The data suggests that: (a) GHD in children increases CYP3A activity in a non-sex-dependent manner, (b) rhGH treatment for 30 days to GHD children results in a sexually dimorphic effect on CYP3A activity, with a significant decrease in males toward normalization in relation to controls and non-significant changes in females. The results of this study may have important clinical implications for GHD children, since changes in CYP3A activity importantly affect the metabolism of both steroid hormones and CYP3A substrate drugs.

These results reveal that HIV-infected individuals have a significant abnormality in systemic K+ equilibrium. This abnormality, which leads to the development of hyperkalemia after the L-arginine challenge, may be related, in part, to a failure in the aldosterone response to hyperkalemia. These results provide a new basis for understanding the pathogenesis of hyperkalemia in HIV individuals, and demonstrate that the risk of HIV-associated hyperkalemia exists even in the absence of amiloride-mimicking drugs or overt hyporeninemic hypoaldosteronism.

Abstract-Data remain insufficient to place the decreased response to L-arginine in hypertensive patients within a consistent pathophysiological sequence. The aim of the present study in patients with essential hypertension was to assess the relationships between the response to L-arginine and a set of relevant clinical and laboratory parameters. In this prospective, interventional study, we administered L-arginine to untreated hypertensive individuals and healthy control subjects and measured the clearance of inulin and of para-aminohippurate and a set of biochemical and clinical variables. L-Arginine infusion revealed major differences between control subjects and 1 subgroup (group B) of hypertensive individuals. Group B hypertensives (nϭ18) had no increase in inulin clearance and no decrease in renal vascular resistance with L-arginine; however, in another subset of hypertensive patients (group A, nϭ27), the insulin clearance increased and renal vascular resistance decreased similar to the control group (group C, nϭ11). The ambulatory blood pressure monitoring in group B showed both an increased mean diastolic pressure and a "nondipper" pattern in the nocturnal regulation of arterial pressure. These findings in group B were accompanied by significant alterations in optic fundus and left ventricle hypertrophy and increased microalbuminuria (all, PϽ0.05). Furthermore, group B individuals had significantly lower values of HDL cholesterol and a higher baseline atherogenic index, plasma insulin level, and glucose/insulin index. We disclose a previously undescribed relationship between end organ repercussion and decreased renal hemodynamic response to L-arginine. Our results may help to understand the mechanisms that lead to target organ damage in hypertension. Key Words: L-arginine Ⅲ hypertension, essential Ⅲ endothelium Ⅲ blood pressure monitoring, ambulatory D espite intense investigative efforts, major basic aspects of the pathophysiology of essential hypertension remain unclear. In recent years, a great deal of attention has been paid to the involvement of endothelium-related mechanisms in the pathogenesis of arterial hypertension. [1][2][3][4][5][6][7][8] In particular, the role of the vascular and renal regulatory mediator NO in hypertension has been extensively studied through the administration of the NO precursor amino acid L-arginine. 9 -12 In these studies, an alteration in the renal vasodilatory response to L-arginine was described, although the findings that have been reported are less than homogeneous. 9 -12 Therefore, even though the information provided in the aforementioned studies is relevant, the data obtained are incomplete and still must be organized to provide a coherent pathophysiological interpretation. First, to homogenize the information and to eliminate undesired variability, strict criteria are necessary to select patients with essential hypertension. Second, and of extreme importance, no relationships have been sought between the response to L-arginine and markers of severity of hypert...

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