Exercise increases the angiotensin II effects in isolated portal vein of trained rats.

Training in rats adapts the portal vein to respond vigorously to sympathetic stimuli even when the animal is re-exposed to exercise. Moreover, changes in the exercise-induced effects of angiotensin II, a potent venoconstrictor agonist, in venous beds remain to be investigated. Therefore, the present study aimed to assess the effects of angiotensin II in the portal vein and vena cava from sedentary and trained rats at rest or submitted to an exercise session immediately before organ bath experiments. We found that training or exposure of sedentary animals to a single bout of running exercise does not significantly change the responses of the rat portal vein to angiotensin II. However, the exposure of trained animals to a single bout of running exercise enhanced the response of the rat portal vein to angiotensin II. This enhancement appeared to be territory-specific because it was not observed in the vena cava. Moreover, it was not observed in endothelium-disrupted preparations and in preparations treated with N(omega)-nitro-l-arginine methyl ester hydrochloride, indomethacin, BQ-123 or BQ-788. These data indicate that training causes adaptations in the rat portal vein that respond vigorously to angiotensin II even upon re-exposure to exercise. This increased response to angiotensin II requires an enhancement of the vasocontractile influence of endothelin beyond the influence of nitric oxide and vasodilator prostanoids.

Orchidectomy enhances the effects of phenylephrine in rat isolated portal vein.

1. Orchidectomy results in long-term testosterone deprivation similar to that observed in male clinical pathologies, such as hypogonadism and age-related reductions in plasma testosterone concentrations. Although the vascular effects of these sorts of hormone deprivations are known in arteries, they have not been studied to the same extent in veins. 2. The aim of the present study was to determine the effect of orchidectomy, with or without subsequent testosterone replacement (started 23 days after orchidectomy; 10 mg/kg, i.m., testosterone propionate once every 5 days for 3 weeks), on responses of rat isolated portal veins and vena cavae to exogenous phenylephrine (PE). Isolated vessels were mounted in an organ bath and concentration-response curves constructed to PE (10(-10)-10(-4) mol/L), endothelin (ET; 10(-10)-10(-5) mol/L) and KCl (10(-2)-1.2 x 10(-1) mol/L; as a control). 3. Orchidectomy had no effect on contractile responses of either the portal vein or vena cava to KCl. However, orchidectomy enhanced the maximum response (R(max)) of the portal vein, but not the vena cava, to PE. Testosterone replacement had no effect on these responses. The effects of orchidectomy on the R(max) to PE in portal veins were not altered by the nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester (10(-4) mol/L) alone or combined with 10(-5) mol/L indomethacin (a non-selective cyclo-oxygenase inhibitor), but they were abolished following treatment of isolated vessels with the ET(A) and ET(B) receptor antagonists BQ-123 and BQ-788 (both at 10(-6) mol/L). Orchidectomy did not alter portal vein responses to the application of exogenous ET. 4. The results of the present study indicate that orchidectomy-induced decreases in plasma testosterone can increase the venoconstrictor effects of PE on the portal vein and that this effect involves activation of both ET(A) and ET(B) receptors by locally produced ET.

Exercise increases the phenylephrine effects in isolated portal vein of trained rats.

Physical exercise evokes an extensive circulatory redistribution. However, the influence of exercise upon the effects of sympathomimetic agonists in veins was not well studied. Thus, the present study aimed to determine whether a single bout of exercise modifies the effects of sympathomimetic agonists in veins and whether this exercise-induced modification may be altered by exercise training. The results have shown that the training did not change the responsiveness of the rat portal vein, but exposure of trained animals to a single bout of exercise enhanced the phenylephrine Rmax in these preparations. Such exercise-induced modifications of vascular response were territory-specific since similar modifications of response to phenylephrine were not observed in vena cava. Moreover, this exercise-induced augmentation of phenylephrine Rmax in the portal vein of trained rats was prevented by endothelium removal or in the presence of N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME), indomethacin, BQ-123 or BQ-788. In conclusion, these data indicate that the training adapted the rat portal vein to respond vigorously to sympathetic stimuli even when the animal is exposed to this exercise. This increased response to sympathetic stimuli appears to involve an enhancement of the vasocontractile influence of endothelin that supplants the modulation exerted by nitric oxide (NO) and vasodilator prostanoids.