Exercise Training Improves the Depressed Sensitivity of the Baroreceptors in Spontaneously Hypertensive Rats

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 700-701
Author(s):  
Gustavo J J Silva ◽  
Edson D Moreira ◽  
Carlos E Negrao ◽  
Patricia C Brum ◽  
Eduardo M Krieger
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Systolic Arterial Pressure ◽  
Arterial Baroreflex ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Baroreceptor Function ◽  
Low Intensity Exercise ◽  
The Relationship

P43 We have previously demonstrated that low-intensity exercise traning (ET) diminishes blood pressure and partially restores the sensitivity of the baroreflex bradycardia and tachycardia that are depressed in spontaneously hypertensive rats (SHR). Presently, the influence of the exercise trainig (ET) on the afferent part of the baroreflex (baroreceptor function curve) and its implication on the baroreflex was analysed in SHR and in normal control rats (NCR). NCR and SHR were subdivided in sedentary (S) and ET groups: SHR-S (n=8) and SHR-ET (n=6), and NCR-S (n=8) and NCR-ET (n=8). ET was performed on treadmill, during 60 min, 5 days/wk, at 50% of VO 2 max, for 12 wk. Arterial baroreflex sensitivity was evaluated by bradycardiac responses to phenylephrine (0.5;1;2;4;8 and 16 μg/ml, i.v.) and tachycardiac responses to sodium nitroprusside (0.5;1;2;4;8 and 16 μg/ml, i.v.). Aortic baroreceptor function curve was evaluated under pentobarbital anesthesia (40 mg/kg) during rapid variations of arterial pressure (AT/CODAS, 3kHz per channel). The relationship between changes in baroreceptor discharge (0-100%) and systolic arterial pressure was analysed using a sigmoidal regression. Mean arterial pressure was reduced in SHR-ET compared to SHR-S group (165±7 vs. 183±4 mmHg) but remained inaltared in NCR-ET compared to NCR-S (112±3 vs. 115±3 mmHg). In SHR, ET increased the sensitivity of baroreflex bradycardia (1.9±0.1 vs. 0.7±0.1 bpm.mmHg -1 ) and tachycardia (2.9±0.1 vs. 1.8±0.2 bpm.mmHg -1 ) which were depressed. In NCR-ET baroreflex bradycardia was decreased (1.4±0.1 vs. 1.7±0.1 bpm.mmHg -1 ) but baroreflex tachycardia was increased (4.6±0.5 vs. 3.0±0.2 bpm.mmHg -1 ). ET increased the aortic baroreceptor gaing-sensitivity in both groups: SHR (0.9±0.1 vs. 0.7±0.1 %.mmHg -1 ) and NCR (2.1±0.1 vs. 1.4±0.1 %.mm Hg -1 ). Conclusion:1. ET increases aortic baroreceptor gain-sensitivity in NCR as well in SHR; 2. The improvement of the baroreflex produced by ET in SHR is partially explainedd by the recovery of the baroreceptor sensitivity, which may also participate in the reduction of high blood pressure.

Changes of Blood Pressure Rhythm and Clock Protein Expression Levels in Spontaneously Hypertensive Rats After Ischemia-Reperfusion

2021 ◽  
Author(s):  
Jing Jin ◽  
Yumeng Liu ◽  
Jing Huang ◽  
Dong Zhang ◽  
Jian Ge ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Protein Expression ◽  
Circadian Clock ◽  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Expression Levels ◽  
The Relationship ◽  
Clock Protein

Abstract Objective A variety of circadian patterns of blood pressure after ischemic stroke in patients with essential hypertension appear to be a potential risk of stroke recurrence, but the mechanism is still unclear. This study intends to reveal the changes in blood pressure rhythm and circadian clock protein expression levels in spontaneously hypertensive rats (SHR) after ischemia-reperfusion, and the relationship between the two. Methods Using the SHR middle cerebral artery occlusion experimental model, the systolic blood pressure was continuously monitored for 24 hours after the operation to observe the blood pressure rhythm. The rat tail vein blood was taken every 3h, and the serum CLOCK, BMAL1, PER1 and CRY1 protein expression levels were detected by Elisa. Pearson correlation analysis counted the relationship between SHR blood pressure rhythm and circadian clock protein fluctuation after ischemia-reperfusion. Results The proportion of abnormal blood pressure patterns in the SHR + tMCAO group was significantly higher than that in the SHR group, the serum CLOCK expression was relatively constant, and the circadian rhythm of BMAL1, PER1 and CRY1 protein expression changed significantly. Pearson analysis showed that PER1 protein level was negatively correlated with dipper (r = -0.565, P = 0.002) and extreme-dipper (r = -0.531, P = 0.001) blood pressure, and was significantly positively correlated with non-dipper blood pressure (r = 0.620, P < 0.001). Conclusion The rhythm pattern of blood pressure after ischemia-reperfusion in SHR is obviously disordered, and it is closely related to the regulation of Per1 gene.

