INVESTIGADORES
PERAL Maria De Los Angeles
artículos
Título:
NITRIC OXIDE MODULATES REACTIVITY TO ANGIOTENSIN II IN INTERNAL MAMMARY ARTERIAL GRAFTS IN HYPERTENSIVE PATIENTS WITHOUT ASSOCIATED RISK FACTORS
Autor/es:
JOO TURONI C; MARAÑÓN R,; PROTO V; HERRERA NICASIO; PERAL DE BRUNO M
Revista:
CLINICAL AND EXPERIMENTAL HYPERTENSION
Editorial:
taylor & Francis
Referencias:
Lugar: New York; Año: 2011 vol. 33 p. 27 - 33
ISSN:
1064-1963
Resumen:
Abstract
We investigated the effects of extraendothelial nitric oxide (NO) on angiotensin II (Ang II) reactivity in internal mammary
artery (IMA) rings, as well as the impact of hypertension without associated risk factors in this response. Vascular
reactivity, NO levels, and resting membrane potentials were determined in hypertensive (HT) and normotensive (NT)
IMA rings. Only rings with endothelial dysfunction were included. Ang II produced a dose-dependent contraction that
was higher in HT rings. Response to Ang II was potentiated by N-nitro L-arginine methyl ester (L-NAME) in NT but
not in HT rings. The antioxidant agents tempol and diphenyleneiodonium (DPI) reverted the hyperreactivity to Ang II
in HT rings. Extraendothelial NO was present in both NT and HT rings. However, NT rings showed higher values.
L-NAME and S-methyl-L-thiocitrulline inhibited NO release in all cases. L-arginine reverted this inhibition. Both tempol
and DPI increased NO release in both NT and HT rings. The number of vascular smooth muscle cells (VSMC) and
anti-a-actin positive areas were lower in HT than in NT rings, without variations in wall thickness or wall/lumen ratio.
With regard to resting membrane potential, we found in HT rings that the depolarization induced by Ang II was
abolished by tempol. These findings suggest that extraendothelial NO counterregulates Ang II contractility in IMA
rings; however, its action could be altered in hypertensive situations even though the patients did not have associated
risk factors. We suggest two mechanisms: increased oxidative stress and a decreased ability of nNOS in VSMC to
produce NO.