Background: Congestive heart failure (CHF) commonly leads to the secondary onset of pulmonary hypertension (PH). In primary forms of PH, endothelial dysfunction instigates adverse changes of the pulmonary vasculature, ultimately impairing pulmonary blood flow distribution. In this study, we utilized synchrotron radiation microangiography to determine the extent of endothelial dysfunction, and whether it adversely impacts on pulmonary blood flow distribution, in a Dahl rat model of CHF with secondary PH. Methods: High salt-fed Dahl salt-sensitive (Dahl-S) and salt-resistant rats (Dahl-R) were anesthetized and microangiography was performed to assess pulmonary blood flow distribution and dynamic changes in vessel internal diameter (ID) in response to i) acetylcholine (3.0 μg/kg/min), ii) sodium nitroprusside (5.0 μg/kg/min), and iii) the ET-1A receptor antagonist, BQ-123 (1 mg/kg). Results: A high salt diet induced CHF and secondary PH in Dahl-S rats. The development of PH was attributable to ‘reactive’ pulmonary endothelial dysfunction, evident by impaired vasodilatory responses to acetylcholine, an enhanced vasodilatory response to BQ-123, an elevated expression of endothelial ET-1 and eNOS protein, and extensive pulmonary vascular remodeling. Consequently, pulmonary blood flow distribution was significantly impaired. Conclusions: The development of PH secondary to CHF is associated with impaired pulmonary blood flow distribution and endothelial dysfunction, which appears comparable to that previously reported for primary PH. However, ET-1 modulation of pulmonary vessels in primary PH differs regionally compared to secondary PH. Accordingly, such discrepancies should be considered in future studies investigating underlying pathomechanisms of primary and secondary forms of PH.