Final answer:
To combat a sudden increase in MAP, the kidney engages its autoregulatory mechanisms: constriction of afferent arterioles via the myogenic mechanism, tubuloglomerular feedback, and sympathetic nervous system.
Step-by-step explanation:
The combined response of the three glomerular filtration rate (GFR) autoregulatory mechanisms to a sudden increase in mean arterial pressure (MAP) is the activation of the myogenic mechanism leading to constriction of the afferent arteriole, activation of tubuloglomerular feedback, and the release of vasoconstrictive substances. The myogenic mechanism reacts to increased blood pressure by causing smooth muscle cells in the afferent arteriole wall to contract, effectively resisting the increased pressure to maintain stable GFR.
Simultaneously, the tubuloglomerular feedback mechanism, involving the juxtaglomerular apparatus (JGA) and macula densa cells, determines that high GFR is causing less sodium chloride reabsorption and responds by releasing ATP and adenosine, which cause afferent arteriolar constriction. Lastly, increased sympathetic nervous system activity during high MAP may also release norepinephrine and epinephrine, leading to systemic and localized vasoconstriction, further regulating GFR.