Renal arterial 20-hydroxyeicosatetraenoic acid levels: regulation by cyclooxygenase

2003 ◽  
Vol 284 (3) ◽  
pp. F474-F479 ◽  
Author(s):  
Monica K. Cheng ◽  
John C. McGiff ◽  
Mairead A. Carroll
Keyword(s):  
Salt Intake ◽  
Renin Angiotensin System ◽  
Renal Arteries ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Sprague Dawley Rats ◽  
Cox 2 ◽  
Potent Vasoconstrictor ◽  
Cytochrome P 450 ◽  
Cox 1

20-HETE, a potent vasoconstrictor, is generated by cytochrome P-450 ω-hydroxylases and is the principal eicosanoid produced by preglomerular microvessels. It is released from preglomerular microvessels by ANG II and is subject to metabolism by cyclooxygenase (COX). Because low-salt (LS) intake stimulates the renin-angiotensin system and induces renal cortical COX-2 expression, we examined 20-HETE release from renal arteries (interlobar and arcuate and interlobular arteries) obtained from 6- to 7-wk-old male Sprague-Dawley rats fed either normal salt (0.4% NaCl) or LS (0.05% NaCl) diets for 10 days. With normal salt intake, the levels of 20-HETE recovered were similar in arcuate and interlobular arteries and interlobar arteries: 30.1 ± 8.5 vs. 24.6 ± 5.3 ng · mg protein−1 · 30 min−1, respectively. An LS diet increased 20-HETE levels in the incubate of either arcuate and interlobular or interlobar renal arteries only when COX was inhibited. Addition of indomethacin (10 μM) to the incubate of arteries obtained from rats fed an LS diet resulted in a two- to threefold increase in 20-HETE release from arcuate and interlobular arteries, from 39.1 ± 13.2 to 101.8 ± 42.6 ng · mg protein−1 · 30 min−1( P < 0.03), and interlobar arteries, from 31.7 ± 15.1 to 61.9 ± 29.4 ng · mg protein−1 · 30 min−1( P < 0.05) compared with release of 20-HETE when COX was not inhibited. An LS diet enhanced vascular expression of cytochrome P-4504A and COX-2 in arcuate and interlobular arteries; COX-1 was unaffected. Metabolism of 20-HETE by COX is proposed to represent an important regulatory mechanism in setting preglomerular microvascular tone.

Peripheral and central angiotensin II regulates expression of genes of the renin-angiotensin system

1992 ◽  
Vol 262 (5) ◽  
pp. E651-E657 ◽  
Author(s):  
K. Kohara ◽  
K. B. Brosnihan ◽  
C. M. Ferrario ◽  
A. Milsted
Keyword(s):  
Northern Blot Analysis ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Expression Of Genes ◽  
Sprague Dawley Rats ◽  
Renin Mrna ◽  
Lower Brain Stem

We investigated whether angiotensin (ANG) II has the potential to regulate expression of genes of the renin-angiotensin system (RAS) in peripheral and central tissues. ANG II (0.1 or 6.0 nmol/h) was infused by osmotic minipump into male Sprague-Dawley rats (225-250 g) for 5 days, either intravenously or intracerebroventricularly. We measured angiotensinogen mRNA in liver, adrenal glands, and brain (hypothalamus and lower brain stem), renin mRNA in the kidney, and angiotensin-converting enzyme (ACE) mRNA in the lung and testis by Northern blot analysis. We demonstrated that plasma ANG II increases the levels of liver angiotensinogen mRNA, decreases kidney renin mRNA, and decreases lung ACE mRNA. Intracerebroventricular administration of ANG II resulted in a different pattern of responses of the peripheral RAS components. Liver angiotensinogen mRNA was increased, and kidney renin mRNA was decreased by both doses of ANG II, whereas lung ACE mRNA remained unresponsive at either dose. Centrally mediated influences of ANG II are most likely indirect since plasma ANG II concentration was not changed. This study has revealed that ANG II has profound diverse effects that influence the regulation of its formation. Further, results indicate that genes of the RAS responded to exogenous ANG II in both tissue- and route-specific ways.

