Abstract
A model of psychosocial stress-induced hypertension in the rat, and examined effects of the prostaglandin E precursor, gamma-linoleic acid (GLA) on the development of hypertension during psychosocial stress. In the 1st study, male rats were housed 4/cage for an acclimation period of 21 days, followed by a 14-day control period. An experimental group (N = 12) was then placed in isolation cages for 14 days, then regrouped for a 7-day recovery period. Controls (N = 12) remained group-housed. Eight animals per group were sacrificed after the experimental period, and 4/group after recovery for organ weight analysis. Mean systolic blood pressure (BP) was similar between groups during the control period (126 .+-. 2 and 125 .+-. 2 mm Hg), but increased during isolation, reaching 140 .+-. 2 mm Hg (P < 0.001) by day 14. During recovery BP returned to control levels. No changes in heart rate, heart weight/body weight or adrenal weight were seen. The 2nd study utilized a protocol similar to that of the experimental group of the 1st study, minus the recovery period. On day 1 of the control period 28-day osmotic pumps were implanted i.p., releasing olive oil or GLA in olive oil. Four groups of rats (N = 8/group) received either olive oil (controls), 0.018 mg GLA/h, 0.040 mg GLA/h or 0.040 mg GLA/h with no stress. Organ weights were obtained following stress in groups 1-3. Controls developed a sustained elevation in BP within 24 h of isolation. Animals receiving 0.018 mg GLA/h developed elevated BP upon isolation, but the BP was less than that of controls on days 1 (P < 0.05) and 14 (P < 0.001) of isolation. Animals receiving 0.040 mg GLA/h demonstrated a greatly attenuated rise in BP vs. controls (P < 0.001) on all isolation days. GLA in unstressed rats had no effect on BP. Heart rate, heart weight/body weight, and adrenal weight were unchanged in all groups. Evidently, isolation is a useful tool for investigating reversible psychosocial stress-induced hypertension, and GLA, while not affecting BP in unstressed animals, produces a dose-dependent attenuation of the BP response to chronic stress.