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Nitric oxide, the kidney, and hypertension
V Lahera1, J Navarro-Cid, V Cachofeiro
1Department of Physiology, Medical School, Complutense University, Madrid, Spain.
American Journal of Hypertension
|January 1, 1997
Summary
Nitric oxide (NO) synthesis inhibition acutely impairs sodium excretion and renal blood flow. Chronically, it elevates blood pressure and damages kidneys, suggesting NO
Area of Science:
- Physiology
- Nephrology
- Cardiovascular Research
Background:
- Nitric oxide (NO) is crucial for regulating systemic and renal hemodynamics.
- NO synthesis inhibition affects renal sodium excretion and renovascular resistance.
Purpose of the Study:
- To investigate the role of NO in regulating renal excretory function and blood pressure.
- To explore the consequences of NO synthesis inhibition on renal hemodynamics and kidney damage.
Main Methods:
- Administration of NO synthesis inhibitors and L-arginine analogs in experimental models.
- Assessment of systemic blood pressure, renal hemodynamics, and sodium excretion.
- Evaluation of renal vascular and parenchymal damage.
Main Results:
- Acute NO inhibition reduced sodium excretion and increased renovascular resistance without altering systemic blood pressure.
- Chronic NO inhibition led to elevated blood pressure, sodium retention, and renal damage.
- Antihypertensive therapy mitigated blood pressure increase and kidney deterioration.
Conclusions:
- NO plays a significant role in regulating systemic and renal hemodynamics and excretory function.
- Diminished NO production contributes to hypertension development and progression.
- Alterations in the L-arginine-NO pathway may be implicated in human essential hypertension.