Human physiology — In vasodilation, what sequence of effects do proper neural/endothelial signals cause in blood vessels (consider mediator release, vascular smooth muscle tone, and systemic pressure)?

Introduction:
Vasodilation is the widening of blood vessels due to decreased vascular smooth muscle tone. This question tests understanding of the linked events: mediator release from endothelium, smooth muscle relaxation, and the impact on systemic hemodynamics.

Given Data / Assumptions:

• Endothelial cells can release nitric oxide (NO) in response to neural and shear stress signals.
• NO diffuses into adjacent smooth muscle and activates intracellular pathways that reduce tone.
• Widespread arteriolar dilation lowers total peripheral resistance, tending to decrease blood pressure.

Concept / Approach:
Connect signaling (NO release) to mechanism (smooth muscle relaxation) to outcome (pressure drop). Evaluate each option as part of the same physiological cascade rather than as isolated events.

Step-by-Step Solution:

Verification / Alternative check:
Pharmacologic vasodilators (e.g., nitroglycerin) mimic NO signaling and predictably lower vascular tone and blood pressure, confirming the mechanism.

Why Other Options Are Wrong:

Common Pitfalls:
Assuming vasodilation always lowers blood pressure regardless of cardiac output; local vasodilation can occur without large systemic pressure changes if compensated by baroreflexes.

Final Answer:
All of the above.