Chonnam Med J.  2016 May;52(2):81-90. 10.4068/cmj.2016.52.2.81.

Altered Nitric Oxide System in Cardiovascular and Renal Diseases

Affiliations
  • 1Department of Physiology, Chonnam National University Medical School, Gwangju, Korea. julee@jnu.ac.kr
  • 2Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.

Abstract

Nitric oxide (NO) is synthesized by a family of NO synthases (NOS), including neuronal, inducible, and endothelial NOS (n/i/eNOS). NO-mediated effects can be beneficial or harmful depending on the specific risk factors affecting the disease. In hypertension, the vascular relaxation response to acetylcholine is blunted, and that to direct NO donors is maintained. A reduction in the activity of eNOS is mainly responsible for the elevation of blood pressure, and an abnormal expression of iNOS is likely to be related to the progression of vascular dysfunction. While eNOS/nNOS-derived NO is protective against the development of atherosclerosis, iNOS-derived NO may be proatherogenic. eNOS-derived NO may prevent the progression of myocardial infarction. Myocardial ischemia/reperfusion injury is significantly enhanced in eNOS-deficient animals. An important component of heart failure is the loss of coronary vascular eNOS activity. A pressure-overload may cause severer left ventricular hypertrophy and dysfunction in eNOS null mice than in wild-type mice. iNOS-derived NO has detrimental effects on the myocardium. NO plays an important role in regulating the angiogenesis and slowing the interstitial fibrosis of the obstructed kidney. In unilateral ureteral obstruction, the expression of eNOS was decreased in the affected kidney. In triply n/i/eNOS null mice, nephrogenic diabetes insipidus developed along with reduced aquaporin-2 abundance. In chronic kidney disease model of subtotal-nephrectomized rats, treatment with NOS inhibitors decreased systemic NO production and induced left ventricular systolic dysfunction (renocardiac syndrome).

Keyword

Nitric oxide; Hypertension; Atherosclerosis; Ischemia/reperfusion injury; Heart failure; Nephrogenic diabetes insipidus; Ureteral obstruction; Cardio-renal syndrome

MeSH Terms

Acetylcholine
Animals
Aquaporin 2
Atherosclerosis
Blood Pressure
Cardio-Renal Syndrome
Diabetes Insipidus, Nephrogenic
Fibrosis
Heart Failure
Humans
Hypertension
Hypertrophy, Left Ventricular
Kidney
Mice
Myocardial Infarction
Myocardium
Neurons
Nitric Oxide*
Rats
Relaxation
Renal Insufficiency, Chronic
Risk Factors
Tissue Donors
Ureteral Obstruction
Acetylcholine
Aquaporin 2
Nitric Oxide

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