scholarly journals Different susceptibilities to cerebral infarction in spontaneously hypertensive (SHR) and normotensive Sprague-Dawley rats.

Stroke ◽  
1986 ◽  
Vol 17 (3) ◽  
pp. 520-525 ◽  
Author(s):  
P Coyle
Keyword(s):  
Cerebral Infarction ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Sprague Dawley Rats

High-NaCl diets increase natriuretic and diuretic responses in salt-resistant but not salt-sensitive SHR

1991 ◽  
Vol 260 (6) ◽  
pp. F890-F897 ◽  
Author(s):  
M. S. Mozaffari ◽  
S. Jirakulsomchok ◽  
Z. H. Shao ◽  
J. M. Wyss
Keyword(s):  
Arterial Pressure ◽  
Renal Denervation ◽  
Isotonic Saline ◽  
Renal Nerves ◽  
Sprague Dawley ◽  
Volume Loading ◽  
Spontaneously Hypertensive ◽  
Volume Load ◽  
Sprague Dawley Rats ◽  
Wistar Kyoto

This study tested the hypothesis that NaCl-sensitive spontaneously hypertensive rats (SHR-S) display a defect in natriuretic and diuretic responses to acute volume loading that contributes to the rise in arterial pressure observed when the rats are fed a high-NaCl diet. Seven-week-old SHR-S and NaCl-resistant SHR rats (SHR-R) and normotensive (Wistar-Kyoto and Sprague-Dawley rats) were fed high- or basal NaCl diets. After 2.5 wk on the diets, preinstrumented conscious rats received an intravenous infusion (5% body wt; 0.5 ml/min) of isotonic saline, and urine was collected through a bladder catheter for 90 min. Control rats on the high-NaCl diet (compared with basal) excreted a significantly greater percentage of Na+ and volume load. In contrast, SHR-S on high-NaCl diet (compared with basal) had a very small increase in natriuretic response and no increase in diuretic response to volume expansion. The effect of renal denervation on natriuretic and diuretic responses to volume load was tested. In SHR-R on 1 and 8% NaCl diets, renal denervation had little or no effect on these responses, suggesting that renal nerves do not play a prominent role in the dietary NaCl-induced increases in the natriuretic and diuretic responses to volume load. These results demonstrate that NaCl-resistant rats rapidly adapt to diets high in NaCl content with increased natriuretic and diuretic responses to acute volume loading. The failure of SHR-S to adapt to the dietary challenge may result in volume loading and a secondary increase in arterial pressure after feeding.

Ameliorating effects of cloperastine on dysfunction of the urinary bladder caused by cerebral infarction in conscious rats

2009 ◽  
Vol 87 (11) ◽  
pp. 893-899 ◽  
Author(s):  
Gen Yamamoto ◽  
Fumio Soeda ◽  
Tetsuya Shirasaki ◽  
Kazuo Takahama
Keyword(s):  
Urinary Bladder ◽  
Cerebral Infarction ◽  
Flow Rate ◽  
Bladder Capacity ◽  
Left Middle Cerebral Artery ◽  
Sprague Dawley ◽  
Urinary Bladder Dysfunction ◽  
Sprague Dawley Rats ◽  
Urethral Resistance ◽  
Effective Doses

We investigated the effects of the centrally acting antitussives dextromethorphan and cloperastine on urinary bladder dysfunction 24 h after cerebral infarction in rats using the cystometry technique. First, cystometrography was performed in conscious male Sprague–Dawley rats. Cerebral infarction was then induced by occlusion of the left middle cerebral artery. Twenty-four hours after cerebral infarction, the effect of each drug on micturition disorder was estimated for 5 parameters: bladder capacity, maximum voiding pressure, micturition latency, flow rate, and urethral resistance. Cerebral infarction markedly reduced bladder capacity, micturition latency, and flow rate and increased urethral resistance. After cerebral infarction, intravenous dosing of saline had no effect on these parameters. Dextromethorphan (20 mg/kg) and cloperastine (2.5 and 5.0 mg/kg) at antitussive effective doses significantly increased bladder capacity and micturition latency. Unlike dextromethorphan, cloperastine ameliorated decreases in flow rate and increases in urethral resistance caused by cerebral infarction. These results suggest that cloperastine may have therapeutic value for the treatment of disorders of the micturition reflex associated with cerebral infarction, and that the drug may become a base compound from which to develop more active drugs for such disorders.

scholarly journals Effects of dietary salt on angiotensin peptides in kidney.

