiuretic hormone (ADH/vasopressin)

  • Angiotensin II

  • Aldosterone (indirect via Na⁺/water retention)

• Vasodilator: Atrial natriuretic peptide (ANP)

Kidney: Long-Term MAP & Chemistry Control

• Filters plasma; variable water reabsorption sets blood volume (BV).

• ADH is principal short-to-medium term hormone:

  • Stimulus: ↓ MAP or ↑ osmolarity.

  • Effect: ↑ water reabsorption → ↓ urine output → ↑ BV → ↑ MAP.

  • Bonus: ADH also produces vasoconstriction (V₁ receptors) – “pressin” aspect.

• Over hours–days, the renin-angiotensin-aldosterone system (RAAS) adds Na⁺ retention & further vasoconstriction.

Integrated Example Scenarios

• Hemorrhage → ↓ BV → ↓ venous pressure (volume receptors) & ↓ MAP (baroreceptors).

  • Reflex: Massive sympathetic discharge → ↑ HR/contractility, vasoconstriction, RAAS & ADH activation → restores pressure & volume.

• High-intensity sprint (exercise)

  • Proprioceptors + cortex anticipate demand → ↑ sympathetic tone even before MAP drops.

  • Targeted dilation in muscle arterioles (β₂) despite global sympathetic-mediated vasoconstriction elsewhere.

• Hypercapnia (↑ CO₂)/Acidosis

  • Chemoreceptors → ↑ MAP + ↑ ventilation; faster pulmonary circulation allows more rapid CO₂ off-loading and O₂ loading, ameliorating pH.

Quick Ethical & Clinical Relevance

• Autonomic blockers (β-blockers, α-blockers) exploit receptor specificity to treat hypertension, arrhythmias, pheochromocytoma.

• Over-aggressive vasoconstriction (ex: septic vasopressors, cocaine) risks ischemia in tissues lacking β₂ escape.

• Understanding low-pressure receptors guides fluid resuscitation strategy vs. vasopressor selection in shock management.

Key Equations & Numbers (to memorize)

• \text{MAP} = \text{CO} \times \text{TPR}.

• Normal systemic arterial MAP: \approx 93\;\text{mmHg} (calculated as \text{DP} + \frac{1}{3}(\text{SP}-\text{DP})).

• Venous (central) pressure: \approx 2\;\text{–}\;5\;\text{mmHg} → foundation for calling venous sensors “low-pressure”.

• Typical reflex latency: baroreceptor response within 1–2 heartbeats; hormonal/renal responses minutes–hours.