Summary

The nitric oxide and the angiotensin II plays an important role in the regulation of cardiovascular and hidrossaline homeostasis. We study the effect of nitric oxide on the cardiovascular and hidroelectrolytic alterations induced by application of angiotensin II into the subfornical organ. In male Holtzman rats 250-300g we study the effect of application of L-NAME (an inhibitor of nitric oxide sintase) and the effect of L-arginine and sodium nitroprussiate on the water intake, sodium potassium and urinary volume, arterial blood pressure and heart rate induced by injection of angiotensin II into subfornical organ. The injection of angiotensin II into the subfornical organ induced an increase in the water intake. The injection of L-NAME before angiotensin II into the subfornical organ produced a decreased in water intake induced by angiotensin II. The injection of L-arginine and sodium nitroprussiate before angiotensin II into the subfornical organ produced an increase in water intake induced by angiotensin II. The angiotensin II injected into the subfornical organ induced an increased in the sodium and potassium renal excretion. The L-NAME injected before angiotensin II produced a decreased in these effects of angiotensin II.The sodium nitroprussiate and the L-arginine injected before angiotensin II induced an increased in these effects of angiotensin II. About the urinary volume the angiotensin II injection into the subfornical organ produced an increased in the urinary volume. The L-NAME injection before angiotensin II produced a decreased in this effect. The sodium nitroprusssiate and the L-arginine injection before angiotensin II induced an incresased in this effect. The injection of angiotensin II into subfornical organ induced an increased in arterial blood pressure with a drop in the heart rate. The L-NAME injected before angiotensin II produced a decreased in the mean arterial pressure and a decreased in the heart rate produced by angiotensin II. The sodium nitroprussiate and the L-arginine injected before angiotensin II produced a decreased in the arterial pressure and a decreased in heart rate induced by angiotensin II. These results showed the important role of the nitric oxide of the subfornical organ in control of the cardiovascular regulatory mechanism and in the regulation of the volume and osmolarity of the extracellular fluid. These results have a strongly support in the methodology utilized. We utilized drugs that blocked released and generated the nitric oxide. The another important point in this research is that we can postulate the influence of the cardiovascular regulatory center. When the arterial blood pressure increased the important regulatory mechanism is released with a drop in the heart rate (reflex bradicadia)