1995 ◽  
Vol 6 (4) ◽  
pp. 1209-1215
Author(s):  
Q C Meng ◽  
J Durand ◽  
Y F Chen ◽  
S Oparil
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Angiotensin Peptides ◽  
Sprague Dawley Rats ◽  
Wistar Kyoto

This study used a novel simple method for the extraction, separation, identification, and quantitation of angiotensin-like immunoactivity from tissue to examine the effects of altering dietary NaCl intake on intrarenal angiotensin I, II, and III levels in salt-sensitive, spontaneously hypertensive rats, salt-resistant Wistar-Kyoto rats, and Sprague-Dawley rats. Seven-week-old male spontaneously hypertensive rats, Wistar-Kyoto rats, and Sprague-Dawley rats were assigned randomly to a diet containing either 8% (high) or 1% (basal) salt and were maintained on these diets for 3 wk. Rats were then decapitated without prior anesthesia, and kidneys were rapidly (< 30 s) removed, snap frozen in liquid nitrogen, and stored at -80 degrees C. Frozen tissue was extracted in 2 M acetic acid and then subjected to solid-phase extraction with the cation exchange resin AG 50W X4. Angiotensin peptides were separated by reversed-phase high-performance liquid chromatography on a phenyl silica gel column with an eluent consisting of 20% acetonitrile in 0.1 M ammonium phosphate buffer, pH 4.9, and quantitated by radioimmunoassay. The elution of standard peptides under isocratic conditions revealed clear resolution of angiotensin I, II, and III and the (1-7) and (3-8) peptides. Recoveries of both labeled and unlabeled angiotensin peptide standards from the extraction step were > 90%. Renal angiotensin II stores were significantly higher in spontaneously hypertensive rats than in Wistar-Kyoto or Sprague-Dawley rats, independent of diet. Renal angiotensin II and III were further suppressed during dietary salt supplementation in both salt-resistant strains but not in the spontaneously hypertensive rat. These findings are consistent with an enhanced (compared with Wistar-Kyoto and Sprague-Dawley rats) role for angiotensin II in the kidney of the salt-sensitive, spontaneously hypertensive rat, particularly under conditions of dietary salt supplementation.

scholarly journals Pre-existing hypertension and pregnancy induced hypertension reveal molecular differences in placental proteome in rodents

2021 ◽  
Author(s):  
Sheon Mary ◽  
Heather Small ◽  
Florian Herse ◽  
Emma Carrick ◽  
Arun Flynn ◽  
...  
Keyword(s):  
Gestational Hypertension ◽  
Tissue Injury ◽  
Cardiovascular Complications ◽  
Trophoblast Invasion ◽  
Future Research ◽  
Chronic Hypertension ◽  
Label Free ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Sprague Dawley Rats

Pre-existing or new onset of hypertension affects pregnancy and is one of the leading causes of maternal and fetal morbidity and mortality. In certain cases, it also leads to long term maternal cardiovascular complications. The placenta is a key player in the pathogenesis of complicated hypertensive pregnancies, however the pathomechanisms leading to an abnormal placenta are poorly understood. In this study we compared the placental proteome of two rat models: a pre-existing hypertension pregnancy model (stroke-prone spontaneously hypertensive, SHRSP) and the transgenic RAS activated gestational hypertension model (transgenic for human angiotensinogen Sprague-Dawley rats, SD-PE). Label-free proteomics using nano LC-MS/MS was performed for identification and quantification of proteins. Between the two models, we found widespread differences in the expression of placental proteins including those related to hypertension, inflammation and trophoblast invasion; whereas pathways such as regulation of serine endopeptidase activity, tissue injury response, coagulation and complement activation were enriched in both models. We present for the first time the placental proteome of SHRSP and SD-PE and provide insight into the molecular make-up of models of hypertensive pregnancy. Our study informs future research into specific preeclampsia and chronic hypertension pregnancy mechanisms and translation of rodent data to the clinic.

scholarly journals Importance of Flaxseed and its Components in the Management of Hypertension

2019 ◽  
Vol 28 (03) ◽  
pp. 153-160
Author(s):  
Kailash Prasad
Keyword(s):  
Protein Hydrolysate ◽  
Therapeutic Agents ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Flax Oil ◽  
Patient Status ◽  
Long Duration ◽  
Sprague Dawley Rats ◽  
Treatment Of Hypertension ◽  
Dose Dependent

