Effects of arachidonic acid and indomethacin on the in vitro release of prostaglandins by aortic strips of spontaneously hypertensive rats

1978 ◽  
Vol 56 (3) ◽  
pp. 509-511 ◽  
Author(s):  
R. Quirion ◽  
F. Rioux ◽  
D. Regoli
Keyword(s):  
Arachidonic Acid ◽  
Intravenous Injection ◽  
Spontaneously Hypertensive Rats ◽  
In Vitro Release ◽  
Hypotensive Effect ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Vitro Release

Aortic strips removed from spontaneously hypertensive (SH) rats and preincubated with arachidonic acid (1.0 × 10−5 g/ml) for 15 min produced two times more prostaglandin (PG) like material than aortae unexposed to the precursor of PG biosynthesis. The stimulating effect of arachidonic acid was largely inhibited by indomethacin (1.0 × 10−5 g/ml). Also, the release of PG-like material by aortic strips derived from SH rats treated with an intravenous injection of indomethacin (10 mg/kg) was inhibited by 74% compared with the control tissues. These results raised the possibility that the in vivo conversion of arachidonic acid by large arteries of SH rats may contribute to the hypotensive effect of this PG precursor in SH rats.

Abstract 181: Overexpression of Arachidonic Acid Cytochrome P450 Expoxygenases Prevents the Development of High Blood Pressure via Enhancing Atrial Natriuretic Peptide in Spontaneously Hypertensive Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Dao Wen Wang ◽  
Bin Xiao ◽  
Yong Wang ◽  
Xiaojun Xiong ◽  
Darryl C Zeldin
Keyword(s):  
Blood Pressure ◽  
Cytochrome P450 ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Spontaneously Hypertensive Rats ◽  
Hypotensive Effect ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Atrial Natriuretic

Cytochrome P450 (CYP)-derived epoxyeicosatrienoic acids (EETs) have potent vasodilatory and diuretic feature, and therefore potentially hypotensive effect. No in vivo studies, however, were performed to support it. This study investigated the hypothesis via overexpressing CYP epoxygense genes in spontaneously hypertensive rats (SHR). Recombinant adeno-associated virus vector (rAAV) was utilized to mediate long-term transfection of CYP2J2 and CYP2C11 genes, respectively, in adult SHR, and animal systolic blood pressure (SBP) was monitored using arterial caudilis indirect manometric method. Results showed that at 2 months the urinary excretion of stable hydrolysis metabolic product of 14, 15-EE, 14–15-DHET increased by 11 and 8.7 folds in rAAV-2J2 and rAAV-2C11 groups, respectively, compared with AAV-GFP-treated rats. (2) SBP in 2J2- and 2C11-treated rats decreased from 175.0 ± 2.8mHg to 163.5 ± 5.8mmHg and 161.2 ± 6.1 mmHg, respectively, ( p <0.01) at month 2, and it is 165.0 ± 4.7 mmHg and 173.0 ± 12.8 mmHg at month 6 after gene injection (~30mmHg and ~23mmHg lowerer than that in control animals, respectively, p <0.001). (3) Before the rats were sacrificed, cardiac function tests with Pressure-Volume System showed that maximum intracardiac pressure was 202.1 ± 30.0 & 209.1 ± 17.1mmHg in two gene-treated rats, respectively, significantly lower than control (241.2 ± 18.2mmHg, p <0.01) and cardiac output in treatment rats were significantly higher than control (p<0.05). (4) Interestingly, atrial natriuretic peptide (ANP) mRNA were up-regulated 6–14 folds respectively in myocardium of 2J2 and 2C11 groups; furthermore, C-type receptor mRNA of ANP was increased in heart, lung, kidney and aorta. (5) in cultured atrial cells (HLB2G5), exogenous EETs stimulated ANP production. In conclusions, for first time our data indicates overexpression of CYP2J2 or CYP2C11 could prevent development of hypertension in SHR, improve cardiac functions, which may involve up-regulating ANP expression and its receptors in target tissues, which suppresses collagen deposition and cardiovascular remodeling.

scholarly journals In vitro release of arachidonic acid and in vivo responses to respirable fractions of cotton dust.

1986 ◽  
Vol 66 ◽  
pp. 87-90
Author(s):  
T A Thomson ◽  
J H Edwards ◽  
T S Al-Zubaidy ◽  
R C Brown ◽  
A Poole ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
In Vitro Release ◽  
Cotton Dust ◽  
Vitro Release

Stress-induced changes in in vivo and in vitro dopamine-β-hydroxylase activity in spontaneously hypertensive rats

1982 ◽  
Vol 28 (3) ◽  
pp. 340-346 ◽  
Author(s):  
Keisuke Fujita ◽  
Ryoji Teradaira ◽  
Takashi Inoue ◽  
Hisahide Takahashi ◽  
Hidehiro Beppu ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Hydroxylase Activity ◽  
Spontaneously Hypertensive ◽  
Induced Changes

scholarly journals Time-Related Alteration in Flow- (Shear Stress-) Mediated Remodeling in Resistance Arteries from Spontaneously Hypertensive Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Odile Dumont ◽  
Gilles Kauffenstein ◽  
Anne-Laure Guihot ◽  
Nathalie C. Guérineau ◽  
Pierre Abraham ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
High Flow ◽  
Low Flow ◽  
Resistance Arteries ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Cross Section Area

