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AT1 receptor antagonist telmisartan administered peripherally inhibits central responses to angiotensin II in conscious rats.
TLDR
It is demonstrated that, following peripheral administration, the AT1 receptor antagonist telmisartan can penetrate the blood-brain barrier in a dose- and time-dependent manner to inhibit centrally mediated effects of Ang II.
Arginase is a major pathway of L-arginine metabolism in nephritic glomeruli.
TLDR
Competition between arginase and NOS pathways suggests a regulatory mechanism of L-arginine metabolism within the glomerulus, with implications for the pathogenesis of injury and scarring in glomerulonephritis.
Cellular localization of inducible nitric oxide synthase in experimental endotoxic shock in the rat.
TLDR
Findings provide a direct demonstration of the cellular localization of inducible NO synthase after lipopolysaccharide, which was monocytes and macrophages in multiple organs, principally liver and spleen.
The relaxant properties in guinea pig airways of S-nitrosothiols.
TLDR
The data reveal that RS-NO are generally potent airway smooth muscle relaxants with at least a partial effect through stimulation of cyclic GMP.
Arginine metabolism in experimental glomerulonephritis: interaction between nitric oxide synthase and arginase.
L-Arginine is metabolized by two pathways: 1) by nitric oxide synthase (NOS) to nitric oxide (NO) and 2) by arginase forming urea and L-ornithine. Inflammatory responses may involve a balance between
Induction of nitric oxide synthase in rat immune complex glomerulonephritis.
TLDR
The results provide the first direct evidence for the presence and localization of inducible NOS in glomeruli and support a significant role for NO in the pathogenesis of immune complex glomerulonephritis.
Inducible nitric oxide synthase in inflammation
TLDR
The evidence is reviewed for a role for nitric oxide (NO) as a chemical indicator of inflammation and inflammatory diseases.
Inducible nitric oxide synthase in inflammation
TLDR
The evidence is reviewed for a role for nitric oxide (NO) as a chemical indicator of inflammation and inflammatory diseases.
Relaxation of human bronchial smooth muscle by S-nitrosothiols in vitro.
TLDR
Consistent with the role of cyclic GMP (cGMP) in mediating relaxation responses, S-nitroso-N-acetyl cysteine (S-NO-AC) increased tissue cGMP levels 4-fold, and 8-bromo-cG MP caused modest tissue relaxation which was potentiated by the phosphodiesterase inhibitor, dipyridamole (1 microM).
L-arginine depletion inhibits glomerular nitric oxide synthesis and exacerbates rat nephrotoxic nephritis.
TLDR
Effects of L-arginine depletion on glomerular NO synthesis and the course of accelerated nephrotoxic nephritis (NTN) are examined, showing that arginine depletion, which inhibits glomerULAR NO synthesis in NTN, leads to increased proteinuria.
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