Why the study?
Does chronic nitric oxide blockade with L-NNA alter pulmonary vasculature and right ventricular hypertrophy in stroke-prone spontaneously hypertensive rats?
Does chronic nitric oxide blockade with L-NNA alter pulmonary vasculature and right ventricular hypertrophy in stroke-prone spontaneously hypertensive rats?
Chronic nitric oxide blockade enhances pulmonary vascular changes and right ventricular hypertrophy in a subset of stroke-prone spontaneously hypertensive rats.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for NO blockade in pulmonary vascular remodeling; leaves open any clinical relevance in hypertension.
To determine the effects of chronic nitric oxide (NO) blockade on the pulmonary vasculature, 58-day-old spontaneously hypertensive rats of the stroke-prone substrain (SHRSP) and Wistar-Kyoto rats (WKY) received N(omega)-nitro-L-arginine (L-NNA; 15 mg. kg(-1). day(-1) orally for 8 days). Relaxation to acetylcholine (ACh) in hilar pulmonary arteries (PAs), the ratio of right ventricular (RV) to body weight (RV/BW) to assess RV hypertrophy (RVH), and the percent medial wall thickness (WT) of resistance PAs were examined. L-NNA did not alter the PA relaxation, RV/BW, or WT in WKY. Although the PA relaxation and RV/BW in control SHRSP were comparable to those in WKY, the WT was increased (31 +/- 2 vs. 19 +/- 1%). L-NNA-treated SHRSP showed two patterns: in one group, the relaxation, RV/BW, and WT were comparable to those in the control SHRSP; in the other, impaired relaxation (36 +/- 7 vs. 88 +/- 4% for WKY) was associated with an increase in WT (37 +/- 1%) and RV/BW (0. 76 +/- 0.05). Thus the abnormal pulmonary vasculature in SHRSP at <10 wk of age is not accompanied by impaired relaxation in PAs or RVH; however, impaired relaxation is associated with increased WT and RVH.
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Mathew et al. (2000) studied this question.
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