Cardiac and renal hyperplasia in newborn spontaneously hypertensive rats

1987 ◽  
Vol 72 (3) ◽  
pp. 271-275 ◽  
Author(s):  
Jaroslav Kunes ◽  
Stephen C. Pang ◽  
Marc Cantin ◽  
Jacques Genest ◽  
P. Hamet
Keyword(s):  
Body Weight ◽  
Dna Content ◽  
Spontaneously Hypertensive Rats ◽  
Weight Ratio ◽  
Total Body Weight ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Relative Dna Content ◽  
Wistar Kyoto ◽  
Total Body

1. Cardiac hyperplasia in newborn spontaneously hypertensive rats (SHR) has been noted by our group as well as by other investigators. The present study was designed to establish whether early (neonatal) hyperplasia is confined to the heart or is a generalized phenomenon in this hypertensive model. 2. The ventricles, kidney and liver of newborn SHR, Wistar and Wistar-Kyoto (WKY) rats were analysed for their protein and DNA content. 3. Total organ weight and the organ/body weight ratio of the heart and kidney but not of the liver were significantly greater in the SHR than in the control rats, irrespective of total body weight. 4. The higher relative DNA content (per 100 mg of tissue or 100 g body weight) indicated that hyperplasia rather than hypertrophy was responsible for the enlarged heart as well as the kidney of newborn SHR. 5. The cause of this selective cardiac and renal hyperplasia is not yet known: it may be due to putative ‘haemodynamic growth stimuli’, an intrinsic genetic abnormality of cells in the heart and kidney, circulating growth-promoting factors, or innervation.

Myocardial meta-[125I]iodobenzylguanidine uptake in awake genetically hypertensive rats at different ages: an autoradiographic study

1999 ◽  
Vol 77 (6) ◽  
pp. 398-406 ◽  
Author(s):  
Carole Schwebel ◽  
Andrée Durand ◽  
Diane Godin-Ribuot ◽  
Olivier Provendier ◽  
Pierre Demenge
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Weight Ratio ◽  
Autoradiographic Study ◽  
Mibg Uptake ◽  
Hypertensive Rats ◽  
Heterogeneous Distribution ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Arterial Blood ◽  
Wistar Kyoto

The purpose of this work was to evaluate changes in myocardial meta-[125I]iodobenzylguanidine ([125I]MIBG) uptake and distribution with age in awake spontaneously hypertensive rats (SHR) with respect to Wistar-Kyoto (WKY) rats. Rats were randomly divided into two groups, one for measuring myocardial [125I]MIBG uptake and distribution 4 h after its injection and the second for evaluating myocardial catecholamine concentrations. Mean arterial blood pressure, cardiac hypertrophy index (heart/body weight ratio), and heart rate were significantly higher with increasing age in SHR compared with matched WKY rats. Myocardial catecholamine concentrations and turnover did not differ between the two strains and were significantly decreased with increasing age. Myocardial [125I]MIBG uptake determined by gamma counting was similar in WKY rats and SHR and did not vary significantly with age when expressed as uptake density. However, in both strains of rats, [125I]MIBG uptake determined by autoradiography was significantly greater at the base of the heart than at the apex and midventricular levels, and the uptake values of young rats were significantly higher than those of older rats. In 21-week-old WKY rats and SHR, the highest [125I]MIBG uptake values were found in the right ventricle. Thus, quantitative autoradiography allowed detection of significant changes in myocardial [125I]MIBG uptake and showed its heterogeneous distribution in the rat heart.Key words: spontaneously hypertensive rats (SHR), Wistar-Kyoto rats, myocardial meta-[125I]iodobenzylguanidine uptake, sympathetic drive.

