Dietary obesity and weight cycling: effects on blood pressure and heart rate in rats

1989 ◽  
Vol 256 (6) ◽  
pp. R1209-R1219 ◽  
Author(s):  
R. J. Contreras ◽  
V. L. Williams

The overconsumption of rich and palatable foods and "yo-yo" dieting are feeding patterns involved in obesity and possibly hypertension in humans. We therefore examined the effects of diet-induced obesity and weight cycling on the blood pressure and heart rate levels of 60-day-old male normotensive Sprague-Dawley (S-D) and spontaneously hypertensive (SHR) rats. Six months on a high-fat and high-sucrose diet (HF/M) produced a greater obesity in S-D rats than in SHR rats. The caloric intakes of S-D rats fed the HF/M diet were greater than the caloric intakes of pellet-fed controls, whereas those of SHR rats were similar. The obesity of both strains was associated with hyperinsulinemia, heavier white (retroperitoneal) and brown (interscapular) fat pads, heavier heart weights, and tachycardia. Despite these changes, diet-induced obesity failed to increase systolic blood pressure obtained under light ether anesthesia or mean arterial pressure in the conscious state. Paradoxically, the blood pressures of SHR rats fed HF/M diet were reduced perhaps as a result of the high polyunsaturated fat component of the diet. A second S-D dietary obese group was alternated between 2-wk periods of unrestricted HF/M diet and 50% restricted pellet chow. Although their body weights were similar to pellet-fed controls, three cycles of weight loss and weight regain resulted in the consumption of increased dietary fat, increased food efficiency, heavier fat pads, and hyperinsulinemia. Heart rate and to some extent blood pressure fluctuated with diet, being elevated during HF/M feeding and reduced during restricted pellet feeding. Although weight cycling intensified the physiological responses to food ingestion, we found that weight cycling in dietary obese S-D rats did not elevate blood pressure levels.

1982 ◽  
Vol 60 (2) ◽  
pp. 208-212 ◽  
Author(s):  
Alexis Gairard ◽  
Alain Berthelot ◽  
René Schleiffer ◽  
Fanny Pernot

In male Sprague–Dawley rats, hypertensive development was diminished for 10 weeks when parathyroidectomy (PTX) was performed 1 week before deoxycorticosterone plus saline (DOCA + NaCl) treatment. In young spontaneously hypertensive male rats (SHR, Okamoto strain) parathyroidectomy performed after weaning lessened hypertensive levels and lowered heart rate for 24 weeks. When mineralocorticoid or genetic hypertension was established, parathyroidectomy did not significantly change blood pressure levels. High dietary calcium in PTX–SHR rats reestablished normal serum calcium but not systolic blood pressure to the level of sham SHR. From our present and previously reported results, it appears that the parathyroid gland is necessary for the total development of hypertension in both models.


1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.


2006 ◽  
Vol 21 (4) ◽  
pp. 192-196 ◽  
Author(s):  
José Ricardo Sousa Ayres de Moura ◽  
Nelson Sass ◽  
Sérgio Botelho Guimarães ◽  
Paulo Roberto Leitão de Vasconcelos ◽  
Rosiane Mattar ◽  
...  

PURPOSE: To evaluate the effects of L-arginine oral supplementation in spontaneously hypertensive pregnant rats (SHR). METHODS: Thirty SHR and ten Wistar-EPM-1 virgin female rats were used in the study. Before randomization, females were caged with males of the same strain (3:1). Pregnancy was confirmed by sperm-positive vaginal smear (Day 0). Wistar-EPM-1 rats served as counterpart control (C-1). SHR rats were randomized in 4 groups (n=10): Group Control 2, non-treated rats; Group L-Arginine treated with L-arginine 2%; Group Alpha-methyldopa treated with Alpha-methyldopa 33mg/Kg; Group L-Arginine+Alpha-methyldopa treated with L-arginine 2%+Alpha-methyldopa 33mg/Kg. L-arginine 2% solution was offered ad libitum in drinking water and Alpha-methyldopa was administered by gavage twice a day during the length of pregnancy (20 days). Blood pressure was measured by tailcuff plethysmography on days 0 and 20. Body weight was measured on days 0, 10 and 20. Results were expressed as mean ± SD (Standard Deviation). One-Way ANOVA/Tukey (or Kruskal-Wallis/Dunn, as appropriate) was used for group comparisons. Statistical significance was accepted as p<0.05. RESULTS: There was no significant weight gain in isolated L-arginine treated SHR. Mean blood pressure decreased in L-arginine-treated SLR compared with untreated-SHR rats. CONCLUSION: L-arginine oral supplementation reduces blood pressure in spontaneously hypertensive rats during pregnancy.


