Programing Effect Of Maternal High Fat/High Sucrose Diet On Cardiovascular Responses And Fos Expression following Air Jet And Restraint Stress
Authors: Polson Jaimie W , Prestipino Louise , Jayaratne Sachini K 
Published: November 2023

A high fat/high sucrose diet (HFS) and/or obesity during pregnancy are known stressors for programing hypertension in the adult offspring. Although the exact causative mechanisms are not fully elucidated, exaggerated cardiovascular (CV) and autonomic responses to psychological stress may be a contributing factor. However, the precise nature of the stressor and the central neural pathways via which the programed responses are mediated remain unknown. Our aim was to investigate the effect of a HFS maternal diet on blood pressure (BP) of adult male offspring at rest and in response to 2 psychological stressors of varying intensities. The central pathways involved in mediating these responses were also investigated by quantifying Fos expression in key CV control regions of the brain. The 2 stressors chosen were air jet stress (AJS), considered a moderate stressor, and restraint stress (RS), considered more severe in nature. Sprague Dawley dams were fed a HFS (21% fat, 34% (w/w) sucrose vs control, 4.8% fat, 0% sucrose) diet ad libitum for 4 weeks prior to mating until weaning. Adult offspring (9–12 months) were implanted with radiotelemetry BP transmitters and BP was recorded at rest for 24 hours, in response to the stress tests, and throughout a 2‐hour recovery period. CV parameters, including heart rate (HR) and mean BP (MnBP) were derived from the BP waveform. Following recovery, rats were perfused with 4% paraformaldehyde and brains processed immunohistochemically for Fos expression. Resting MnBP was similar between groups both at night (HFS, 101±2.3 mmHg; control, 97±2.5 mmHg) and day (HFS, 96±0.7 mmHg; control, 93±3.5 mmHg). There was also no difference in HR between groups. Interestingly, MnBP in HFS offspring was approximately 10 mmHg higher than controls in the resting period immediately preceding the stress tests. This suggests that even mild environmental perturbations, such as the presence of researchers in the laboratory, may have an impact on BP responses in HFS offspring. HFS offspring also exhibited greater increases in MnBP upon commencement of AJS (HFS, 25±5.4 mmHg; control, 13±3.1 mmHg) and delayed recovery. At 45 minutes post‐stress, MnBP was at 15% baseline in HFS, compared to 3.5% baseline in controls. RS caused similar increases in MnBP in both groups (HFS, 29±5.0 mmHg, control, 30±8.6 mmHg). Interestingly, initial analysis indicated that although RS produced greater CV responses than AJS in control offspring, this was not observed in HFS. Consistent with this, in control rats, RS evoked a 5‐fold increase in Fos labeling throughout the brainstem compared to baseline, while AJS caused a 3‐fold increase. Future analysis will determine the degree of Fos labeling in HFS offspring. The results suggest that maternal HFS programs a pro‐hypertensive phenotype characterised by exaggerated and extended BP responses to mild to moderate stress. RS evoked greater responses than AJS in control rats only, and this was consistent with greater Fos labelling in key CV nuclei in controls. Fos labelling in HFS is in progress.