Aortic stiffness and pulse pressure amplification in Wistar-Kyoto and spontaneously hypertensive rats

2007 ◽  
Vol 292 (5) ◽  
pp. H2506-H2512 ◽  
Author(s):  
Emmanuel Cosson ◽  
Monique Herisse ◽  
Dominique Laude ◽  
Frédérique Thomas ◽  
Paul Valensi ◽  
...  
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Aortic Stiffness ◽  
Spontaneously Hypertensive Rats ◽  
Age Effect ◽  
Strain Effect ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto

In humans, increased body weight and arterial stiffness are significantly associated, independently of blood pressure (BP) level. The finding was never investigated in rodents devoid of metabolic disorders as spontaneously hypertensive rats (SHR). Using simultaneous catheterization of proximal and distal aorta, we measured body weight, intra-arterial BP, heart rate and their variability (spectral analysis), aortic pulse wave velocity (PWV), and systolic and pulse pressure (PP) amplifications in unrestrained conscious Wistar-Kyoto (WKY) rats and SHR between 6 and 24 wk of age. Aortic proximal systolic and diastolic pressure, PP, and mean BP were significantly higher in SHR than in WKY rats and increased significantly with age (with the exception of PP). PP amplification increased with age but did not differ between strains. PWV was significantly associated with heart rate variability. PWV was significantly higher (via two-way variance analysis) in SHR than in WKY rats (strain effect) and increased markedly with age in both strains (age effect). Adjustment of PWV to mean BP attenuated markedly both the age and the strain effects. After adjustment for body weight, either alone or associated with mean BP, the age effect was not more significant, but the strain effect was markedly enhanced. In conscious unanesthetized SHR and WKY rats, aortic stiffness is consistently associated with body weight independent of age and mean BP. An intervention study should consider in the objectives systolic BP and PP amplifications measured in conscious animals, central control of body weight, and autonomic nervous system.

Body fluid volumes in prehypertensive spontaneously hypertensive rats

1983 ◽  
Vol 244 (5) ◽  
pp. H652-H655 ◽  
Author(s):  
M. M. Mullins
Keyword(s):  
Volume Expansion ◽  
Body Fluid ◽  
Spontaneously Hypertensive Rats ◽  
Interstitial Fluid ◽  
Extracellular Fluid ◽  
Plasma Aldosterone ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Total Body

To ascertain the effect of aldosterone on body fluid volumes in neonatal, prehypertensive spontaneously hypertensive rats (SHR), we studied these animals at 12 days using age-matched Wistar-Kyoto (WKY) as normotensive controls. Some pups of each strain were treated with spironolactone (1.5 micrograms/g body wt) on days 10-12. Total body water (TBW, by dessication) and extracellular fluid (ECF, Na2 35SO4 space) volumes were significantly larger in SHR than in WKY, whereas plasma volumes (125I-serum albumin space) were not different. Thus the enlarged ECF was due to preferential expansion of the interstitial fluid (ISF) space. Treatment of SHR with spironolactone reduced TBW and ISF to values not different from untreated WKY and also reduced plasma volume to some extent. These results indicate 1) significant ISF volume expansion occurs in SHR prior to elevation of blood pressure, and 2) the previously observed elevation in plasma aldosterone in SHR at this age probably mediates the volume expansion.

scholarly journals Alteration of RhoA Prenylation Ameliorates Cardiac and Vascular Remodeling in Spontaneously Hypertensive Rats

2016 ◽  
Vol 39 (1) ◽  
pp. 229-241 ◽  
Author(s):  
Jian Yang ◽  
Yu-Ning Chen ◽  
Zao-Xian Xu ◽  
Yun Mou ◽  
Liang-Rong Zheng
Keyword(s):  
Cardiac Hypertrophy ◽  
Spontaneously Hypertensive Rats ◽  
Weight Ratio ◽  
Heart Weight ◽  
Farnesyl Pyrophosphate ◽  
Hypertensive Rats ◽  
Cross Sectional ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Aortic Remodeling

