OBJECTIVE: To study the effect of pregnancy on die kinetics of vascular relaxation. STUDY DESIGN: Aortic rings from rats in early (D8), late (D16) and term (D22) gestation and from nonpregnant (NP) rats were placed in organ chambers for isometric tension recording, precontracted with high-K+ (60 mM), and then allowed to relax in normal-K+ physiology salt solution. The time to reach 50% (t50) and 80% (t80) relaxation was determined in the presence or absence of a cyclooxygenase (COX) inhibitor (indomethacin) plus a nitric oxide synthase (NOS) inhibitor (L-NAME. or after removal of the endothelium. RESULTS: Relaxation was signifcantly faster at term (see figure). Similar differences were seen after L-NAME + indomethacin or deendothelization. Within each pregnancy group, inhibition of COX and NOS did not change the rates of relaxation, whereas de-endothelization caused a significant increase in both t50 and t80 in all groups. (Figure Presented) CONCLUSIONS: The rate of vascular relaxation depends on the endothelium but not on the NOS or COX systems. Term gestation is associated with acceleration of vascular relaxation, a finding which may explain some of the vascular changes reported in pregnancy. The differences in relaxation between term and other stages of pregnancy or the nonpregnant state cannot be ascribed to an endothelium-dependent factor. We speculate that it is due to an intrinsic change in the vascular smooth muscle.
|Original language||English (US)|
|Journal||Acta Diabetologica Latina|
|Issue number||1 PART II|
|State||Published - Dec 1 1997|
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism