Pressure and Hemodynamic Effects

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The BP effects of Ang II are mediated via a combination of mechanisms including vasoconstriction, stimulation of renal tubular sodium resorption, and its effects on the central and sympathetic nervous tissues (100,101). Because hypertension exacerbates diabetic vascular complications (102), it is likely that the BP-lowering effects of ACE inhibitors are a major contributor to the reduction of vascular complications in diabetic patients with hypertension (9,93). However, there is growing evidence that ACE inhibitors may also provide beneficial vascular effects in diabetes in the absence of systemic hypertension. Several large studies have demonstrated that ACE inhibition can reduce renal, retinal, and cardiovascular complications in normotensive diabetic patients (1,5,8). Although a small reduction in systemic BP within the normotensive range may contribute to the vasoprotective effects of ACE inhibition, the magnitude of these effects is greater than that which would be predicted based on the magnitude of these BP-lowering effects alone. Local upregulation or sensitization of the RAS can result in tissue specific increases in Ang II action, which may not significantly affect systemic BP. These local changes in the RAS can affect hemodynamics and pressure within certain vascular structures, such as the renal glomerulus. RAS inhibition has been shown to alleviate glomerular capillary hypertension caused by efferent arteriolar vasoconstriction induced by diabetes (103106). Thus, in addition to systemic BP control, ACE inhibition can also affect local hemodynamics and pressure. Multiple mechanisms may mediate the detrimental vascular effects associated with mechanical stress caused by hypertension. Mechanical stretch stimulates cardiomyocytes to release Ang II, which induces an autocrine hypertrophic response (107). A recent report has shown that mechanical stretch also induces Ang II-independent activation of the AT1 receptor (45). Interestingly, this mechanical stretch response blocked the AT1 antagonist candesartan but not by the Ang II competitive inhibitor (Sar1,Ile8)-Ang. Additionally, increased shear stress and mechanical stretch can activate vascular calcium transport, transforming growth factor-^, and purinoceptors (108-111).

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