These findings suggest that radiographic imaging has a relatively high diagnostic yield in children with SNHL. These findings may be of value in counseling patients and guiding the management of their SNHL.

Abstract-The systemic renin-angiotensin system (RAS) plays an important role in blood pressure (BP) regulation during the development of 2-kidney, 1 clip (2K1C) hypertension. Its contributions decrease with time after constriction of the renal artery. During the chronic phase, the peripheral RAS returns to normal, but the hypertension is sustained for months. We hypothesized that in this phase the brain RAS contributes to the maintenance of high BP. To test the hypothesis, we studied the role of brain RAS by decreasing the synthesis of angiotensinogen (AGT) and the angiotensin II (Ang II) type 1a receptor (AT 1 R) with intracerebroventricular injections of antisense oligonucleotides (AS-ODNs). The response of systolic BP (SBP) to AS-ODNs to AGT mRNA was studied in 2K1C rats at 6 months after clipping, and the response to AS-ODNs to AT 1 R mRNA was studied at 10 months after clipping. Key Words: rats Ⅲ renin-angiotensin system Ⅲ brain Ⅲ hypertension, 2K1C Ⅲ antisense T he renin-angiotensin system (RAS) plays an important role in blood pressure (BP) regulation during the development of renovascular hypertension. 1 In the rat model of unilateral renovascular hypertension (the 2-kidney, 1 clip Goldblatt [2K1C] hypertensive rat), renal stenosis elevates the RAS. The contributions of RAS in this model vary depending on the time after constriction of the renal artery. 2 In the acute phase of 2K1C hypertension, plasma renin activity rises, and the increase in BP is RAS dependent. Both plasma renin activity and plasma angiotensin II (Ang II) concentrations normalize in the chronic phase despite the continued high BP. To explain the antihypertensive effects of ACE inhibitors when the circulating RAS is not overtly activated, the concept of tissue RAS has been used. It is proposed that in 2K1C hypertension, the RAS in various tissues is activated, and the products act in a paracrine fashion and are not detectable in plasma. 3,4 An activation of tissue RAS in the acute phase of 2K1C hypertension has been extensively discussed. [3][4][5][6][7][8][9] By contrast, few studies have examined the mechanism of maintained hypertension in the chronic phase, 9,10 although clinically, this is much more relevant. Most renovascular hypertensive patients present with chronic high BP. We have shown that inhibiting the brain RAS in adult spontaneously hypertensive rats (SHR) significantly reduces hypertension. 11 Baltatu et al 12 have reported that the transgenic rat [TGR(ASrAoGEN)], which has permanent inhibition of brain-specific angiotensinogen (AGT) synthesis, shows a reduction of hypertension induced by a low-dose of Ang II. Therefore, we hypothesize that as the 2K1C hypertension progresses chronically, the brain RAS contributes to elevated BP in the absence of peripheral RAS elevation.To test this hypothesis, we used antisense (AS) oligodeoxynucleotides (ODNs), which we previously designed to inhibit components of the brain RAS, including AGT mRNA and Ang II type 1a receptor (AT 1 R) mRNA. 13-15 AS-ODN has some advantages over drugs:...