Key Points
- To examine how chronic renal hypertension affects endothelium-dependent vascular relaxation and direct nitric oxide release in isolated arteries.
- Sprague-Dawley rats were randomly allocated to uninephrectomized control or one-kidney one-clip Goldblatt renal hypertension groups for 10 weeks.
- In the presence of indomethacin, isolated superior mesenteric arteries were evaluated using a nitric oxide-specific microelectrode to simultaneously record nitric oxide release and relaxation.
- Basal nitric oxide concentrations were unchanged, but acetylcholine-stimulated nitric oxide release and vascular relaxation were significantly diminished in hypertensive arteries.
- Relaxations induced by the nitric oxide donor SNAP were also impaired in arteries from renal hypertensive animals.
- Superoxide dismutase and l-arginine failed to restore nitric oxide concentration or relaxation, whereas asymmetric dimethyl l-arginine reduced both responses.
Structured PICO
PPopulationSprague-Dawley rats
IInterventionOne-kidney one-clip (Goldblatt hypertension) renal hypertension model
CComparatorUninephrectomized normotensive controls
OOutcomeEndothelium-dependent relaxation and nitric oxide (NO) concentration in isolated superior mesenteric arteriessurrogate
Reduced endothelium-dependent relaxations in the superior mesenteric artery from renal hypertensive rats are driven, at least in part, by diminished nitric oxide release.