The insulin resistance-systemic vascular resistance-isolated diastolic hypertension axis: a metabolic framework for an overlooked hypertension phenotype.
Level 5 - mechanism / opinion, no new human data
Narrative review and mechanistic framework without original empirical data or systematic review methodology.
PubMed 42325680 · doi:10.3389/fcvm.2026.1834237
What was done
This narrative review synthesized mechanistic, hemodynamic, and epidemiological evidence connecting insulin resistance and compensatory hyperinsulinemia to isolated diastolic hypertension (IDH). The authors examined physiological pathways across neural, vascular, and renal domains and evaluated the utility of clinical insulin resistance surrogates for metabolic phenotyping.
What was found
The abstract reports no empirical numbers or quantitative effect estimates. It presents a conceptual framework linking insulin resistance to increased systemic vascular resistance and IDH via: (1) neural activation (sympathetic and renin-angiotensin-aldosterone signaling); (2) vascular dysfunction (endothelial insulin resistance, reduced nitric oxide bioavailability, inflammation, and microvascular remodeling); and (3) renal mechanisms (preserved sodium retention, salt sensitivity, and volume expansion).
Why it matters
It outlines a pathophysiological rationale for viewing isolated diastolic hypertension as a metabolically driven resistance-vessel phenotype, suggesting that insulin resistance surrogates could aid in risk stratification.
Limits
As a narrative review, it presents no original data, quantitative effect estimates, or systematic review methodology. Whether treating insulin resistance improves clinical cardiovascular outcomes in IDH remains to be determined.
Cited by
- context High diastolic blood pressure is primarily driven by insulin resistance.