scholarly journals Effect of hereditary obesity on renal expressions of NO synthase, caveolin-1, AKt, guanylate cyclase, and calmodulin

2005 ◽  
Vol 68 (6) ◽  
pp. 2766-2772 ◽  
Author(s):  
Zhen Li ◽  
Bernardo Rodruguez-Iturbe ◽  
Z. Ni ◽  
A. Shahkarami ◽  
L. Sepassi ◽  
...  
Keyword(s):  
Guanylate Cyclase ◽  
No Synthase ◽  
Caveolin 1 ◽  
Hereditary Obesity

Effect of renal injury-induced neurogenic hypertension on NO synthase, caveolin-1, AKt, calmodulin and soluble guanylate cyclase expressions in the kidney

2007 ◽  
Vol 292 (3) ◽  
pp. F974-F980 ◽  
Author(s):  
Y. Bai ◽  
S. Ye ◽  
R. Mortazavi ◽  
V. Campese ◽  
N. D. Vaziri
Keyword(s):  
Arterial Pressure ◽  
Guanylate Cyclase ◽  
Renal Injury ◽  
Soluble Guanylate Cyclase ◽  
Left Kidney ◽  
Renal Tissue ◽  
No Synthase ◽  
No Production ◽  
Caveolin 1 ◽  
Nos Isoforms

Single injection of a small quantity of phenol into the cortex of one kidney in rats results in development of persistent hypertension (HTN) which is thought to be mediated by activation of renal afferent and efferent sympathetic pathways and sodium retention. Nitric oxide (NO) plays a major role in regulation of renal vascular resistance, tubular Na+ reabsorption, pressure natriuresis, and thereby systemic arterial pressure. The present study was performed to test the hypothesis that chronic renal injury-induced HTN may be associated with dysregulation of NO system in the kidney. Accordingly, urinary NO metabolite (NOx) and cGMP excretions as well as renal cortical tissue (right kidney) expressions of NO synthase (NOS) isoforms [endothelial, neuronal, and inducible NOS, respectively (eNOS, nNOS, and iNOS)], NOS-regulatory factors (Caveolin-1, phospho-AKt, and calmodulin), and second-messenger system (soluble guanylate cyclase [sGC] and phosphodiesterase-5 [PDE-5]) were determined in male Sprague-Dawley rats 4 wk after injection of phenol (50 μl of 10% phenol) or saline into the lower pole of left kidney. The phenol-injected group exhibited a significant elevation of arterial pressure, marked reductions of urinary NOx and cGMP excretions, downregulations of renal tissue nNOS, eNOS, Phospho-eNOS, iNOS, and alpha chain of sGC. However, renal tissue AKt, phospho-AKT, Calmodulin, and PDE-5 proteins were unchanged in the phenol-injected animals. In conclusion, renal injury in this model results in significant downregulations of NOS isoforms and sGC and consequent reductions of NO production and cGMP generation by the kidney, events that may contribute to maintenance of HTN in this model.

Capillary hydraulic conductivity is decreased by nitric oxide synthase inhibition

1995 ◽  
Vol 268 (5) ◽  
pp. H1856-H1861 ◽  
Author(s):  
R. E. Rumbaut ◽  
M. K. McKay ◽  
V. H. Huxley
Keyword(s):  
Nitric Oxide ◽  
Hydraulic Conductivity ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
No Synthase ◽  
Capillary Water ◽  
Cell Monolayers ◽  
Study Support ◽  
Oxide Synthase

