Relationship between Hypertensive Left Ventricular Hypertrophy and Levels of Endothelin and Nitric Oxide.

Abstract

To investigate the relationship between hypertensive left ventricular hypertrophy (LVH) and levels of endothelin (ET) and nitric oxide (NO), and to provide an experimental basis for prevention and treatment of hypertensive LVH. Fifty eight hypertensive patients and 14 healthy controls were studied. All patients were examined by echocardiography. Left ventricular mass (LVM) and left ventricular mass index (LVMI) were calculated using Devereux RB formula. Hypertensive patients were divided into a LVH (+) group (n=21) and a LVH (-) group (n=37), and the levels of endothelin and nitric oxide in the peripheral venous blood were measured. The mean ET level was significantly higher in the LVH (+) group than in LVH (-) group (p < 0.05), but the NO level was significantly lower in the LVH (+) group. The ET/NO ratio was significantly higher in the LVH (+) group than in LVH (-) group (p< 0.01). For the stepwise multiple regression analysis, the LVMI of hypertensive patients served as a dependent variable, and age, sex, BMI, MAP, ET, NO, and ET/NO served as independent variables. Only MAP, ET, and NO were found to have significant correlation to hypertensive LVH. ET had a significant positive correlation, and NO a significant negative relation to LVMI, but ET/NO showed no correlation to hypertensive LVH. ET and NO are involved in hypertensive LVH; the independent action of ET and NO in the pathogenesis of hypertensive LVH may weaken the relation between ET/NO and hypertensive LVH. (Hypertens Res 2000; 23: 377-380)

Evidence for altered ETB receptor characteristics during development and progression of ventricular cardiomyocyte hypertrophy

“…Increased plasma levels of ETs are positively correlated with severity of LVH in humans (15). There are conflicting data, however, regarding whether plasma ET-1 levels are elevated in SHRs.…”

“…Increased plasma levels of ET-1 occur during hypertension and heart failure and correlate with severity of LVH (15). ET receptor antagonists attenuate LVH in some experimental models in vivo (17,20).…”

Differential Effects of an Anti-Oxidant Intervention on Cardiomyocyte Expression of Adrenomedullin and Intermedin and their Receptor Components in Chronic Nitric Oxide Deficiency

“…NO levels are reduced in the plasma of hypertensive patients with left ventricular hypertrophy (LVH) [7]. NOdeficient hypertension induced by treatment of rats with the NOS inhibitor, N G -nitro-L-arginine methyl ester (L-NAME) is characterised in myocardium by hypertrophy, fibrosis, ischemia and necrosis [8].…”

G.ALPHA.13 Induces PreproET-1 Gene Expression via JNK.

“…Gα13 regulates Na/H exchanger activity (7,8), extracellular signal regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK) (9 -11), nuclear factor κB (NF-κB) (12) and the activity of the low molecular weight GTPase, Rho (13 -15), and is also capable of neoplastic transformation, induction of apoptosis, and stimulation of actin reprotein kinases (ERK, JNK, and p38) (23,24). Because of its vasoconstrictor and growth-promoting action, numerous studies indicate that ET-1 is involved in the pathogenesis of a broad spectrum of renal and cardiovascular diseases (21,22,(25)(26)(27). Previous studies have demonstrated that ET-1 induced ET-1 production through ETAR and/or ETBR-mediated pathways, suggesting that a sustained ET-1 autocrine loop contributes to the progression of cardiovascular and renal diseases (28)(29)(30)(31)(32).…”