1999 ◽  
Vol 87 (6) ◽  
pp. 2025-2031 ◽  
Author(s):  
Holger Kraiczi ◽  
Jarkko Magga ◽  
Xiang Ying Sun ◽  
Heikki Ruskoaho ◽  
Xiaohe Zhao ◽  
...  

We investigated whether the effect of long-term intermittent hypoxia (LTIH) on cardiovascular function may be modified by preexisting genetic traits. To induce LTIH experimentally, cycles of 90-s hypoxia (nadir 6%) followed by 90-s normoxia were applied to six Wistar-Kyoto and six spontaneously hypertensive rats during 8 h daily. Comparison with the same number of control animals after 70 days revealed no alteration of intra-arterial blood pressure or heart rate. Blood pressure responsiveness to a brief hypoxic stimulus was enhanced in the LTIH animals, regardless of strain, whereas the hypoxia-induced increase in heart rate was abolished. In the spontaneously hypertensive but not the Wistar-Kyoto rats, LTIH increased left ventricular weight-to-body weight ratio and content of atrial natriuretic peptide mRNA. Expression of B-type natriuretic peptide was unchanged (Northern blot). Slightly increased right ventricular weight-to-body weight ratios in the LTIH animals were associated with higher right ventricular atrial natriuretic peptide and B-type natriuretic peptide mRNA amounts. Consequently, the effects of LTIH on different components of cardiovascular function appear incompletely related to each other and differentially influenced by constitutional traits.


2002 ◽  
Vol 10 (3) ◽  
pp. 199-210 ◽  
Author(s):  
Adamu Alemayehu ◽  
Laura Breen ◽  
Drahomira Krenova ◽  
Morton P. Printz

Evidence exists implying multiple blood pressure quantitative trait loci (QTL) on rat chromosome 2. To examine this possibility, four congenic strains and nine substrains were developed with varying size chromosome segments introgressed from the spontaneously hypertensive rat (SHR/lj) and normotensive Wistar-Kyoto rat (WKY/lj) onto the reciprocal genetic background. Cardiovascular phenotyping was conducted with telemetry over extended periods during standard salt (0.7%) and high-salt (8%) diets. Our results are consistent with at least three independent pressor QTL: transfer of SHR/lj alleles to WKY/lj reveals pressor QTL within D2Rat21-D2Rat27 and D2Mgh10-D2Rat62, whereas transfer of WKY/lj D2Rat161-D2Mit8 to SHR/lj reveals a depressor locus. Our results also suggest a depressor QTL in SHR/lj located within D2Rat161-D2Mgh10. Introgressed WKY/lj segments also reveal a heart rate QTL within D2Rat40-D2Rat50 which abolished salt-induced bradycardia, dependent upon adjoining SHR/lj alleles. This study confirms the presence of multiple blood pressure QTL on chromosome 2. Taken together with our other studies, we conclude that rat chromosome 2 is rich in alleles for cardiovascular and behavioral traits and for coordinated coupling between behavior and cardiovascular responses.


2017 ◽  
Vol 49 (2) ◽  
pp. 96-104 ◽  
Author(s):  
Sareema Adnan ◽  
James W. Nelson ◽  
Nadim J. Ajami ◽  
Venugopal R. Venna ◽  
Joseph F. Petrosino ◽  
...  

Gut dysbiosis has been linked to cardiovascular diseases including hypertension. We tested the hypothesis that hypertension could be induced in a normotensive strain of rats or attenuated in a hypertensive strain of rats by exchanging the gut microbiota between the two strains. Cecal contents from spontaneously hypertensive stroke prone rats (SHRSP) were pooled. Similarly, cecal contents from normotensive WKY rats were pooled. Four-week-old recipient WKY and SHR rats, previously treated with antibiotics to reduce the native microbiota, were gavaged with WKY or SHRSP microbiota, resulting in four groups; WKY with WKY microbiota (WKY g-WKY), WKY with SHRSP microbiota (WKY g-SHRSP), SHR with SHRSP microbiota (SHR g-SHRSP), and SHR with WKY microbiota (SHR g-WKY). Systolic blood pressure (SBP) was measured weekly using tail-cuff plethysmography. At 11.5 wk of age systolic blood pressure increased 26 mmHg in WKY g-SHRSP compared with that in WKY g-WKY (182 ± 8 vs. 156 ± 8 mmHg, P = 0.02). Although the SBP in SHR g-WKY tended to decrease compared with SHR g-SHRSP, the differences were not statistically significant. Fecal pellets were collected at 11.5 wk of age for identification of the microbiota by sequencing the 16S ribosomal RNA gene. We observed a significant increase in the Firmicutes:Bacteroidetes ratio in the hypertensive WKY g-SHRSP, as compared with the normotensive WKY g-WKY ( P = 0.042). Relative abundance of multiple taxa correlated with SBP. We conclude that gut dysbiosis can directly affect SBP. Manipulation of the gut microbiota may represent an innovative treatment for hypertension.


