Oxidative stress-related factors in Bartter's and Gitelman's syndromes: relevance for angiotensin II signalling.

Background: Bartter's and Gitelman's syndromes (BS/GS) have a blunted Gq protein-mediated cell signalling despite high circulating angiotensin II (Ang II) levels. This is associated with reduced Galphaq gene expression, intracellular inositol trisphosphate and Ca(++) release, PKC activity and cell reactivity. Ang II is a powerful stimulator of vascular oxidases but BS/GS patients show reduced total volatile LDL oxidation products and reduced LDL susceptibility to oxidation suggesting low level of oxidative stress.

The Li+/Na+ exchange in hypertension.

The red cell membrane Li+/Na+exchange is a heteroexchange that operates in either direction across the cell membrane. It binds either Li+ or Na+ on one side of the membrane and it exchanges the transported species for either Li+ or Na+ on the opposite side in a stoichiometric ratio of 1:1. In the population, Li+/Na+exchange is unimodally distributed but skewed to the right.

Kidney transplant in Gitelman's syndrome. Report of the first case.

This paper is the first report of a patient with Gitelman's syndrome who, after developing a chronic nephropathy leading to end-stage renal disease, underwent kidney transplantation. The clinical findings of this disease, which include hypokalemia, high angiotensin II and aldosterone levels, sustained hyporesponsiveness to the pressor action of angiotensin II and norepinephrine, normo/hypotension and hypovolemia; the clinical course after kidney transplantation highlights the importance and the need for carefully controlling the hemodynamic status of these patients. In fact, the persistence of normo/hypotension and hypokalemia, in the presence of increased levels of Ang II and aldosterone to which the transplanted kidney should normally respond, raises interesting questions about the mechanisms responsible for the regulation of patient's vascular tone and potassium homeostasis after transplantation, which could expose the patient to post-transplant hypoperfusive renal failure and its long-term complications.

Oxidative stress in kidney transplant patients with calcineurin inhibitor-induced hypertension: effect of ramipril.

In patients with cyclosporine-induced hypertension, upregulation of the nitric oxide system and oxidative stress were shown, which could induce hypertension, remodeling, and chronic rejection by increasing nitric oxide catabolism. However, it is still debated whether cyclosporine and tacrolimus exert a different action. The aim of the current study was to compare the effects of cyclosporine and tacrolimus on markers of oxidative stress and endothelial dysfunction in kidney transplant patients with posttransplant hypertension.