Localization of components of the renin–angiotensin system in the suprachiasmatic nucleus of normotensive Sprague–Dawley rats

2004 ◽  
Vol 1008 (2) ◽  
pp. 212-223 ◽  
Author(s):  
Martin Alexander Thomas ◽  
Gerta Fleissner ◽  
Marion Stöhr ◽  
Stefan Hauptfleisch ◽  
Björn Lemmer
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Renin Angiotensin System ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sprague Dawley Rats

Modulation of the intrahepatic renin–angiotensin system after stimulation of the gastric sodium monitor in the rat

1999 ◽  
Vol 98 (1) ◽  
pp. 57-64
Author(s):  
V. Z. C. YE ◽  
K. A. DUGGAN
Keyword(s):  
Renin Angiotensin System ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Sprague Dawley Rats ◽  
Sodium Load ◽  
Ace Activity ◽  
Stimulation Of

Changes in the rate of formation of angiotensin II (ANG II) participate in mediating the natriuresis that occurs in direct response to a gastric sodium stimulus (upper-gut sodium monitor). As this natriuresis is also dependent on intrahepatic events, we investigated whether changes in hepatic and plasma angiotensinogen levels and hepatic angiotensin-converting enzyme (ACE) activity might explain the decrease in ANG II synthesis. Male Sprague–Dawley rats, equilibrated on a low-sodium diet, were anaesthetized and received a sodium load of 1.5 mmol/kg (using 3× normal saline) either intragastrically or intravenously. Blood and livers were sampled before and at various times after sodium administration. ACE activity in serum and tissues was determined by generation of histidyl-leucine. Angiotensinogen was determined by radioimmunoassay of angiotensin I generated by incubation in the presence of exogenous renin. Plasma angiotensinogen had decreased significantly by 15 min after sodium administration (P< 0.005), while hepatic angiotensinogen was also decreased significantly from 30 min after the sodium load (P< 0.01). Hepatic ACE activity decreased in response to sodium (P< 0.005) from 30 min. We conclude that stimulation of the gastric sodium monitor regulates angiotensinogen synthesis and secretion by the liver, as well as hepatic ACE activity.

scholarly journals Sodium Thiosulfate Improves Hypertension in Rats with Adenine-Induced Chronic Kidney Disease

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 147
Author(s):  
Chien-Ning Hsu ◽  
Chih-Yao Hou ◽  
Guo-Ping Chang-Chien ◽  
Sufan Lin ◽  
Hung-Wei Yang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Oral Administration ◽  
Sodium Thiosulfate ◽  
Renin Angiotensin System ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Targeting Therapy ◽  
Sprague Dawley Rats

Hypertension is highly prevalent in chronic kidney disease (CKD). Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with vasodilator properties. We, hence, investigated whether oral administration of sodium thiosulfate (STS), a clinically applicable H2S-based therapy, can exert a protective effect against hypertension in an adenine-induced CKD rat model. Eight-week-old male Sprague–Dawley rats were fed with 0.5% adenine chow for 3 weeks to induce CKD. After 1 week, the rats were divided into two groups: one without and one with STS (2 g/kg body weight/day) in drinking water for 2 weeks. Treatment with STS lowered systolic and diastolic blood pressure by 7 and 9 mm Hg, respectively. Renal H2S-generating enzyme expression was inhibited by CKD, while STS therapy increased plasma levels of H2S and thiosulfate. Additionally, restoration of nitric oxide bioavailability and rebalance of the renin–angiotensin system may contribute to the protective effects of STS. Our data suggest that the oral administration of STS improves hypertension in an adenine-induced CKD model, which brings us closer to the clinical translation of H2S-targeting therapy in CKD-induced hypertension.

scholarly journals Chronic intermittent hypoxia increases blood pressure and expression of FosB/ΔFosB in central autonomic regions

2011 ◽  
Vol 301 (1) ◽  
pp. R131-R139 ◽  
Author(s):  
W. David Knight ◽  
Joel T. Little ◽  
Flavia R. Carreno ◽  
Glenn M. Toney ◽  
Steven W. Mifflin ◽  
...  
Keyword(s):  
Intermittent Hypoxia ◽  
Renin Angiotensin System ◽  
Brain Regions ◽  
Ventrolateral Medulla ◽  
Chronic Intermittent Hypoxia ◽  
Preoptic Nucleus ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Sprague Dawley Rats ◽  
Obstructive Sleep

