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• W2049164029 abstract "Circulatory homoeostasis depends on the equilibrium between vasoconstricting and vasodilating forces regulating blood pressure, as well as the equilibrium between procoagulant and fibrinolytic factors regulating blood rheology. Several lines of evidence suggest an interplay of these two functions, so that changes tipping the balance towards increased vasoconstriction and elevation of blood pressure result also in a hypercoagulable state with elevated risk of atherothrombotic cardiovascular events. A major class of vasoactive peptides is the kallikrein–kinin system, whose importance came to focus when it was discovered that the angiotensin-converting enzyme (ACE) and the kininase II that inactivates bradykinin are actually one and the same [1]. This led to the realization that many of the haemodynamic and metabolic consequences of ACE inhibition are attributable to bradykinin, which is in keeping with the original designation of ACE inhibiting polypeptides as ‘bradykinin potentiating factors’ [2]. Bradykinin exerts most of its physiologically relevant functions via the B2 type receptor [3], which is constitutively abundant in many vascular and visceral tissues, whereas the B1 receptor is mostly inducible by inflammation, tissue damage and various manipulations [4]. Physiological B2 receptor-mediated functions include, depending on circumstances, both vasodilation and vasoconstriction (via activation of the arachidonic acid cascade), stimulation of the sympathoadrenal system, nociception via sensory nerve stimulation and enhanced insulin-dependent glucose transport across cell membranes, leading to improved glucose tolerance. Interestingly, the absence of functional B2 receptors induces upregulation and overexpression of B1 receptors that can compensate for most of the haemodynamic effects of bradykinin [5,6], but not the metabolic ones, leading to a state of insulin resistance [7]. Another B2 receptor-mediated action of bradykinin is its interaction with components of the coagulation system. The salutary effects of ACE inhibition post-myocardial infarct have been demonstrated by numerous long-term outcome trials, but have been attributed mostly to inhibition of angiotensin, with its long-known vasculotoxic and tissue-damaging properties [8], as well as its recently reported procoagulant properties via increase in plasminogen activator inhibitor-1 [9]. Indeed, antihypertensive therapy with angiotensin AT1 receptor blockade was shown to tip the coagulation-fibrinolysis balance in favour of the latter by influencing several markers of blood rheology and endothelial function [10]. However, recent reports have revealed another aspect of the influence of ACE inhibition on the fibrinolytic balance, namely the bradykinin B2 receptor-mediated enhanced fibrinolysis via stimulation of tissue-type plasminogen activator [11]. Against this background of multiple interactions between angiotensin, bradykinin and various factors of the coagulation cascade affecting vasoregulation and blood rheology, in this issue of the journal, Amphilochiadis et al. [12] provide another new piece of evidence. These authors have published a series of papers describing a novel vasopressor peptide named ‘new pressor protein’ (NPP), characterized by a close amino acid sequence homology with the beta-fragment of activated coagulation factor XII (Hageman factor). This FXIIa-derived peptide was shown to elicit a potent vasoconstricting response, associated with tachycardia and a sympathoadrenal activation with massive release of catecholamines. Peptides derived from cleavage of FXIIa have previously been shown to produce hypotension and to activate the kallikrein–kinin system [13,14]. Because bradykinin and some of its B2 receptor-specific analogues have been shown to stimulate the adrenal medulla [15], Amphilochiadis et al. [12] hypothesized that the NPP too may exert some of its effects via the B2 receptor of bradykinin. Indeed, they demonstrate convincingly that this is the case, because these effects are potentiated by ACE inhibition with captopril and blocked to a large extent by the specific B2 receptor antagonist HOE-140. It is unclear from their studies whether the NPP itself directly activates the B2 receptor and shares it with bradykinin, or whether it exerts the largest part of its action indirectly, by stimulating the generation or otherwise potentiating the effects of bradykinin. This, of course, could have been clarified by measurement of the plasma levels of bradykinin before and after injection of the NPP. Be that as it may, these studies shed light on a new interface between vasoactive peptides and the coagulation system. Although the practical implications of this finding are still speculative, it is not difficult to envision clinical situations, where pharmacological manipulation of certain components could enhance tissue perfusion and end-organ protection." @default.
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• W2049164029 date "2004-06-01" @default.
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• W2049164029 title "Hypertension, vasoactive peptides and coagulation factors" @default.
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• W2049164029 doi "https://doi.org/10.1097/00004872-200406000-00007" @default.
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