Nitric oxide inhibition accelerates hypertension and induces perivascular inflammation in rats

Nan Kuang Hsieh, Jia Yi Wang, Jiang Chuan Liu, Shwun De Wang, Hsing I. Chen

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

1. Inflammatory changes in peripheral arteries have been reported in animal models of hypertension. Whether they occur in cerebral arteries (CA) with hypertension induced by deprivation of endogenous nitric oxide (NO) remains unknown. 2. In the present study, we compared the arteriolar injury score (AIS) and perivascular inflammation in CA between hypertensive and normotensive rats following NO deprivation with the NO synthase inhibitor Nω- nitro-L-arginine methyl ester (L-NAME). Five-week-old male spontaneously hypertensive rats (SHR) and Wistar -Kyoto (WKY) rats were fed with L-NAME (1 mg/mL) for 4 weeks. 3. Nitric oxide deprivation resulted in time-dependent elevations in tail-cuff pressure (representing systolic blood pressure (SBP)) in both SHR and WKY rats. The magnitude of increase in SBP was larger in SHR (+81.0 ± 3.2 vs +25.0 ± 2.2 mmHg; P <0.01). Arteriolar hyalinosis and AIS in various segments of the CA were assessed with periodic acid-Schiff staining and inflammatory cells were immunostained with the antibody against macrophage/monocyte marker (ED1). The ED1+ cells appeared in the middle CA of L-NAME-treated SHR as early as 2 weeks after treatment. These cells were not observed in L-NAME-treated WKY rats and untreated SHR. More ED1+ cells were found in L-NAME-treated SHR than L-NAME-treated WKY rats after 4 weeks treatment. 4. The AIS and number of ED1+ cells around the perivascular area of the internal carotid artery were significantly higher in L-NAME-treated compared with untreated rats (AIS: 137 ± 28 vs 46 ± 10 for WKY rats, respectively; 169 ± 18 vs 53 ± 6 for SHR, respectively (P <0.01); ED1+ cells: 7.9 ± 0.6 vs 1.3 ± 0.9 for WKY rats, respectively; 13.6 ± 2.7 vs 2.1 ± 0.9 for SHR, respectively (P <0.01)), although SBP was higher in untreated SHR than in L-NAME-treated WKY rats (170 ± 4 vs 137 ± 4 mmHg, respectively; P <0.05). 5. These findings suggest that ED1+ cells appeared in the middle CA of L-NAME-SHR as early as 2 weeks after treatment. Chronic inhibition of NO accelerates hypertension and induces perivascular inflammation.

Original languageEnglish
Pages (from-to)212-218
Number of pages7
JournalClinical and Experimental Pharmacology and Physiology
Volume31
Issue number4
DOIs
Publication statusPublished - Apr 2004
Externally publishedYes

Fingerprint

Inbred SHR Rats
NG-Nitroarginine Methyl Ester
Nitric Oxide
Inbred WKY Rats
Hypertension
Inflammation
Blood Pressure
Cerebral Arteries
Middle Cerebral Artery
Wounds and Injuries
Periodic Acid
Internal Carotid Artery
Nitric Oxide Synthase
Tail
Monocytes
Animal Models
Arteries
Cell Count
Macrophages
Staining and Labeling

Keywords

  • Arteriolar injury score
  • Cerebral arteries
  • ED1-positive cells
  • Hypertension
  • Nitric oxide deprivation
  • Perivascular inflammation

ASJC Scopus subject areas

  • Physiology
  • Pharmacology (medical)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Nitric oxide inhibition accelerates hypertension and induces perivascular inflammation in rats. / Hsieh, Nan Kuang; Wang, Jia Yi; Liu, Jiang Chuan; Wang, Shwun De; Chen, Hsing I.

In: Clinical and Experimental Pharmacology and Physiology, Vol. 31, No. 4, 04.2004, p. 212-218.

Research output: Contribution to journalArticle

Hsieh, Nan Kuang ; Wang, Jia Yi ; Liu, Jiang Chuan ; Wang, Shwun De ; Chen, Hsing I. / Nitric oxide inhibition accelerates hypertension and induces perivascular inflammation in rats. In: Clinical and Experimental Pharmacology and Physiology. 2004 ; Vol. 31, No. 4. pp. 212-218.
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