Our findings that the mid-frequency band variability of arterial pressure was reduced in diabetic patients suggest that sympathetic modulation of the cardiovascular system is impaired, corroborating other studies in such patients using this and other approaches.

Angiotensin II (ANG II) and vasopressin (AVP) act together with the mechanical effect of aortic constriction in the onset of acute aortic coarctation hypertension. Blockade of ANG II and AVP V 1 receptors demonstrated that ANG II acts on the prompt (5 min) rise in pressure whereas AVP is responsible for the maintenance (30-45 min) of the arterial pressure elevation during aortic coarctation. Hormone assays carried out on blood collected from conscious rats submitted to aortic constriction 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, presumably due to the inhibitory effect of the sinoaortic baroreceptors. The lack of afferent feedback from the kidneys for AVP 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 prompt increase in proximal pressure followed by a progressive decline to lower hypertensive levels, revealing a significant role for the integrity of the neuroaxis in the maintenance of the aortic coarctation hypertension through the release of AVP. In conclusion, the important issue raised by this model of hypertension is the likelihood of a link between some vascular territory -probably renal -below the coarctation triggering the release of AVP, with this vasoconstrictor hormone participating with Ang II and the mechanical effect of aortic constriction in the acute aortic coarctation hypertension. Key words Mechanical vs renal factorFor a long time two schools of thought have attributed different mechanisms to chronic aortic coarctation hypertension. Whereas one school suggested that the mechanical effect of aortic constriction was the main factor promoting high blood pressure (1-3), others (4-6) argued that a renal factor was involved in the arterial pressure elevation. However, it was only in 1968 (7) that studies on young dogs with hypertension induced by chronic aortic coarctation hypertension provided a clear-cut demonstration that both factors, i.e., mechanical and renal factors, were operative in this model for hypertension. Later, these observations were confirmed in adult dogs submitted to aortic constriction, indicating a major role for the renal mechanisms in the development of hypertension, associated with a role played by aortic constriction (8).