Effect of pregnancy on aortic and carotid vascular function
Authors: Zynda Megan , Klatt Kimberly A. , Vallejo‐Elias Johana , Cooper Kimbal E. , Eckman Delrae M. 
Published: November 2023

Objective/Introduction

Normal pregnancy is associated with substantial cardiovascular changes to meet the metabolic demands of the placenta, growing fetus and mother. These changes include an increase in uterine blood flow, plasma volume, elevated cardiac output and a reduction in systemic vascular resistance. To accommodate these changes, the maternal aorta must undergo structural and functional changes to accommodate elevated compliance, distensibility and diameter. This study was designed to determine whether pregnancy alters the carotid artery in a manner similar to that observed in the aorta.

Methods

Thoracic aorta (TA) and carotid arteries (CA) from non‐pregnant (NP, n=5) and late pregnant (P, d20g ± 1 day, n=5) Sprague‐Dawley rats were removed, cleaned of connective tissue, cut into 3mm long ring segments. Ring segments were mounted onto two triangular tungsten wires (approximately 125 μm diameter) and hung vertically in an isolated organ chamber to assess smooth muscle function in the absence and presence of 50 mM [K+]O and 1μM phenylephrine (PE). In addition, endothelial function was assessed using stepwise increases in acetylcholine (ACh, 0.001μM to 100μM) in the absence and presence of L‐NAME and indomethacin to determine the contribution of NOS and COX to smooth muscle and endothelial function. Finally, arterial segments were then challenged to stepwise increases (100μM) circumferential stretch (0μm to 3000μm) in the absence and presence of elastase (0.5mg/ml) and collagenase type 1 (0.5mg/ml) to determine whether P alters stretch‐induced force development.

Results

P‐ and NP‐TA segments exhibited significantly greater PE (1μm) and [K+]O‐induced constriction than P‐ and NP‐ CA. L‐NAME significantly augmented PE‐induced constriction in TA and CA from NP and P rats while indomethacin significantly attenuated PE‐induced constriction in TA and CA from NP and P rats. In contrast, 50 mM [K+]O ‐induced constrictions were unaffected by either L‐NAME or indomethacin in arteries from NP and P rats. L‐NAME significantly attenuated ACh‐induced relaxation in TA and CA from NP and P rats while Indomethacin was without effect. Preliminary studies suggest that force development to stepwise increases in circumferential stretch were similar in TA and CA from NP and P rats. Collagenase type 1 had little effect on force development in TA from NP and P rats, while significantly attenuating force development in CA from both NP and P rats. Elastase attenuated force development TA and CA from NP and P rats. Data was considered significant if P<0.05.

Summary/Conclusion

These data suggest that pregnancy does not alter agonist‐induced constriction and/or endothelial‐dependent dilation in TA and CA from NP and P rats. Interestingly, PE‐induced constriction was augmented in the presence of L‐NAME and attenuated in indomethacin. Furthermore, our data suggests that collagenase appears to play a greater role in force development in the CA than in the TA, while elastase attenuated force development in TA at higher levels of active force development while attenuating force development in CA at lower levels active stretch. Taken together, these data demonstrate that elastin and collagen contribute differentially to active force development in TA and CA.

Support or Funding Information

MWU start‐up funds (DME) and Biomedical Sciences graduate student research support (MZ, DME).