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Endothelial function in hypertension
P Mattei1, A Virdis, L Ghiadoni
1Cattedra di Medicina Interna, Clinica Medica I, University of Pisa, Italy.
Insights
Essential hypertension is linked to endothelial dysfunction, affecting nitric oxide (NO) pathways in blood vessels. This study suggests impaired kidney function in hypertensive patients, potentially due to superoxide anions impacting NO production.
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Endothelial Function
Background:
- Endothelial dysfunction is observed in essential hypertension affecting forearm and coronary circulation.
- Impaired nitric oxide (NO) release and altered agonist-induced vasodilation are key features.
- The L-arginine-NO pathway and cyclooxygenase-dependent factors contribute to endothelial dysfunction.
Purpose of the Study:
- To investigate the role of the L-arginine-NO pathway in human kidney function in essential hypertension.
- To assess the impact of aging on endothelium-dependent vasodilation in the kidney.
- To explore the mechanisms behind blunted renal response to L-arginine in hypertensive individuals.
Main Methods:
- Analysis of data from kidney donors regarding intrarenal infusion of acetylcholine.
- Systemic infusion of L-arginine in normotensive and hypertensive subjects.
- Assessment of renal vasodilation, natriuresis, and intrarenal NO production.
Main Results:
- Aging impairs endothelium-dependent vasodilation in the kidney, similar to other circulations.
- L-arginine infusion induced renal vasodilation and natriuresis in normotensive individuals, mediated by NO.
- Hypertensive patients showed blunted renal vasodilation and NO production in response to L-arginine, possibly due to superoxide anions.
Conclusions:
- Endothelial dysfunction is present in the kidney of essential hypertensive patients.
- Superoxide anions may be a common mechanism underlying renal endothelial dysfunction in hypertension.
- Findings highlight the importance of the L-arginine-NO pathway in renal regulation and its impairment in hypertension.
Abstract:
Endothelial dysfunction has been documented both in the forearm and coronary beds of essential hypertensive patients. Impairment in the tonic release of nitric oxide (NO) is secondary to hypertension, while the alteration in agonist-induced endothelium-dependent vasodilation seems to be a primary defect caused both by an alteration of the L-arginine-NO pathway and the production of cyclooxygenase-dependent EDCFs, such as prostanoids or superoxide anions. These latter substances curtail endothelium-dependent vasodilation mainly by inactivating NO production. Although experimental data clearly indicate that the L-arginine-NO pathway participates in the regulation of renal hemodynamics and renal excretory function under basal and stimulated conditions, data in humans are scanty and confounded by methodological approaches. A posteriori interpretation of data obtained with intrarenal infusion of acetylcholine in kidney donors suggests that endothelium dependent vasodilation in the kidney is impaired by aging, a phenomenon well documented in the forearm and coronary circulation. Systemic infusion of L-arginine induced renal vasodilation and natriuresis in normotensive subjects, an effect which seems to be mediated mainly by intrarenal NO production. Moreover the few available data suggest that both renal vasodilation and renal production of NO in response to L-arginine are blunted in patients with essential hypertension and that superoxide anions, may be, at least partially, responsible for this alteration of the L-arginine-NO pathway. In conclusion, endothelial dysfunction has been well documented in the forearm and coronary circulation of patients with essential hypertension. Available data suggest that endothelial, dysfunction is also detectable in the kidney and that a common mechanism, probably superoxide anions, can account for this abnormality.