A cell exposed to epinephrine shows an intracellular response within seconds. Which pathway best explains this speed?
AEpinephrine diffuses through the plasma membrane and binds directly to a nuclear receptor
BEpinephrine binds a surface GPCR, activating adenylyl cyclase to produce cAMP, which activates PKA to phosphorylate existing enzymes
CEpinephrine enters the nucleus and acts as a transcription factor, rapidly inducing gene expression
DEpinephrine directly binds ribosomes and stimulates immediate protein synthesis
Epinephrine is water-soluble and cannot cross the membrane. It binds a Gs-coupled GPCR on the surface, activating adenylyl cyclase to convert ATP into cAMP. cAMP activates PKA, which phosphorylates pre-existing enzymes — a cascade that unfolds in seconds because no new protein synthesis is required. Options A and C describe steroid hormone mechanisms; option D is not a real signaling pathway.
Question 2 True / False
Steroid hormones act faster than peptide hormones because they bypass receptors and enter the cell directly.
TTrue
FFalse
Answer: False
While steroid hormones are lipid-soluble and do diffuse through the membrane, this does not make them faster. They must still bind intracellular receptors, translocate to the nucleus, alter transcription, and wait for new mRNA and protein to be synthesized — a process taking hours. Peptide hormones acting through second messengers modify existing enzymes within seconds to minutes, making them substantially faster despite never entering the cell.
Question 3 Short Answer
What is receptor downregulation, and what is its physiological consequence for target tissue sensitivity?
Think about your answer, then reveal below.
Model answer: Downregulation is a reduction in the number of functional receptors on a target cell in response to chronically elevated hormone levels. The consequence is decreased sensitivity — the tissue responds less to the same hormone concentration over time.
When receptors are continuously stimulated, cells accelerate receptor internalization and degradation faster than replacement, reducing receptor density. This feedback prevents overstimulation. Clinically, it explains insulin resistance in hyperinsulinemia and why patients on long-term exogenous steroids develop dependence — their tissues have downregulated endogenous receptor pathways.