Gamma linolenic acid attenuates cardiovascular responses to stress in borderline hypertensive rats

The purpose of the present study was to investigate the effects of gamma linolenic acid (GLA) on cardiovascular responses to psychosocial stress (isolation) and to pressor hormones in the genetically borderline hypertensive rat (SHR×WKY). Adult male SHR×WKY were divided into two groups following five weeks of group housing. One group (GLA) received eight weeks constant flow osmotic pumps releasing 0.04 mg GLA in olive oil/kg‐hr, while the second group received dummy pumps (DUM). One week following pump implantation, each group was divided into two subgroups and exposed to a four‐week experimental period of either continued group housing (no stress) or isolation (stress). A two‐week recovery period of group housing followed the experimental period. Blood pressure and heart rate were determined weekly by the tail cuff technique. At the end of the recovery period, animals in the no stress condition were anesthetized and received an arterial cannula for NOR and ANG infusion and direct BP recording. Then the responses to an ED 50 of NOR and ANG were determined. All animals were then killed for determination of heart weight and adrenal weight. All groups had mean control period systolic BP values ranging from 143–146 mm Hg. In the no stress condition, neither GLA nor DUM altered BP over the course of the study. However, BP increased in the DUM group durign all four weeks of the isolation period vs the control period (p<0.01), whereas BP increased only in week 1 in the GLA group (p<0.05). Heart rate increased during stress in the DUM group (p<0.05), but not in the GLA group. Vascular reactivity to NOR was unaffected by GLA administration. In contrast, GLA increased the duration of the pressor response to ANG (p<0.01), but tended to decrease the magnitude of the pressor response (p<0.09) vs DUM. GLA had no effect on heart weight/body weight ratio. Adrenal weight/body weight ratio was lower in the DUM/no stress group than all other treatment groups. These data indicate that GLA administration attenuates the cardiovascular responses to chronic stress in animals with a genetic predisposition to hypertension, in the absence of an effect on resting BP. They also demonstrate a limitation of GLA effect, in mature animals, to epigenetic pressor factors. Furthermore, GLA action may involve an alteration of the cardiovascular responses to ANG, but not NOR. These findings suggest that GLA may be useful in preventing the neurogenic triggering of hypertension by chronic stress in genetically stress‐sensitive animals.