Uncontrolled and Resistant Hypertension: From Guideline Updates to RAAS Mechanisms-RAAS Across the Cardiovascular-Kidney-Metabolic Continuum: Why Hypertension Becomes Resistant

RAAS Across the Cardiovascular-Kidney-Metabolic Continuum: Why Hypertension Becomes Resistant

Video Transcription

Video Summary

The speaker explains how renin-angiotensin system (RAS) activation drives resistant hypertension across cardiovascular, kidney, and metabolic disease. Using clinical examples, he describes three main mechanisms: volume retention, persistent neurohormonal activation, and increased vascular resistance. He emphasizes confirming true resistant hypertension, then identifying the dominant cause, such as CKD, obesity, diabetes, sleep apnea, heart failure, or primary aldosteronism. Treatment should match the phenotype, using ACE/ARBs, ARNIs, diuretics, mineralocorticoid antagonists, or non-steroidal MRAs as appropriate. Key message: more RAS blockade is not always better; therapy must be targeted and monitored.

Meta Tag

Concept Renin-Angiotensin-Aldosterone System

Concept Primary Hypertension

Concept Refractory Hypertension

Concept Sodium Retention

Concept Vasoconstriction

Keywords

renin-angiotensin system

resistant hypertension

RAS blockade

chronic kidney disease

mineralocorticoid antagonists

Renin-Angiotensin-Aldosterone System

Primary Hypertension

Refractory Hypertension

Sodium Retention

Vasoconstriction