Chronic intermittent hypoxia (CIH) models repetitive bouts of arterial hypoxemia that occur in humans suffering from obstructive sleep apnea. CIH has been linked to persistent activation of arterial chemoreceptors and the renin-angiotensin system, which have been linked to chronic elevations of sympathetic nerve activity (SNA) and mean arterial pressure (MAP). Because Fos and FosB are transcription factors involved in activator protein (AP)-1 driven central nervous system neuronal adaptations, this study determined if CIH causes increased Fos or FosB staining in brain regions that regulate SNA and autonomic function. Male Sprague Dawley rats were instrumented with telemetry transmitters for continuous recording of MAP and heart rate (HR). Rats were exposed to continuous normoxia (CON) or to CIH for 8 h/day for 7 days. CIH increased MAP by 7–10 mmHg without persistently affecting HR. A separate group of rats was killed 1 day after 7 days of CIH for immunohistochemistry. CIH did not increase Fos staining in any brain region examined. Staining for FosB/ΔFosB was increased in the organum vasculosum of the lamina terminalis (CON: 9 ± 1; CIH: 34 ± 3 cells/section), subfornical organ (CON: 7 ± 2; CIH: 31 ± 3), median preoptic nucleus (CON 15 ± 1; CIH: 38 ± 3), nucleus of the solitary tract (CON: 9 ± 2; CIH: 28 ± 4), A5 (CON: 3 ± 1; CIH: 10 ± 1), and rostral ventrolateral medulla (CON: 5 ± 1; CIH: 17 ± 2). In the paraventricular nucleus, FosB/ΔFosB staining was located mainly in the dorsal and medial parvocellular subnuclei. CIH did not increase FosB/ΔFosB staining in caudal ventrolateral medulla or supraoptic nucleus. These data indicate that CIH induces an increase in FosB/ΔFosB in autonomic nuclei and suggest that AP-1 transcriptional regulation may contribute to stable adaptive changes that support chronically elevated SNA.

Effect of salt deprivation on blood pressure in rats

1989 ◽  
Vol 256 (5) ◽  
pp. H1426-H1431 ◽  
Author(s):  
C. E. Ott ◽  
W. J. Welch ◽  
J. N. Lorenz ◽  
S. A. Whitescarver ◽  
T. A. Kotchen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Salt Intake ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
The Other ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Sprague Dawley Rat ◽  
Low Salt

In most cases blood pressure (BP) is directly related to NaCl intake. In some studies, BP is increased by low salt intake. The effect of Na and Cl deprivation or selective Na deprivation on BP in the normotensive Sprague-Dawley rat was investigated. In study 1, rats were uninephrectomized and fed low NaCl, normal NaCl, or low Na-normal Cl for 3 wk. BP was higher (P less than 0.05) in rats fed low NaCl and low Na-normal Cl than normal NaCl. Plasma renin activity was stimulated by low NaCl intake but was not different between the other two groups. After captopril treatment, BP was lower in the low NaCl group (73.1 +/- 3.6 mmHg) than in the normal-NaCl (99.2 +/- 6.7 mmHg) or low Na-normal Cl (92.0 +/- 6.7 mmHg) groups. In study 2, intact rats (n = 8 per group) were fed low (less than 0.01%), normal (1%), or high NaCl (4%) for 1 wk. BP and heart rate were higher in the low-NaCl group (P less than 0.05) than in the other two groups. Plasma volumes were not different among the groups. In study 3, two groups of eight rats were given either low NaCl or 2% NaCl for 2 wk. BP (131.4 +/- 3.6 mmHg) and heart rate (402 +/- 11 beats/min) were higher in the low-NaCl group than in the 2% NaCl group (121.1 +/- 3.2 mmHg and 369 +/- 9 beats/min, respectively). In the normotensive Sprague-Dawley rat, low NaCl intake elevated BP when compared with normal or high NaCl intake. Part of the increase in the uninephrectomized, Cl-supplemented group is not dependent on the renin-angiotensin system.

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