Background: In our previous study, farnesyl pyrophosphate synthase (FPPS) was shown to be increased in spontaneously hypertensive rats (SHR) and in mice with angiotensin-II induced cardiac hypertrophy. Overexpression of FPPS induced cardiac hypertrophy and fibrosis in mice, accompanied by an increase in the synthesis of farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP). In the present study, we investigated the mechanisms of reversing cardiovascular remodeling in SHR by inhibiting FPPS. Methods and Results: Six-week-old rats were given vehicle or an FPPS inhibitor (alendronate, 100 ug/kg/d) daily for twelve weeks by osmotic mini-pump. The results demonstrated that FPPS inhibition attenuated cardiac hypertrophy and fibrosis in SHR as shown by the heart weight to body weight ratio, echocardiographic parameters, and histological examination. In addition, FPPS inhibition attenuated aortic remodeling as shown by reduced media thickness, media cross-sectional area and collagen of the aorta as well as SBP, DBP, MBP. Furthermore, 12 weeks of alendronate treatment significantly decreased FPP and GGPP levels, RhoA activation and geranylgeranylation in the heart and aorta, all of which were significantly upregulated in SHR compared with normotensive Wistar-Kyoto rats. Conclusion: Taken together, these results indicate that chronic treatment with alendronate decreases the development of cardiac and aortic remodeling, by a pathway which involves inhibition of the geranylgeranylation and activation of RhoA.

Blood pressure and heart rate development in young spontaneously hypertensive rats

1998 ◽  
Vol 274 (3) ◽  
pp. H794-H800 ◽  
Author(s):  
Jeffrey G. Dickhout ◽  
Robert M. K. W. Lee
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Weight ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Genetic Trait ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Hypertension Development ◽  
Rate Development

The course of hypertension development in young spontaneously hypertensive rats (SHR) was studied by the measurement of changes in systolic blood pressure (BP), body weight, and heart rate (HR) at 2, 3, 4, and 6 wk of age. To achieve this, we compared inbreeding lines of SHR and Wistar-Kyoto rats (WKY) to determine if differences in BP, body weight, or HR were present among inbreeding lines of the same strain or between strains. The effect of these differences on the eventual level of BP was then assessed. We found that BP began to diverge between SHR and WKY at 4 wk of age. Significant differences in systolic BP (24 mmHg) between SHR inbreeding lines at 4 wk of age did not affect the BP at 8 wk (172 vs. 170 mmHg). Pulse pressure was significantly higher in SHR than in WKY at 4 wk of age. HR was elevated in SHR over age-matched WKY at 3 wk of age and positively correlated to the level of BP attained by individual animals at 6 wk ( P = 0.037). Moreover, WKY inbreeding lines showing elevated HR developed higher BP (145 vs. 127 mmHg) at 10–12 and 20 wk of age. The prehypertensive tachycardia in SHR was investigated further and found to result from an increased intrinsic HR. Because HR at 3 wk is a genetic trait that can be partitioned into inbreeding lines, and inbreeding lines most expressive of this trait showed the highest eventual BP, we conclude that prehypertensive tachycardia may be an important first step during hypertension development in SHR. Moreover, early elevations in HR are highly predictive ( r = 0.41) of hypertension occurrence in the animal population studied.

Disparate Effects of Methyldopa and Clonidine on Cardiac Mass and Haemodynamics in Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 449s-452s ◽  
Author(s):  
Shozo Ishise ◽  
Barbara L. Pegram ◽  
E. D. Frohlich
Keyword(s):  
Heart Rate ◽  
Total Peripheral Resistance ◽  
Spontaneously Hypertensive Rats ◽  
Peripheral Resistance ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. Wistar-Kyoto and spontaneously hypertensive rats were given either methyldopa (400 mg day−1 kg−1) or clonidine (0.1 or 0.3 mg day−1 kg−1) for 3 weeks commencing at 20 weeks of age. 2. Both drugs significantly decreased mean arterial pressure in spontaneously hypertensive but not Wistar-Kyoto rats. Heart rate was significantly increased in spontaneously hypertensive rats by methyldopa, whereas clonidine significantly decreased heart rate. The higher dose of clonidine also decreased heart rate in Wistar-Kyoto rats. Both cardiac output and total peripheral resistance decreased slightly, but not significantly, with both agents. 3. Methyldopa, but not the lower equipotent depressor dose of clonidine, reduced left ventricular hypertrophy in spontaneously hypertensive rats. However, the higher dose of clonidine also significantly decreased the heart to body weight ratio despite an increased total peripheral resistance presumably due to the α-adrenergic agonist effect. 4. Minimal changes in organ blood flows were noted with both drugs. 5. These results suggest that neither systemic haemodynamics nor central inhibition of adrenergic drive are primary factors responsible for the regression of hypertrophy.