Hypertension is a major risk factor for cardiovascular disorders. As flow-mediated outward remodeling has a key role in postischemic revascularization, we investigated this remodeling in mesenteric resistance arteries of normotensive (WKY) and spontaneously hypertensive rats (SHRs) aged 3 to 9 months. Sequential ligation of mesenteric resistance arteries allowed modifying blood flowin vivo, thus exposing arteries to low, normal, or high flow. After 1, 3, 8, or 24 weeks, arteries were isolated forin vitrostudy. High flow (HF) induced outward hypertrophic remodeling in WKY rats after 1 week and persisted until 24 weeks without change in wall to lumen ratio. In SHRs, diameter increase was delayed, occurring only after 3 weeks. Nevertheless, it was reduced at 8 weeks and no longer significant after 24 weeks. In parallel, media cross-section area increased more with time in SHRs than in WKY rats and this was associated with increased contractility and oxidative stress with decreased NO-dependent relaxation. Low flow induced progressive inward remodeling until 24 weeks in both strains with excessive hypertrophy in SHRs. Thus, a chronic increase in flow induced transitory diameter expansion and long-lasting hypertrophy in SHRs. This could contribute to the higher susceptibility of hypertensive subjects to ischemic diseases.

Physical exercise decreases neuronal activity in the posterior hypothalamic area of spontaneously hypertensive rats

2005 ◽  
Vol 98 (2) ◽  
pp. 572-578 ◽  
Author(s):  
Joseph A. Beatty ◽  
Jeffery M. Kramer ◽  
Edward D. Plowey ◽  
Tony G. Waldrop
Keyword(s):  
Physical Exercise ◽  
Neuronal Activity ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Hypothalamic Area ◽  
Spontaneously Hypertensive ◽  
Firing Rates ◽  
The Impact

Recently, physical exercise has been shown to significantly alter neurochemistry and neuronal function and to increase neurogenesis in discrete brain regions. Although we have documented that physical exercise leads to molecular changes in the posterior hypothalamic area (PHA), the impact on neuronal activity is unknown. The purpose of the present study was to determine whether neuronal activity in the PHA is altered by physical exercise. Spontaneously hypertensive rats (SHR) were allowed free access to running wheels for a period of 10 wk (exercised group) or no wheel access at all (nonexercised group). Single-unit extracellular recordings were made in anesthetized in vivo whole animal preparations or in vitro brain slice preparations. The spontaneous firing rates of PHA neurons in exercised SHR in vivo were significantly lower (8.5 ± 1.6 Hz, n = 31 neurons) compared with that of nonexercised SHR in vivo (13.7 ± 1.8 Hz, n = 38 neurons; P < 0.05). In addition, PHA neurons that possessed a cardiac-related rhythm in exercised SHR fired significantly lower (6.0 ± 1.8 Hz, n = 11 neurons) compared with nonexercised SHR (12.1 ± 2.4 Hz, n = 18 neurons; P < 0.05). Similarly, the spontaneous in vitro firing rates of PHA neurons from exercised SHR were significantly lower (3.5 ± 0.3 Hz, n = 67 neurons) compared with those of nonexercised SHR (5.6 ± 0.5 Hz, n = 58 neurons; P < 0.001). Both the in vivo and in vitro findings support the hypothesis that physical exercise can lower spontaneous activity of neurons in a cardiovascular regulatory region of the brain. Thus physical exercise may alter central neural control of cardiovascular function by inducing lasting changes in neuronal activity.

scholarly journals Administration with Quinoa Protein Reduces the Blood Pressure in Spontaneously Hypertensive Rats and Modifies the Fecal Microbiota

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2446
Author(s):  
Huimin Guo ◽  
Yuqiong Hao ◽  
Xin Fan ◽  
Aurore Richel ◽  
Nadia Everaert ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Alpha Diversity ◽  
Treated Group ◽  
Fecal Microbiota ◽  
Potential Candidate ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Despite the well-established role of quinoa protein as the source of antihypertensive peptides through in vitro enzymolysis, there is little evidence supporting the in vivo antihypertensive effect of intact quinoa protein. In this study, in vivo study on spontaneously hypertensive rats (SHRs) was conducted by administering quinoa protein for five weeks. Gastrointestinal content identification indicated that many promising precursors of bioactive peptides were released from quinoa protein under gastrointestinal processing. Quinoa protein administration on SHRs resulted in a significant decrease in blood pressure, a significant increase in alpha diversity, and microbial structure alternation towards that in non-hypertension rats. Furthermore, blood pressure was highly negatively correlated with the elevated abundance of genera in quinoa protein-treated SHRs, such as Turicibacter and Allobaculum. Interestingly, the fecal microbiota in quinoa protein-treated SHRs shared more features in the composition of genera with non-hypertension rats than that of the captopril-treated group. These results indicate that quinoa protein may serve as a potential candidate to lower blood pressure and ameliorate hypertension-related gut dysbiosis.

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