Objectives: 

Genetic hypertension, social stress as well as ischemia/reperfusion are supposed to be connected to the changes in bioavailability of NO which can be manifested by alterations in vascular reactivity. The aim of the work was to study the effect of mesenteric ischemia/ /reperfusion on the crowding stress-induced changes in endothelium-dependent relaxation of the rat superior mesenteric artery (SMA) of normotensive Wistar rats (W) and spontaneously hypertensive rats (SHR).

Materials: 

Males of SHR and W rats were exposed to crowding for 8 weeks. Crowding was induced by placement of 5 rats per cage (70cm2/100g of body weight). Controls were kept of 4 rats per cage (160cm2/100g of body weight). In anesthetized rats, ischemia of the mesentery lasted 60 min and reperfusion 30 min. Sham-operated animals served as controls. Endothelium-dependent (acetylcholine-induced) relaxation of SMA rings was studied in vitro under isometric conditions. Blood pressure (BP) was measured using tail-cuff plethysmography.

Results: 

In control conditions, SHR rats had significantly higher BP compared to W (185±2 vs 111±1 mmHg). Moreover, SMA of SHR rats responded to acetylcholine with smaller relaxation than that of W rats. Crowding stress induced the further increase of blood pressure of SHR (193±2 mmHg), but not of W rats (112±2 mmHg). In vascular functional studies responses of SMA to acetylcholine (the total response and NO-mediated portion of relaxation) were depressed in the crowded SHR animals (*P<0.05). Wistar rats responded to stress with depression only in L-NAME-resistant vasodilation. Mesenteric ischemia/reperfusion did not induce any further impairement of the response of SMA to acetylcholine either in W or SHR group.

Conclusions: 

The results showed damaging effect of crowding stress on endothelium-dependent relaxation of SMA of SHR rats. Ischemia/reperfusion did not influence the changes in relaxation evoked by stress.

Supported by the APVV-0523-10 and VEGA 2/0084/10.