Hemodynamic Homeostasis · §8 · MAP → sensors → controllers → effectors → MAP

The hemodynamic interaction map (sensor to MAP to feedback)

The hemodynamic interaction map has 7 nodes and 11 directed edges. Two sensors — the PIEZO baroreceptor and the NKCC2 macula densa — feed a fast baroreflex arc (seconds) and a slow RAAS/kidney integral arc (hours–days) that converge on MAP and close back to the sensors. Edge identities are cited [L]; the reproduced loop shapes are sim-verified [V].

The package’s wiring is a directed graph from sensors to MAP and back: 7 nodes, 11 edges. A fast loop (MAP → baroreceptor → baroreflex − SVR/HR → MAP) acts in seconds; a slow loop (MAP → macula densa → renin/TGF → RAAS/kidney → volume → MAP) acts over hours–days. Edge identities cited [L], loop shapes reproduced [V].

Two loops, two time-scales, one defended variable

The control architecture is two nested loops sharing the same output, which is what lets one variable be both quickly buffered and durably defended. The fast loop runs MAP → baroreceptor(PIEZO) → baroreflex −(−)→ SVR/HR → MAP in seconds (research target RP2); the slow loop runs MAP → macula densa(NKCC2) → renin(−)/TGF(+) → RAAS/kidney integrator → volume → MAP over hours to days (RP3). The fast loop attenuates; the slow loop sets the reference; together they make a defended setpoint.

The disease axes sit on these loops, which is why the map is more than a diagram. Essential hypertension is a rightward reset of the kidney integral reference; chronic heart failure is collapse of the cardiac high-output basin; and the hypotensions are individual node failures along the same edges. Carotid-body and cardiopulmonary afferents enter the map as cited seams from the cardiorespiratory package, keeping one canonical home for each result.

Directed edges (sign: 0 read-only, + raises, − lowers)

Each edge carries a sign, a grade and a named mechanism, so the map is auditable rather than schematic. The edges whose loop role is reproduced in the engine are graded [V]; the edges that import an external molecular or pharmacological identity are graded [L].

source→ targetsigngrademechanism
MAPbaroreceptor0[L] citedarterial wall stretch ~ pressure; PIEZO1/2 transduction (Zeng 2018)
MAPmacula_densa0[L] citeddistal NaCl delivery ~ GFR ~ pressure; NKCC2 chemosensing (slow)
baroreceptorbaroreflex+[L] citedafferent firing -> NTS -> autonomic outflow set
baroreflexvascular_resistance-[V] sim-reproducedfast negative feedback: pressure up -> sympathetic withdrawal -> SVR down (RP2)
baroreflexMAP-[V] sim-reproducednet fast buffering of a pressure step, residual ~ step/(1+G) (RP2)
macula_densaraas_endocrine-[L] citedhigh luminal NaCl -> renin DOWN (inverse); low NaCl -> renin UP
macula_densakidney_volume_integrator+[V] sim-reproducedtubuloglomerular feedback: high NaCl -> afferent constriction -> GFR down
raas_endocrinevascular_resistance+[L] citedAngII vasoconstriction raises SVR
raas_endocrinekidney_volume_integrator+[L] citedaldosterone/AngII raise Na/volume retention -> raises the defended reference
kidney_volume_integratorMAP+[V] sim-reproducedintegral (pressure-natriuresis) control sets the slow defended MAP reference (RP3, Guyton infinite gain)
vascular_resistanceMAP+[V] sim-reproducedOhm hydraulic: MAP = CVP + CO x SVR (RP1)