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.

scholarly journals Spinal and peripheral mechanisms contributing to hyperactive voiding in spontaneously hypertensive rats

1998 ◽  
Vol 275 (4) ◽  
pp. R1366-R1373 ◽  
Author(s):  
Katarina Persson ◽  
Raj K. Pandita ◽  
John M. Spitsbergen ◽  
William D. Steers ◽  
Jeremy B. Tuttle ◽  
...  
Keyword(s):  
Marked Reduction ◽  
Spontaneously Hypertensive Rats ◽  
Electrical Field Stimulation ◽  
Bladder Function ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto

The influence of noradrenergic mechanisms involved in micturition in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats was investigated using continuous cystometry in in vivo and in vitro studies on isolated bladder and urethral tissues. Compared with WKY rats, SHR had a significantly lower bladder capacity (SHR: 0.7 ± 0.05 ml; WKY rats: 1.3 ± 0.06 ml; P < 0.001), micturition volume (SHR: 0.4 ± 0.04 ml, WKY rats: 1.2 ± 0.05 ml; P < 0.001), and an increased amplitude of nonvoiding (unstable) bladder contractions. The effects of intrathecal and intra-arterial doxazosin on cystometric parameters were more pronounced in SHR than in WKY rats. There was a marked reduction in nonvoiding contractions after intrathecal (but not intra-arterial) doxazosin in SHR. Norepinephrine (0.1 μM–1 mM) failed to evoke contractions in bladder strips from WKY rats, in contrast to a weak contractile response in SHR. The response to electrical field stimulation was significantly less in bladder strips from SHR than from WKY rats. In WKY rats, norepinephrine produced concentration-dependent inhibition (87 ± 5%, n = 6) of nerve-evoked bladder contractions. Almost no inhibition (11 ± 8%, n = 6) was found in SHR. Alterations in bladder function of SHR appear to be associated with changes in the noradrenergic control of the micturition reflex, in addition to an increased smooth muscle and decreased neuronal responsiveness to norepinephrine. The marked reduction in nonvoiding contractions after intrathecal doxazosin suggests that the bladder hyperactivity in SHR has at least part of its origin in supraspinal and/or spinal structures.

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

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.

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.

Intravital Studies on Cerebral Arteries in Hypertensive and Normotensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 81s-82s ◽  
Author(s):  
Barbro B. Johansson ◽  
Ludwig M. Auer ◽  
Ichiro Sayama
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Cerebral Arteries ◽  
Cortical Surface ◽  
Percentage Increase ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cranial Window ◽  
Wky Rats ◽  
Wistar Kyoto

1. The diameters of main cortical surface branches of the middle cerebral artery were continuously monitored through a closed cranial window in spontaneously hypertensive rats (SHR) and in normotensive Wistar Kyoto (WKY) rats by aid of a multichannel video-angiometer under resting conditions and under maximal vasodilatation induced by hypercapnia. 2. Initial mean arterial pressure was 172 ± sem 9 mmHg in SHR and 103 ± 5 mmHg in WKY rats; during hypercapnia the corresponding values were 183 ± 9 and 127 ± 7 mmHg. 3. The resting diameter of the arteries was 55 ± 1 μm in SHR (n = 53) and 87 ± 1 μm in WKY rats (n = 53; P < 0.001). The percentage increase in diameter during vasodilatation (Paco2 70 mmHg) was larger in SHR (54%) than in WKY rats (36%). However, the maximum lumen diameter remained significantly smaller in SHR (84 ± 2 μm compared with 117 ± 5 μm in WKY rats; P < 0.001). No significant further dilatation was seen in either group after α-adrenoceptor blockade. 4. The smaller diameter of cortical arteries during vasodilatation is consistent with the concept that hypertensive vascular hypertrophy encroaches on the lumen in vivo. The larger percentage increase in diameter of cortical arteries in hypertensive rats corroborates Folkow's hypothesis on the haemodynamic consequences of an altered media/lumen ratio in hypertension. 5. There is no evidence that an enhanced sympatho-adrenergic tone prevents maximum vasodilatation during hypercapnia in SHR.

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