2018 ◽  
Vol 9 (3) ◽  
pp. 1657-1671 ◽  
Author(s):  
Shyan Yea Chay ◽  
Annas Salleh ◽  
Nor Fazila Sulaiman ◽  
Najib Zainal Abidin ◽  
Mohamad Ariff Hanafi ◽  
...  

Winged bean seed hydrolysate is found to reduce blood pressure in spontaneously hypertensive rats. Peptide of non-Current Good Manufacturing Practice grade demonstrates toxicity and is not suitable for testing in animals.


1955 ◽  
Vol 33 (3) ◽  
pp. 436-447 ◽  
Author(s):  
H. G. Downie ◽  
J. A. F. Stevenson

Although the blood pressure is one of the important criteria in the standardization of hemorrhagic shock in the dog, it has rarely been used for this purpose in the rat. A method resembling the reservoir technique developed by Wiggers and Werle (1942) for the dog using blood pressure as the criterion has been modified for use with the rat. Male Sprague-Dawley rats weighing approximately 400 gm. were used. In the standardization of this technique the blood pressure was reduced to 30 mm. Hg in a 10-min. period of hemorrhage and then maintained at this level by subsequent small hemorrhages into the reservoir until reinfusion indicated the beginning of vascular collapse, at which time all the blood in the reservoir was returned. Considering that those animals which lived longer than 48 hr. were survivors, in a series of 27 animals, 21 died and 6 survived—a mortality rate of 78%.During the hypotensive period there was a consistent and steady drop in the respiratory rate and rectal temperature. The heart rate declined initially and tended to recover as the hypotensive period progressed. After reinfusion the blood pressure rose but. did not reach prehemorrhage levels. Hemorrhage into the bowel and convulsions were significant postreinfusion findings.


1998 ◽  
Vol 275 (2) ◽  
pp. R426-R438 ◽  
Author(s):  
Ping Su ◽  
K. Maya Kaushal ◽  
Deanna L. Kroetz

The mechanism-based cytochrome P-450 (CYP) inhibitor 1-aminobenzotriazole (ABT) was characterized as an inhibitor of renal arachidonic acid metabolism and administered to spontaneously hypertensive rats (SHRs) to determine the effect of reduced eicosanoid production on mean arterial pressure (MAP). A single intraperitoneal dose of ABT to Sprague-Dawley rats caused a dose-dependent loss of renal CYP content, arachidonic acid metabolism, and CYP4A protein. In the cortex and outer medulla, ABT showed a high degree of selectivity for the CYP4A enzymes, reflected by the potent inhibition of 19- and 20-hydroxyeicosatetraenoic acid (19- and 20-HETE) formation. A 50 mg/kg dose of ABT reduced cortical 20-HETE formation to 16.1 ± 0.82% of control and outer medullary 20-HETE formation to 23.8 ± 0.45% of control. In contrast, there was no inhibition of renal epoxygenase activity at this dose. Renal CYP content, arachidonic acid ω- and (ω-1)-hydroxylase activity, and CYP4A protein levels gradually return to control levels by 72 h after a single dose of ABT. Cortical 20-HETE formation recovered from 17.9 ± 3.15% of control at 6 h to 84.8 ± 4.67% of control at 72 h after ABT administration. A single injection of ABT to 7-wk-old SHRs caused an acute reduction in MAP, which remained suppressed for at least 12 h. The effect was maximal within 4 h and averaged 17–23 mmHg during the 4- to 12-h period after administration. 20-HETE formation was inhibited 85% in the cortex and 70–80% in the outer medulla during the period when MAP was reduced. A structurally related ABT analog 1-hydroxybenzotriazole had no effect on blood pressure or renal arachidonic acid metabolism. These results identify ABT as a selective inhibitor of renal CYP4A activity and provide further support for a role for 20-HETE in the regulation of blood pressure.


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