Vasopressor mechanisms in acute aortic coarctation hypertension

Abstract

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).

Hemodynamic responses to acute aortic coarctation in conscious sinoaortic denervated rats

“…Partial aortic occlusion with the maintenance of the pressure distal to the cuff precisely at 50 mmHg (8) keeps the renal perfusion pressure well below the lower limit of renal blood flow autoregulation (10) providing a powerful stimulus for renin (1,4) and vasopressin release (2,3,6,11,12). In addition, this maneuver induces a marked mechanical increase in aortic resistance which represents a substantial challenge for circulatory homeostasis (6).…”

Increased hypothalamic angiotensin-(1–7) levels in rats with aortic coarctation-induced hypertension

“…The elevated plasma Ang levels may result from the augmented plasma renin activity arising from the reduced perfusion pressure of the kidney below the constriction previously reported in CH rats [5,6,[25][26][27]31], suggesting that activation of the enzyme contributes to the increased production of Ang peptides. Similarly, augmented Ang I and Ang II levels as a result of increased plasma renin activity have also been reported in two-kidney, one-clip (2K, 1C) hypertensive rats [13], another renovascular hypertensive rat model characterized by RAS hyperactivity.…”

“…The physiopathogenesis of acute aortic coarctation hypertension has been well documented [5,6,[25][26][27]31]. Clamping the aorta between the renal arteries initially results in arterial and cardiac hypertrophy in response to the development of high blood pressure [5,6].…”

“…Clamping the aorta between the renal arteries initially results in arterial and cardiac hypertrophy in response to the development of high blood pressure [5,6]. Involvement of angiotensin II (Ang II) in this hypertensive process has been demonstrated by blockade of Ang II receptors or measurement of plasma renin activity, which was significantly increased following aortic constriction [5,6,[25][26][27]31]. On the other hand, the response of critical cardiovascular target organs to the increased renin-angiotensin system (RAS) in this model of hypertension has not been characterized.…”

Cardiac surgery and hypertension: a dangerous association that must be well known

“…They deduced that hypertension and arch obstruction appeared relating to unparalleled growth of the transverse aortic arch proximal to the repair site. But the renal factor, i.e., aortic constriction below the coarctation triggering the release of vasopressin and involved by angiotensin II offered a more plausible explanation for hypertension resulting from acute aortic coarctation [39].…”