scholarly journals Regulation and function of renal medullary cyclooxygenase-2 during high salt loading

10.2741/4476 ◽  
2017 ◽  
Vol 22 (1) ◽  
pp. 128-136 ◽  
Author(s):  
Tianxin Yang
Keyword(s):  
Cyclooxygenase 2 ◽  
High Salt ◽  
Salt Loading ◽  
And Function

scholarly journals Nephron-Specific Disruption of Polycystin-1 Induces Cyclooxygenase-2–Mediated Blood Pressure Reduction Independent of Cystogenesis

2020 ◽  
Vol 31 (6) ◽  
pp. 1243-1254
Author(s):  
Jayalakshmi Lakshmipathi ◽  
Yang Gao ◽  
Chunyan Hu ◽  
Deborah Stuart ◽  
Jonathan Genzen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Arterial Pressure ◽  
Knockout Mice ◽  
Salt Intake ◽  
Blood Pressure Reduction ◽  
Cyclooxygenase 2 ◽  
High Salt ◽  
Salt Loading ◽  
High Salt Intake ◽  
And Control

BackgroundHypertension often occurs before renal function deteriorates in autosomal dominant polycystic kidney disease (ADPKD). It is unknown whether the Pkd1 gene product polycystin-1—the predominant causal factor in ADPKD—itself contributes to ADPKD hypertension independent of cystogenesis.MethodsWe induced nephron-specific disruption of the Pkd1 gene in 3-month-old mice and examined them at 4–5 months of age.ResultsKidneys from the Pkd1 knockout mice showed no apparent renal cysts, tubule dilation, or increased cell proliferation. Compared with control mice, Pkd1 knockout mice exhibited reduced arterial pressure during high salt intake; this associated with an increased natriuretic, diuretic, and kaliuretic response during the first 2–3 days of salt loading. The lower arterial pressure and enhanced natriuresis during high salt loading in Pkd1 knockout mice were associated with lower urinary nitrite/nitrate excretion and markedly increased urinary PGE2 excretion, whereas GFR, plasma renin concentration, and urinary endothelin-1 excretion were similar between knockout and control mice. Kidney cyclooxygenase-2 protein levels were increased in Pkd1 knockout mice during high salt intake; administration of NS-398, a selective cyclooxygenase-2 inhibitor, abolished the arterial pressure difference between the knockout and control mice during high salt intake. Total kidney Na+/K+/2Cl− cotransporter isoform 2 (NKCC2) levels were greatly reduced in Pkd1 knockout mice fed a high salt diet compared with controls.ConclusionsThese studies suggest that nephron polycystin-1 deficiency does not itself contribute to ADPKD hypertension and that it may, in fact, exert a relative salt-wasting effect. The work seems to comprise the first in vivo studies to describe a potential physiologic role for nephron polycystin-1 in the absence of cysts, tubule dilation, or enhanced cell proliferation.

scholarly journals Breast cancer cell cyclooxygenase-2 expression alters extracellular matrix structure and function and numbers of cancer associated fibroblasts

Oncotarget ◽  
2017 ◽  
Vol 8 (11) ◽  
pp. 17981-17994 ◽  
Author(s):  
Balaji Krishnamachary ◽  
Ioannis Stasinopoulos ◽  
Samata Kakkad ◽  
Marie-France Penet ◽  
Desmond Jacob ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Extracellular Matrix ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Structure And Function ◽  
Cyclooxygenase 2 ◽  
Cancer Associated Fibroblasts ◽  
Matrix Structure ◽  
And Function

Prolonged NOS inhibition in the brain elevates blood pressure in normotensive rats

1998 ◽  
Vol 275 (2) ◽  
pp. R410-R417 ◽  
Author(s):  
Atsushi Sakima ◽  
Hiroshi Teruya ◽  
Masanobu Yamazato ◽  
Rijiko Matayoshi ◽  
Hiromi Muratani ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
High Salt ◽  
Salt Loading ◽  
Salt Diet ◽  
Intracerebroventricular Infusion ◽  
Air Jet ◽  
Sd Rats ◽  
Low Salt ◽  
The Brain

