229 The relationship between serum insulin level and blood pressure in stroke-prone spontaneously hypertensive rats with hypoinsulinemia

1993 ◽  
Vol 11 (5) ◽  
pp. S499
Author(s):  
Zhang Weiguo ◽  
Liu Lisheng
2021 ◽  
Author(s):  
Jing Jin ◽  
Yumeng Liu ◽  
Jing Huang ◽  
Dong Zhang ◽  
Jian Ge ◽  
...  

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.


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

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.


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