Vascular biology – If a disease kills vascular endothelial cells, what happens to the normal cellular processes that mediate vasodilation?

Introduction:
Endothelial cells regulate vascular tone by releasing vasoactive mediators, including nitric oxide (NO), prostacyclin, and endothelium-derived hyperpolarizing factors. This question probes the consequences of endothelial loss on vasodilation and downstream hemodynamics.

Given Data / Assumptions:

• Endothelium synthesizes NO via endothelial nitric oxide synthase (eNOS).
• NO diffuses to vascular smooth muscle to activate guanylate cyclase → cGMP → relaxation.
• Endothelial integrity is required for normal shear-stress–dependent dilation.

Concept / Approach:
Killing endothelial cells eliminates a key source of NO and other relaxing factors. Without NO, smooth muscle relaxation through the cGMP pathway is blunted, limiting vasodilation. Consequently, increasing local blood flow and lowering vascular resistance become more difficult, raising perfusion pressure requirements and contributing to dysfunction such as ischemia or hypertension.

Step-by-Step Solution:

Verification / Alternative check:
Experimental endothelial denudation abolishes acetylcholine-induced vasodilation while leaving direct smooth-muscle vasodilators (e.g., nitroprusside) effective, showing endothelium dependency.

Why Other Options Are Wrong:

• Each individual statement (a–c) is correct; therefore “All of the above” is the best choice.
• Autonomic compensation cannot fully restore endothelium-dependent dilation; response patterns change and are often insufficient.

Common Pitfalls:
Confusing endothelium-dependent dilation (e.g., acetylcholine) with endothelium-independent dilation (e.g., nitrates) that bypasses endothelial NO synthesis.

Final Answer:
All of the above