Excess oxygen delivery during muscle contractions in spontaneously hypertensive rats

1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Delivery ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Contractions ◽  
Hypertensive Rats ◽  
Hemoglobin Oxygen Saturation ◽  
Spontaneously Hypertensive ◽  
Tissue Po2 ◽  
Wistar Kyoto

These experiments determined whether a deficit in oxygen supply relative to demand could account for the sustained decrease in tissue PO2 observed during contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR). Relative changes in blood flow were determined from measurements of vessel diameter and red blood cell velocity. Venular hemoglobin oxygen saturation measurements were performed by using in vivo spectrophotometric techniques. The relative dilation [times control (xCT)] of arteriolar vessels during contractions was as large or greater in SHR than in normotensive rats (Wistar-Kyoto), as were the increases in blood flow (2 Hz, 3.50 +/- 0.69 vs. 3.00 +/- 1.05 xCT; 4 Hz, 10.20 +/- 3.06 vs. 9.00 +/- 1.48 xCT; 8 Hz, 16.40 +/- 3.95 vs. 10.70 +/- 2.48 xCT). Venular hemoglobin oxygen saturation was lower in the resting muscle of SHR than of Wistar-Kyoto rats (31.0 +/= 3.0 vs. 43.0 +/- 1.9%) but was higher in SHR after 4- and 8-Hz contractions (4 Hz, 52.0 +/- 4.8 vs. 43.0 +/- 3.6%; 8 Hz, 51.0 +/- 4.6 vs. 41.0 +/- 3.6%). Therefore, an excess in oxygen delivery occurs relative to oxygen use during muscle contractions in SHR. The previous and current results can be reconciled by considering the possibility that oxygen exchange is limited in SHR by a decrease in anatomic or perfused capillary density, arteriovenular shunting of blood, or decreased transit time of red blood cells through exchange vessels.

scholarly journals Aging Additively Influences Insulin- and Insulin-Like Growth Factor-1-Mediated Endothelial Dysfunction and Antioxidant Deficiency in Spontaneously Hypertensive Rats

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 676
Author(s):  
Kunanya Masodsai ◽  
Yi-Yuan Lin ◽  
Sih-Yin Lin ◽  
Chia-Ting Su ◽  
Shin-Da Lee ◽  
...  
Keyword(s):  
Growth Factor ◽  
Endothelial Dysfunction ◽  
Spontaneously Hypertensive Rats ◽  
No Production ◽  
Organ Bath ◽  
Insulin Like Growth Factor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Nos Inhibitors ◽  
Wistar Kyoto

This study aimed to investigate the aging-related endothelial dysfunction mediated by insulin and insulin-like growth factor-1 (IGF-1) and antioxidant deficiency in hypertension. Male spontaneously hypertensive rats (SHRs) and age-matched normotensive Wistar–Kyoto rats (WKYs) were randomly divided into 24-week-old (younger) and 48-week-old (older) groups, respectively. The endothelial function was evaluated by the insulin- and IGF-1-mediated vasorelaxation of aortic rings via the organ bath system. Serum levels of nitric oxide (NO), malondialdehyde (MDA), catalase, and total antioxidant capacity (TAC) were examined. The insulin- and IGF-1-mediated vasorelaxation was significantly impaired in both 24- and 48-week-old SHRs compared with age-matched WKYs and was significantly worse in the 48-week-old SHR than the 24-week-old SHR. After pretreatments of phosphoinositide 3-kinase (PI3K) or NO synthase (NOS) inhibitors, the insulin- and IGF-1-mediated vasorelaxation became similar among four groups. The serum level of MDA was significantly increased, while the NO, catalase, and TAC were significantly reduced in the 48-week-old SHR compared with the 24-week-old SHR. This study demonstrated that the process of aging additively affected insulin- and IGF-1-mediated endothelial dysfunction in SHRs, which could be partly attributed to the reduced NO production and antioxidant deficiency.

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