One enzyme, two messengers
When a Gq protein switches on, it activates the membrane enzyme phospholipase C (PLC). PLC does something elegant: it cuts a single membrane lipid (called PIP2) into two second messengers in one stroke. One half, inositol trisphosphate (IP3), floats away into the cytoplasm; the other half, diacylglycerol (DAG), stays put in the membrane. The cell now has two messages travelling on two different routes from a single cut.
IP3 opens the calcium floodgates
IP3 travels to the endoplasmic reticulum — the cell's internal calcium store — and opens channels there. Intracellular calcium rushes out into the cytoplasm, and its level can jump more than tenfold in a fraction of a second. Calcium is itself a powerful second messenger: it triggers smooth-muscle contraction, glandular secretion, and hormone release, depending on the tissue.
This is why Gq-linked receptors matter so much in blood vessels, airways and the gut, where contraction is the headline action. A drug that activates a Gq receptor on vascular smooth muscle raises calcium and constricts the vessel; an antagonist at the same receptor lets it relax — a logic you will recognise behind many cardiovascular and respiratory medicines.
DAG and PKC: the second arm
Meanwhile DAG, still in the membrane, recruits and activates protein kinase C (PKC) — and PKC works best when the calcium freed by IP3 is also high. So the two arms cooperate: IP3 supplies the calcium, DAG supplies the membrane anchor, and together they switch PKC fully on. Like PKA before it, PKC then phosphorylates a family of effector proteins to change cell behaviour over a longer timescale.
Agonist -> Gq-linked receptor -> Gq ON
Gq -> phospholipase C ON
PIP2 (membrane lipid) cut into TWO messengers:
|-- IP3 (soluble) -> opens ER channels
| -> intracellular calcium SPIKES
| -> contraction / secretion
|-- DAG (membrane) -> activates protein kinase C
+ the high calcium
-> PKC phosphorylates effectors