scholarly journals Duration of Electrically Induced Atrial Fibrillation Is Augmented by High Voltage of Stimulus with Higher Blood Pressure in Hypertensive Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Tomomi Nagayama ◽  
Yoshitaka Hirooka ◽  
Akiko Chishaki ◽  
Masao Takemoto ◽  
Yasushi Mukai ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Blood Pressure ◽  
Arterial Pressure ◽  
High Voltage ◽  
Spontaneously Hypertensive Rats ◽  
Low Voltage ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Stimulus ◽  
Wistar Kyoto

Objective.Many previous clinical studies have suggested that atrial fibrillation (AF) is closely associated with hypertension. However, the benefits of antihypertensive therapy on AF are still inconsistent, and it is necessary to explore the factors augmenting AF in hypertensive rats. The aim of the present study was to investigate the correlation between arterial pressure or voltage stimulus and to the duration of electrically induced AF in normotensive or hypertensive rats.Methods.AF was reproducibly induced by transesophageal atrial burst pacing in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We did the burst pacing at high (20 V) or low (5 V) voltage.Results.Duration of AF did not correlate with systolic blood pressure (SBP) and stimulus voltage in WKY. However, only in SHR, duration of AF with high stimulus voltage significantly correlated with SBP and was significantly longer in high than in low voltage stimulus.Discussion and Conclusion.Duration of AF is augmented by high voltage stimulus with higher blood pressure in SHR.

scholarly journals The Relationship between Periarteritis Nodosa and Blood Pressure in Stroke-prone Spontaneously Hypertensive Rats

1991 ◽  
Vol 32 (4) ◽  
pp. 537-539 ◽  
Author(s):  
Noboru Saito ◽  
Teruhiko Okada ◽  
Shoji Nishiyama
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Periarteritis Nodosa ◽  
Spontaneously Hypertensive ◽  
The Relationship

Arterial baroreflex resetting mediates postexercise reductions in arterial pressure and heart rate

1998 ◽  
Vol 275 (5) ◽  
pp. H1627-H1634 ◽  
Author(s):  
Margaret P. Chandler ◽  
David W. Rodenbaugh ◽  
Stephen E. DiCarlo
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Acute Exercise ◽  
Operating Point ◽  
Arterial Baroreflex ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Single Bout ◽  
Before And After ◽  
The Relationship

We tested the hypothesis that postexercise reductions in arterial pressure and heart rate (HR) are mediated by a lowering of the operating point and a reduction in the gain of the arterial baroreflex. To test this hypothesis, spontaneous changes in arterial pressure and the reflex responses of HR were examined before and after a single bout of mild to moderate dynamic exercise in 19 spontaneously hypertensive rats (SHR, 10 male and 9 female). Eleven SHR subjected to sinoaortic denervation (SAD) (6 male, 5 female) were also studied. All rats were instrumented with an arterial catheter for the measurement of arterial pressure and HR. After exercise, arterial pressure and HR were reduced below preexercise levels. Furthermore, the operating point and spontaneous gain (G) of the arterial baroreflex were reduced. Specifically, after exercise, the spontaneous range of HR (P1, 50%), the pressure at the midpoint of the pressure range (P3, 13%) and the HR at the midpoint of the HR range (H3, 10%), the spontaneous minimum HR (P4, 8%) and maximum HR (10%), and G (76%) were significantly attenuated. SAD significantly attenuated the relationship between arterial pressure and HR by reducing G (males 94%, females 95%). These results demonstrate that acute exercise resulted in a postexercise resetting of the operating point and a reduction in the gain of the arterial baroreflex. Furthermore, these data suggest that postexercise reductions in arterial pressure and HR are mediated by a lowering of the operating point of the arterial baroreflex.