Nitric oxide (NO) has been reported to modulate microvascular permeability to solutes in whole organs, venules, and cultured endothelial cell monolayers. NO derived from L-arginine via NO synthase activates soluble guanylate cyclase in vascular smooth muscle and endothelial cells. While the effects of NO on capillary water permeability have not been characterized, other activators of guanylate cyclase, such as sodium nitroprusside and atrial natriuretic peptide, increase capillary hydraulic conductivity (Lp). We hypothesized that inhibition of NO synthase with the arginine analogue, NG-monomethyl-L-arginine (L-NMMA), would decrease Lp from control levels. Lp was assessed in situ in single perfused frog mesenteric capillaries, first during control conditions (Lcontrolp) and then during superfusion (Ltestp) with either L-NMMA, NG-monomethyl-D-arginine (D-NMMA), a biologically inert enantiomer, or L-NMMA and L-arginine. Superfusion with 1 microM L-NMMA caused a decrease in Lp (Ltestp/Lcontrolp = 0.6 +/- 0.1, P < 0.001), whereas 1 microM D-NMMA was without effect on Lp (Ltestp/Lcontrolp = 1.0 +/- 0.2). The decrease in Lp by 1 microM L-NMMA was not only prevented by the presence of excess L-arginine (100 microM), but Lp increased from control (Ltestp/Lcontrolp = 1.4 +/- 0.2, P < 0.05). Furthermore, superfusion of L-arginine (100 microM) caused an increase in capillary Lp (Ltestp/Lcontrolp = 2.4 +/- 0.9, P < 0.05), whereas D-arginine had no effect on Lp (Ltestp/Lcontrolp = 1.2 +/- 0.3). The results of this study support our hypothesis that inhibition of NO synthase decreases capillary Lp in the intact circulation. In addition, L-arginine increases capillary Lp in our model.(ABSTRACT TRUNCATED AT 250 WORDS)

Ovariectomy upregulates expression of estrogen receptors, NOS, and HSPs in porcine platelets

2002 ◽  
Vol 283 (1) ◽  
pp. H220-H226 ◽  
Author(s):  
Muthuvel Jayachandran ◽  
Virginia M. Miller
Keyword(s):  
Estrogen Receptors ◽  
Hormone Replacement ◽  
Ovarian Hormones ◽  
No Synthase ◽  
Regulatory Proteins ◽  
Caveolin 1 ◽  
Increase Risk ◽  
Shock Proteins ◽  
Risk For Thrombosis ◽  
Platelet Functions

Platelets participate in normal and pathological thrombotic processes. Hormone replacement in postmenopausal women is associated with increase risk for thrombosis. However, little is known regarding how platelets are affected by hormonal status. Nitric oxide (NO) modulates platelet functions and is modulated by hormones. Therefore, the present study was designed to determine how loss of ovarian hormones changes expression of estrogen receptors and regulatory proteins for NO synthase (NOS) in platelets. Estrogen receptors (ERα and ERβ), NOS, heat shock proteins 70 and 90 (HSP70 and HSP90), caveolin-1, -2, and -3, calmodulin, NOS activity, and cGMP were analyzed in a lysate of platelets from gonadally intact and ovariectomized female pigs. Expression of ERβ and ERα receptors, endothelial NOS (eNOS), HSP70, and HSP90 increased with ovariectomy. NOS activity and cGMP also increased; calmodulin was unchanged. Caveolins were not detected. These results suggest that ovarian hormones influence expression of estrogen receptors and eNOS in platelets. Changes in estrogen receptors and NOS could affect platelet aggregation in response to hormone replacement.

Histamine increases venular permeability via a phospholipase C-NO synthase-guanylate cyclase cascade

1993 ◽  
Vol 264 (5) ◽  
pp. H1734-H1739 ◽  
Author(s):  
Y. Yuan ◽  
H. J. Granger ◽  
D. C. Zawieja ◽  
D. V. DeFily ◽  
W. M. Chilian
Keyword(s):  
Phospholipase C ◽  
Guanylate Cyclase ◽  
Permeability Coefficient ◽  
Direct Action ◽  
No Synthase ◽  
Constant Flow ◽  
Apparent Permeability ◽  
Apparent Permeability Coefficient ◽  
Synthase Inhibitor ◽  
Ly 83583