Systemic inhibition of nitric oxide synthase (NOS) evokes hypertension, which is enhanced by salt loading, partly via augmented sympathetic activity. We investigated whether inhibition of brain NOS elevates blood pressure (BP) in normotensive rats and, if so, whether the BP elevation is enhanced by salt loading. After a 2-wk low-salt (0.3%) diet, male Sprague-Dawley (SD) rats were divided into four groups. Groups 1 and 2 received a chronic intracerebroventricular infusion of 0.5 mg ⋅ kg−1 ⋅ day−1of N G-monomethyl-l-arginine (l-NMMA), and groups 3 and 4 were given artificial cerebrospinal fluid (aCSF). Groups 1 and 3 were placed on a high-salt (8%) diet, whereas groups 2 and 4 were on a low-salt diet. On day 9or 10, group 1 showed significantly higher mean arterial pressure (MAP) in a conscious unrestrained state (129 ± 3 mmHg vs. 114 ± 3, 113 ± 1, and 108 ± 3 mmHg in groups 2, 3, and 4, respectively, P < 0.05). On a high-salt diet, response of renal sympathetic nerve activity but not of BP to air-jet stress was significantly larger in rats givenl-NMMA than in rats given aCSF (29 ± 4% vs. 19 ± 3%, P < 0.05). When the intracerebroventricular infusions were continued for 3 wk, MAP was significantly higher in rats givenl-NMMA than in rats given aCSF irrespective of salt intake, although the difference was ∼7 mmHg. Thus chronic inhibition of NOS in the brain only slightly elevates BP in SD rats. Salt loading causes a more rapid rise in BP. The mechanisms of the BP elevation and its acceleration by salt loading remain to be elucidated.

Vascular Lesions in Hypertensive Rats under Salt Loading: Kidney Renin and Lysosomal Enzymes

1976 ◽  
Vol 51 (s3) ◽  
pp. 49s-51s
Author(s):  
N. Saito ◽  
S. Mukaino ◽  
K. Ogino ◽  
C. Kawai
Keyword(s):  
Enzyme Activities ◽  
Cathepsin D ◽  
Normal Diet ◽  
High Salt ◽  
Renin Activity ◽  
Vascular Lesions ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

1. Renal and cerebral vascular lesions occurred more often and earlier in spontaneously hypertensive rats (SHR) given a high salt diet than in SHR given a normal diet. 2. Kidney renin activity was low during high salt loading; the kidney renin activity of rats with hypertensive renal vascular lesions was moderately elevated. Kidney renin activity or cathepsin D activities were higher in stroke-prone SHR (SHRSP) aged 9 months than in stroke-resistant SHR (SHRSR). 3. β-Glucuronidase, cathepsin D and deoxyribonuclease activities were greater in the kidney of Wistar/Kyoto (WK) rats or SHR when there were hypertensive vascular lesions. These three enzyme activities were also greater in the aorta of SHR aged 13–14 months than in the aorta of WK rats. 4. It was supposed that kidney renin activity and lysosomal enzyme activities were related to hypertensive vascular lesions.

scholarly journals Salt Loading Affects Cortisol Metabolism in Normotensive Subjects: Relationships with Salt Sensitivity

2003 ◽  
Vol 88 (9) ◽  
pp. 4180-4185 ◽  
Author(s):  
Michiel N. Kerstens ◽  
Frank G. H. van der Kleij ◽  
Arnold H. Boonstra ◽  
Wim J. Sluiter ◽  
Jan Koerts ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Vascular Resistance ◽  
High Salt ◽  
Percentage Change ◽  
High Salt Diet ◽  
Salt Loading ◽  
Salt Diet ◽  
Cortisol Metabolism ◽  
Normotensive Subjects ◽  
Renal Vascular