Regression of myocardial hypertrophy and influence of adrenergic system

1983 ◽  
Vol 244 (1) ◽  
pp. H97-H101 ◽  
Author(s):  
S. Sen ◽  
R. C. Tarazi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Regression Analysis ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Myocardial Hypertrophy ◽  
Cardiac Response ◽  
Adrenergic System ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Studies of regression of myocardial hypertrophy in spontaneously hypertensive rats (SHR) suggest that the adrenergic system may play an important role in the reversal of hypertrophy. The effect of propranolol on reversal of hypertrophy, however, is still controversial. This study describes the effect of propranolol, given alone or in combination with hydralazine in different ratios for 4 wk, on blood pressure (BP), ventricular weight, and myocardial catecholamine (MC) concentrations. The data show that a certain ratio of propranolol to hydralazine (750:30) leads to moderate BP control (196-156 mmHg) without increased MC (634 vs. 552 ng/g) and moderately reduced hypertrophy. Reduction of BP alone with increased MC (hydralazine alone) or reduction of MC without BP control (propranolol alone) failed to reduce hypertrophy. A significant correlation between both ventricular weight and heart rate with MC (r = 0.6) was obtained by multiple regression analysis. This study suggests that adrenergic factors seem to play an important role in modulating structural cardiac response to variations in arterial pressure.

Contribution of Vasopressin to the maintenance of blood pressure in deoxycorticosterone-salt induced malignant hypertension in spontaneously hypertensive rats

1986 ◽  
Vol 70 (2) ◽  
pp. 191-198 ◽  
Author(s):  
Masao Hiwatari ◽  
Josephine M. Abrahams ◽  
Takao Saito ◽  
Colin I. Johnston
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Left Ventricular ◽  
Malignant Hypertension ◽  
Minor Importance ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

1. In the present study, deoxycorticosterone (DOC) and salt was administered to Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) by using silicone-rubber implants (DOC acetate, 100 mg/kg) and 0.9% NaCl as drinking water. SHR treated with DOC-salt for 4 weeks showed the characteristics of malignant hypertension including marked increases in blood pressure and left ventricular weight with typical histological changes in the kidney. 2. DOC-salt treatment increased plasma vasopressin levels in WKY (from 6.1 ± 0.5 to 8.9 ± 0.8 pmol/l) but significantly more in SHR (from 5.0 ± 0.6 to 15.8 ±1.2 pmol/l). 3. Intravenous administration of the specific antagonist to the pressor effect of vasopressin, d(CH2)5Tyr(Me)AVP (10μg/kg), decreased mean arterial pressure of DOC-salt treated WKY and SHR by 6.6 ± 0.9mmHg (P < 0.05) and 9.7 ± 1.7 mmHg (P < 0.05) respectively. 4. DOC-water treatment also increased plasma AVP levels in SHR to 10.5 ± 0.8 pmol/l, but the vasopressin antagonist had little effect on blood pressure in these rats. 5. Plasma levels of vasopressin were significantly correlated with both mean arterial pressure (r = 0.64) and left ventricular weight (r = 0.74). This suggests a close relationship between plasma AVP and severity of hypertension. 6. The results of the present experiment demonstrate that vasopressin is part of the overall pressor mechanism which contributes to the maintenance of blood pressure in DOC-salt induced malignant hypertension in SHR, but the small fall in pressure produced by the AVP antagonists suggests that the contribution is of only minor importance.

Dietary Estrogen Protects Against NaCl-Sensitive Hypertension in Estrogen-Depleted Female Spontaneously Hypertensive Rats.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 723-724
Author(s):  
Zhiwu Fang ◽  
Scott H. Carlson ◽  
J. Michael Wyss
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Negligible Effect ◽  
Transient Increase ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Beneficial Effects ◽  
Endogenous Estrogen ◽  
Sustained Increase

P169 In male spontaneously hypertensive rats (SHR) a high NaCl diet produces a rapid and sustained increase in hypertension. In contrast, in female SHR a high NaCl diet causes only a small, transient increase in arterial pressure. Elimination of most endogenous estrogen (via ovariectomy) produces mild NaCl-sensitive hypertension in female SHR, but simultaneous ovariectomy and elimination of exogenous dietary plant estrogens (phytoestrogens) nearly quadruples the hypertensive effect of the high NaCl diet, although phytoestrogen removal has a negligible effect on blood pressure in SHR fed a basal NaCl diet. This suggests that phytoestrogens (particularly genistein, the primary dietary phytoestrogen) protect ovariectomized female SHR from NaCl-sensitive hypertension. However, other reports suggest that the beneficial effects of phytoestrogens may only be present when genistein is combined with a high soy diet. The present study tests the hypothesis that genistein can independently reduce NaCl-sensitive hypertension in estrogen-depleted female SHR. Female SHR were ovariectomized at 3 weeks of age and placed on one of four casein-based, non-soy containing, diets (AIN-76A), i.e., a high (8%) or basal (0.6%) NaCl diet with or without genistein (0.06%; the approximate phytoestrogen concentration in the diet) added to the diet. After 5 weeks, femoral arterial catheters were implanted and 3 days later arterial pressures were recorded from all rats. The high NaCl diet increased arterial pressure by 68 ± 6 mm Hg in the phytoestrogen-free SHR, but produced only a 17 ± 5 mm Hg rise in arterial pressure in the genistein-supplemented group (similar to the rise previously observed in ovariectomized SHR fed a normal high NaCl diet). These results demonstrate that dietary genistein reduces NaCl-sensitive hypertension in ovariectomized female SHR. This work was supported by NHLBI Grant HL-37722.

