VASOPRESSOR MECHANISMS IN ACUTE AORTIC COARCTATION HYPERTENSION

Angiotensin II (ANG II) and vasopressin (AVP) act together with the me chanical effect of aortic constriction in the onset of acute aortic co arctation hypertension. Blockade of ANG II and AVP V-1 receptors demon strated that ANG II acts on the prompt (5 min) rise in pressure wherea s AVP is responsible for the maintenance (30-45 min) of the arterial p ressure elevation during aortic coarctation. Hormone assays carried ou t on blood collected from conscious rats submitted to aortic constrict ion supported a role for ANG II in the early stage and a combined role for both ANG II and AVP in the maintenance of proximal hypertension. As expected, a role for catecholamines was ruled out in this model of hypertension, presumable due to the inhibitory effect of the sinoaorti c baroreceptors. The lack of afferent feedback from the kidneys for AV P release from the central nervous system in rats with previous renal denervation allowed ANG II to play the major role in the onset of the hypertensive response. Median eminence-lesioned rats exhibited a promp t increase in proximal pressure followed by a progressive decline to l ower hypertensive levels, revealing a significant role for the integri ty of the neuroaxis in the maintenance of the aortic coarctation hyper tension through the release of AVP. In conclusion, the important issue raised by this model of hypertension is the likelihood of a link betw een some vascular territory - probably renal - below the coarctation t riggering the release of AVP, with this vasoconstrictor hormone partic ipating with Ang II and the mechanical effect of aortic constriction i n the acute aortic coarctation hypertension.