The Effect of ACE Inhibitors Vs. Angiotensin Receptor Blockers on Insulin Resistance in Hypertensive Patients

Insulin resistance is more than a metabolic disorder; it is a complex syndrome influencing blood pressure regulation. Neuro-immune and neuro-humoral system dysfunctions contribute to its pathophysiology, especially in hypertensive individuals, where its prevalence is rising. A key mechanism in insulin resistance involves alterations in the Renin-Angiotensin-Aldosterone System (RAAS). Angiotensin II, a major RAAS component, impairs insulin action through reactive oxygen species (ROS) production, leading to inflammation and insulin signaling disruption. Clinical trials have shown that RAAS inhibition through ACE inhibitors and ARBs significantly improves insulin sensitivity compared to other antihypertensive agents, though long-term ACE inhibitor use does not consistently reduce diabetes risk. Tissue-specific RAAS within adipocytes, muscle, and other organs contributes to the complexity of insulin resistance. This chapter explores how RAAS inhibitors improve insulin sensitivity in hypertensive patients and highlights the different mechanisms involved in insulin resistance in diabetes versus hypertension.