We studied cortisol metabolism together with insulin sensitivity [homeostatic model assessment (HOMA)] and renal hemodynamics in 19 salt-resistant (sr) and nine salt-sensitive (ss) normotensive subjects after a low- and high-salt diet. Results are described as high- vs. low-salt diet. Sum of urinary cortisol metabolite excretion (∑metabolites) increased in sr subjects (3.8 ± 1.6 vs. 3.1 ± 1.1 μg/min per square meter, P &lt; 0.05) and decreased in ss subjects (2.3 ± 1.0 vs. 2.9 ± 1.1 μg/min per square meter, P &lt; 0.05). Plasma 0830 h cortisol decreased in sr subjects but did not change significantly in ss subjects. In all subjects, the absolute blood pressure change correlated negatively with the percentage change in ∑metabolites (P &lt; 0.05) and positively with the percentage change in renal vascular resistance (P &lt; 0.05). ∑metabolites during high-salt diet correlated negatively with the percentage changes in plasma 0830 h cortisol (P &lt; 0.05) and renal vascular resistance (P = 0.05). HOMA did not change in either group, but the percentage change in HOMA correlated positively with the percentage change in plasma cortisol (P = 0.001) and negatively with the percentage change in ∑metabolites (P &lt; 0.01). Parameters of 11β-hydroxysteroid dehydrogenase activity were not different between groups and did not change. In conclusion, these data suggest that cortisol elimination is affected differently after salt loading in sr and ss subjects. Changes in circulating cortisol might contribute to individual sodium-induced alterations in insulin sensitivity.

High-salt diet upregulates kininogen and downregulates tissue kallikrein expression in Dahl-SS and SHR rats

1996 ◽  
Vol 271 (4) ◽  
pp. F824-F830 ◽  
Author(s):  
C. Wang ◽  
C. Chao ◽  
L. M. Chen ◽  
L. Chao ◽  
J. Chao
Keyword(s):  
Blood Pressure ◽  
High Salt ◽  
Transcriptional Level ◽  
Tissue Kallikrein ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
High Salt Diet ◽  
Salt Loading ◽  
Salt Diet ◽  
Sd Rats

Tissue kallikrein cleaves low-molecular-weight (low-M(r)) kininogen to produce the vasoactive kinin peptide. It has been suggested that hypertensive patients with low urinary kallikrein excretion may have a defect in sodium handling. In this study, we examined the effect of a high-salt diet on the expression of tissue kallikrein and kininogen genes in Dahl salt-sensitive rats (Dahl-SS), spontaneously hypertensive rats (SHR), and normotensive Sprague-Dawley rats (SD) by Northern and Western blot analysis and radioimmunoassay. Control and experimental groups received normal and high-salt diets containing 0.4% and 8% NaCl, respectively, for 6 wk. High-salt diet induced a significant time-dependent increase of blood pressure in both strains of hypertensive rats and a slight but significant increase of blood pressure in normotensive SD rats. Hepatic kininogen mRNA levels of both Dahl-SS and SHR on a high-salt diet increased 2.4-fold and 2.0-fold, respectively, while alpha 1-antitrypsin mRNA levels were not changed in rats receiving high-salt diet. Immunoreactive total kininogen and low-M(r) kininogen (58 kDa) levels in sera increased in response to high-salt diet in both strains of hypertensive rats. In SD rats, the low-M(r) kininogen level in sera was unaltered, whereas total kininogen increased in response to high-salt diet. Tissue kallikrein mRNAs in the kidney and salivary glands of Dahl-SS, SHR, and SD rats were reduced, whereas beta-actin mRNA was not altered by high-salt diet. Similarly, immunoreactive intrarenal kallikrein levels were reduced in these rats in response to high-salt diet. These studies show that increases in blood pressure after salt loading in Dahl-SS and SHR are accompanied by increases in low-M(r) kininogen. Tissue kallikrein gene expression in hypertensive Dahl-SS and SHR and normotensive SD rats is suppressed after salt loading. These findings show that reduced renal kallikrein expression and increased kininogen expression is regulated at the transcriptional level during salt loading.

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