Final answer:
Inflammation of the endothelium depletes Nitric oxide (NO), a major vasorelaxant, resulting in vasoconstriction. NO is essential for balancing vasoconstrictive substances such as endothelins, which are powerful vasoconstrictors produced by endothelial cells.
Step-by-step explanation:
Inflammation of the endothelium depletes Nitric oxide (NO), a major vasorelaxant of the arterial muscle wall. This depletion leads to a net vasoconstrictive effect. Nitric oxide is a gas that acts as a ligand, diffusing directly across the plasma membrane to interact with receptors in smooth muscle, inducing relaxation. A very short half-life ensures that NO only functions over short distances.
Nitroglycerin, used in heart disease treatment, works by releasing NO, which causes blood vessels to dilate and restore blood flow. NO's vasodilatory effect is crucial as it helps to balance the vasoconstrictive influence of substances like prostaglandins, endothelins, and products released by activated platelets and leukocytes.
The endothelins are extremely powerful vasoconstrictors produced by endothelial cells, including those in renal blood vessels, and their release can be stimulated by hormones such as angiotensin II, bradykinin, and epinephrine. In healthy individuals, endothelins typically do not affect blood pressure significantly, but in pathological states like diabetic kidney disease, they can be chronically elevated, leading to issues like sodium retention and increased vascular resistance.