Vasopressin withdrawal produces hypotension in the spontaneously hypertensive rat

1985 ◽  
Vol 249 (1) ◽  
pp. H193-H197 ◽  
Author(s):  
E. K. Chiu ◽  
J. R. McNeill
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Pressor Agent

In spontaneously hypertensive rats (SHR) and their normotensive Wistar-Kyoto controls (WKY), prolonged intravenous infusions of either arginine vasopressin (AVP, 8 mU X kg-1 X min-1) or phenylephrine (PE, 20 nmol X kg-1 X min-1) resulted in similar rises in arterial pressure. Heart rate fell greatly in the WKY but not in the SHR. Withdrawal of the PE infusion resulted in moderate decreases in blood pressure and increases in heart rate; these responses were similar in SHR and WKY. At 5 h after PE withdrawal, blood pressure and heart rate returned to basal values. In contrast, withdrawal of the AVP infusion was associated with greater falls in blood pressure and rises in heart rate. Blood pressure and heart rate in both the SHR and the WKY at 5 h after AVP were significantly different from their respective basal values. The effects of AVP withdrawal on either blood pressure or heart rate were significantly greater in the SHR than in the WKY. At 5 h after the withdrawal of AVP, blood pressure in the SHR was reduced to normotensive levels. These results suggest that the withdrawal effect was specific to AVP, was more marked in the SHR, and might not result from only the rise in blood pressure seen during the intravenous infusion of the pressor agent.

Sinoaortic denervation prevents postexercise reductions in arterial pressure and cardiac sympathetic tonus

1997 ◽  
Vol 273 (6) ◽  
pp. H2738-H2745 ◽  
Author(s):  
Margaret P. Chandler ◽  
Stephen E. Dicarlo
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Acute Exercise ◽  
Dynamic Exercise ◽  
Arterial Baroreflex ◽  
Hypertensive Rats ◽  
Experimental Conditions ◽  
Spontaneously Hypertensive ◽  
Single Bout

Arterial pressure, cardiac sympathetic tonus (ST), and heart rate (HR) are reduced after a single bout of dynamic exercise in spontaneously hypertensive rats (SHR). To test if the arterial baroreflex is required for these postexercise responses, intact ( n = 9) and sinoaortic-denervated (SAD) rats ( n = 5) were chronically instrumented with an arterial catheter for the measurement of arterial pressure and HR and for the infusion of cardiac autonomic antagonists. Five days after instrumentation, cardiac ST and parasympathetic tonus (PT) were determined under two experimental conditions (no exercise and postexercise). SAD rats did not alter no-exercise cardiac ST (intact 47 ± 3 vs. SAD 50 ± 3 beats/min); however, no-exercise PT was reduced (intact −24 ± 2 vs. SAD −4 ± 4 beats/min, P < 0.05). Acute exercise reduced arterial pressure (postexertional hypotension, −20 ± 3 mmHg, P < 0.05), cardiac ST (no exercise 47 ± 3 vs. postexercise 24 ± 3 beats/min, P < 0.05), and PT (no exercise −24 ± 2 vs. postexercise −11 ± 2 beats/min, P < 0.05) in intact SHR. In contrast, SAD prevented postexercise reductions in arterial pressure and cardiac ST (no exercise 50 ± 3 vs. postexercise 59 ± 7 beats/min). Furthermore, SAD had no effect on postexercise PT (no exercise −4 ± 4 vs. postexercise −7 ± 4 beats/min). These results demonstrate that the arterial baroreflex is required for the reduction in arterial pressure and cardiac ST that occurs in SHR after a single bout of dynamic exercise.

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