In this study, we hypothesized that histaminergic increases in venular permeability result from a cascade triggered by activation of phospholipase C (PLC), inducing the synthesis of nitric oxide (NO) and activating guanylate cyclase. The apparent permeability coefficient to albumin (Pa) was measured in isolated porcine coronary venules subjected to constant flow and hydrostatic and oncotic pressures. Histamine (2.5, 5, and 10 microM) transiently and progressively increased Pa. The PLC inhibitor 2-nitro-4-carboxyphenyl N,N-diphenylcarbamate (NCDC; 100 microM) decreased baseline permeability and abolished the effect of histamine. The NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA; 10 microM) and the guanylate cyclase inhibitor 6-anilinoquinoline-5,8-quinone (LY 83583; 10 microM) also blocked the histamine-induced hyperpermeability. L-Arginine (3 mM) reversed the inhibition by L-NMMA. NG-monomethyl-D-arginine did not influence the effect of histamine. Furthermore, sodium nitroprusside (10 microM) augmented Pa by two- to threefold; this effect was blocked in the presence of LY 83583 but not altered in the presence of NCDC. The results suggest that histamine increases coronary venular permeability by a direct action on the venular endothelial cells through a PLC-NO synthase-guanylate cyclase-signaling cascade.

scholarly journals Apolipoprotein E Enhances Endothelial-NO Production by Modulating Caveolin 1 Interaction With Endothelial NO Synthase

Hypertension ◽  
2012 ◽  
Vol 60 (4) ◽  
pp. 1040-1046 ◽  
Author(s):  
Lili Yue ◽  
Jing-Tan Bian ◽  
Ivana Grizelj ◽  
Ana Cavka ◽  
Shane A. Phillips ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
No Synthase ◽  
No Production ◽  
Caveolin 1 ◽  
Endothelial No Synthase

A high-fat, refined-carbohydrate diet induces endothelial dysfunction and oxidant/antioxidant imbalance and depresses NOS protein expression

2005 ◽  
Vol 98 (1) ◽  
pp. 203-210 ◽  
Author(s):  
Christian K. Roberts ◽  
R. James Barnard ◽  
Ram K. Sindhu ◽  
Michael Jurczak ◽  
Ashkan Ehdaie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Protein Expression ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Kidney Tissue ◽  
High Fat ◽  
Caveolin 1 ◽  
Induced Hypertension ◽  
Nitric Oxide Deficiency

We tested whether consumption of a high-fat, high-sucrose (HFS) diet can affect endothelium-dependent relaxation, whether this precedes the development of diet-induced hypertension previously noted in this model, and whether it is mediated, in part, by changes in nitric oxide synthase (NOS) and/or NOS regulatory proteins. Female Fischer rats were fed either a HFS diet or standard low-fat, complex-carbohydrate chow starting at 2 mo of age for 7 mo. Vasoconstrictive response to KCl and phenylephrine was similar in both groups. Vasorelaxation to acetylcholine was significantly impaired in the HFS animals, and there were no differences in relaxation to sodium nitroprusside, suggesting that the endothelial dysfunction is due, at least in part, to nitric oxide deficiency. HFS consumption decreased protein expression of endothelial NOS in aorta, renal, and heart tissues, neuronal NOS in kidney, heart, aorta, and brain, and inducible NOS in heart and aorta. Caveolin-1 and soluble guanylate cyclase protein expression did not change, but AKT protein expression decreased in heart and aorta and increased in kidney tissue. Consumption of HFS diet raised brain carbonyl content and plasma hydrogen peroxide concentration and diminished plasma total antioxidant capacity. Because blood pressure, which is known to eventually rise in this model, was not as yet significantly elevated, the present data suggest that endothelial dysfunction precedes the onset of diet-induced hypertension. The lack of a quantitative change in caveolin-1 and soluble guanylate cyclase protein content indicates that alteration in these proteins is not responsible for the endothelial dysfunction. Thus nitric oxide deficiency combined with antioxidant/oxidant imbalance, appears to be a primary factor in the development of endothelial dysfunction in this model.

Sign in / Sign up

Export Citation Format

Share Document