AbstractThis review paper describes the effects of flaxseed and its components (flax oil, secoisolariciresinol diglucoside [SDG], flax lignan complex [FLC], and flaxseed protein hydrolysate [FPH]) on blood pressure (BP) in Sprague Dawley rats (SDR), spontaneously hypertensive rats (SHR), and humans. Flaxseed, flax oil, and FLC had variable effects on BP in humans, while SDG and FPH significantly reduced the BP in SDR and SHR. The effect of SDG was dose-dependent and long lasting. The lowering of BP is mediated through inhibition of soluble epoxide by α-linolenic acid in flax oil, stimulation of guanylate cyclase and inhibition of angiotensin converting enzyme (ACE) by SDG, and inhibition of renin and ACE activity by FPH. Flaxseed, flax oil, and FLC have variable effects on BP (none, slight, and significant). They are effective in lowering BP in individuals with hypertension and metabolic syndrome but ineffective in healthy individuals' ineffectiveness of flaxseed and its compounds in lowering BP may be due to their low doses, long interval of dosing, short duration of consumption, and patient status. In conclusion, the data at present suggest that flaxseed, flax oil, and FLC cannot serve as therapeutic agents for the treatment of hypertension. However, they can be used as an adjunct in the treatment of hypertension. A clinical trial should be conducted of these agents with higher doses which would be given twice daily for long duration. Pure SDG and FPS may serve as therapeutic agents for the treatment of hypertension but they have not been tried in humans.

Distensibility and wall composition of rat cerebral arterioles in hypertension induced by chronic blockade of nitric oxide synthase

1996 ◽  
Vol 54 ◽  
pp. 754-755
Author(s):  
S. M. Ghoneim ◽  
J. M. Chillon ◽  
G.L. Baumbach
Keyword(s):  
Nitric Oxide ◽  
Vessel Wall ◽  
Mass Composition ◽  
Chronic Hypertension ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Sprague Dawley Rats ◽  
Cacodylate Buffer ◽  
Cerebral Arterioles ◽  
Oxide Synthase

We have previously reported that, during chronic hypertension, cerebral arterioles undergo hypertrophy of the vessel wall, accompanied by a paradoxical increase in passive distensibility. We have proposed that this increase may be due to a reduction in the proportion of nondistensible (collagen and basement membrane) to the distensible (smooth muscle, elastin and endothelium) components of the vessel wall. We have recently observed in stroke-prone spontaneously hypertensive rats(SHRSP), that an endothelium derived factor, endothelin, may contribute to hypertrophy, but not to increases in passive ditensibility, of cerebral arterioles vessel wall.The goal of this study was to examine wall mass, composition and passive ditensibility of cerebral arterioles in chronic hypertension induced by decreased availability of another endothelium derived factor, nitric oxide (NO).Four weeks old male Sprague-Dawley rats were treated with LG-nitro-L-arginine methyl ester (LNAME; 10 mg /kg/day) in the drinking water. We examined distensibility of maximally dilated cerebral arterioles in 4 months old Sprague-Dawley rats. Arterioles were then fixed at physiological pressure (2.25% gluterladehyde in 0.10 mol/L cacodylate buffer), the arteriolar segment used for distensibility measurements was removed then immerse fixed, rinsed briefly in 0.1 M cacodylate buffer, osmicated and processed routinely for electron microscopy (TEM).

Antihypertensive effect of progesterone in rats with mineralocorticoid-induced hypertension.

1979 ◽  
Vol 236 (4) ◽  
pp. E366 ◽  
Author(s):  
G Wambach ◽  
J R Higgins
Keyword(s):  
Phase I ◽  
Phase Ii ◽  
Hypotensive Effect ◽  
Sodium Concentration ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Blood Pressures ◽  
Induced Changes

Uninephrectomized, saline-fed male Sprague-Dawley rats were given DOCA 5 mg per week alone or together with progesterone 20 mg per week for 6 weeks (phase I). Subsequently, the doses of DOCA and progesterone were doubled and the rats were studied for an additional 6 wk (phase II). Progesterone prevented DOCA-induced hypertension during phase I. Phase II blood pressures were higher in DOCA-progesterone-treated animals than in controls, but remained lower than in animals treated with DOCA alone. At the end of phase II the animals were killed, and blood samples and skeletal muscle samples were taken for analysis of electrolyte content. DOCA-treated animals were found to have an increased rate of potassium excretion, an increase in muscle sodium concentration, and a decrease in muscle potassium concentration compared to the controls. Progesterone treatment significantly blunted the DOCA-induced changes in muscle electrolyte concentrations and increased the rate of sodium excretion. No hypotensive effect was observed when progesterone in doses similar to those of phase I was administered to spontaneously hypertensive rats. Thus, in experimental mineralocorticoid hypertension, the hypotensive effect of progesterone appears to correlate closely with its mineralocorticoid antagonistic properties.

Sign in / Sign up

Export Citation Format

Share Document