Nitric Oxide Pathway and Blood Vessel Regulation

Vocabulary flashcards covering the components, steps, comparisons, and perturbations of the nitric oxide pathway in vascular smooth muscle regulation.

Muscarinic Acetylcholine Receptor

A G protein-coupled receptor located on endothelial cells lining blood vessels that initiates the nitric oxide pathway upon binding acetylcholine.

Nicotinic Acetylcholine Receptor

A ligand-gated ion channel located at synapses that mediates muscle contraction, distinct from the muscarinic receptor found on endothelium.

Endothelial Cells

Cells lining blood vessels that contain muscarinic receptors and NO synthase, responsible for synthesizing and releasing nitric oxide gas.

Vascular Smooth Muscle Cells

Cells in the blood vessel wall neighboring the endothelium that express guanylyl cyclase and relax in response to nitric oxide signaling.

$$IP_3$$

A signaling molecule produced upon muscarinic receptor activation in endothelial cells that opens calcium channels on the endoplasmic reticulum membrane.

$$Ca^{2+}$$

An ion released from the endoplasmic reticulum into the endothelial cytoplasm by $IP_3$ to stimulate the enzyme NO synthase.

NO Synthase

An endothelial enzyme stimulated by cytoplasmic $Ca^{2+}$ that synthesizes nitric oxide gas from the amino acid arginine.

Arginine

The amino acid precursor used by NO synthase to produce nitric oxide gas in endothelial cells.

Nitric Oxide

A gaseous signaling molecule produced from arginine by NO synthase that diffuses from endothelial cells to activate guanylyl cyclase in smooth muscle cells.

Paracrine Signaling

Local cell-to-cell signaling exhibited by nitric oxide, which acts exclusively on neighboring cells because it is rapidly converted into nitrates and nitrites in extracellular fluid.

Nitrates and Nitrites

Extracellular breakdown products into which nitric oxide gas is rapidly converted, preventing it from acting beyond neighboring cells.

Guanylyl Cyclase

An enzyme in vascular smooth muscle cells that is activated by nitric oxide to convert GTP into cGMP and PPi.

Cyclic GMP (cGMP)

A second messenger produced from GTP by guanylyl cyclase that directly promotes smooth muscle relaxation and vessel dilation.

Adenylyl Cyclase

An enzyme in the epinephrine pathway that converts ATP into cAMP, contrasted with guanylyl cyclase in the nitric oxide pathway.

Vasodilation

The relaxation and widening of blood vessels mediated by acetylcholine acting through the nitric oxide and cGMP signaling pathway.

Vasoconstriction

The narrowing of blood vessels caused by angiotensin II acting via protein kinase C (PKC) on vascular smooth muscle.

Angiotensin II Pathway

A signaling pathway causing vasoconstriction via PKC that shares the common step of $IP_3$-mediated $Ca^{2+}$ release from the endoplasmic reticulum with the NO pathway.

NO Synthase Inhibition

A state where endothelial $IP_3$ and $Ca^{2+}$ still rise after acetylcholine release, but no nitric oxide is synthesized, keeping guanylyl cyclase off and preventing relaxation.

Guanylyl Cyclase Blockade

A state where nitric oxide is still produced and diffuses across to smooth muscle, but muscle relaxation fails because no cGMP forms.

Inhibition of cGMP Breakdown

The blockade of the enzyme degrading cGMP, which causes cGMP concentrations to stay high longer and results in stronger, prolonged smooth muscle relaxation.

Endothelial Denudation

The physical removal of the blood vessel endothelial layer, which prevents relaxation upon acetylcholine addition because muscarinic receptors and NO synthase are absent.

Muscarinic Receptor Blockade

The inhibition of endothelial muscarinic receptors, causing every subsequent step of the pathway—including $IP_3$ production, $Ca^{2+}$ release, NO synthesis, cGMP generation, and muscle relaxation—to fail.