Background: Hypertension remains a major global health burden and a leading cause of cardiovascular morbidity and mortality. Approximately 10% of pregnancies are complicated by hypertensive disorders such as pregnancy-induced hypertension (PIH) and pre-eclampsia. These conditions not only contribute to adverse perinatal outcomes but also predispose women to persistent endothelial dysfunction (ED) and a higher lifetime risk of cardiovascular disease (CVD). PIH is defined as a transient elevation in blood pressure (≥140/90 mmHg) occurring after 20 weeks of gestation in previously normotensive women, without proteinuria or other systemic involvement. It typically resolves after delivery, suggesting a reversible endothelial disturbance. In contrast, chronic hypertension, represented by the spontaneously hypertensive rat (SHR) model, is characterised by sustained, non-pregnancy-related hypertension associated with vascular remodelling, increased arterial stiffness, and irreversible endothelial injury. Understanding the molecular differences between these conditions is crucial to elucidate why some women with PIH women subsequently develop chronic hypertension and CVD earlier in life. Objective: This study aims to characterise long non-coding RNA (lncRNA)-mediated transcriptomic signatures underlying transient (PIH)and chronic (SHR) forms of endothelial dysfunction. Methods: Three rat groups (Control, PIH, and SHR; n = 6 per group) were included in the study. Blood pressure was recorded at gestational day 13, day 19, and postpartum days 7 and 30. Aortic and mesenteric arteries were harvested for RNA sequencing using the DNBSEQ G400RS platform. Differential gene expression, principal component analysis (PCA), correlation heatmaps, and Venn diagram analyses were performed to compare transcriptomic profiles. Results: PIH rats exhibited a transient increase in mean arterial pressure at gestational day 19, which normalised postpartum, whereas SHR maintained persistently elevated blood pressure. A total of 348, 597, and 337 differentially expressed genes (DEGs) were identified in PIH vs Healthy, SHR vs Healthy, and PIH vs SHR, respectively, with 83 shared DEGs. PCA demonstrated clear separation of SHR samples, consistent with chronic endothelial injury, whereas PIH clustered near controls, indicating reversibility. Heatmap and Venn analyses revealed distinct lncRNA expression patterns, with SHR showing greater transcriptomic divergence. Conclusion: PIH and chronic hypertension exhibit distinct molecular programs of endothelial dysfunction. lncRNA-driven regulatory networks appear central to microvascular adaptation and maladaptation, providing novel insights into post-pregnancy cardiovascular risk and potential lncRNA-targeted therapeutic strategies.