Chronic Effects of Central and Systemic Administration of Losartan on Blood Pressure and Baroreceptor Reflex in Spontaneously Hypertensive Rats

1994 ◽  
Vol 7 (6) ◽  
pp. 536-542 ◽  
Author(s):  
Yuhei Kawano ◽  
Kaoru Yoshida ◽  
Hiroaki Matsuoka ◽  
Teruo Omae
1999 ◽  
Vol 277 (3) ◽  
pp. H1200-H1206 ◽  
Author(s):  
Zheng-Zheng Shan ◽  
Sheng-Ming Dai ◽  
Ding-Feng Su

The purpose of this study was to further illustrate the relationship between baroreceptor reflex sensitivity (BRS) and hypertensive end-organ damage (EOD) and to test the hypothesis that impairment of BRS aggravates EOD in hypertension. We studied baroreflex-mediated changes in heart rate [expressed as baroreceptor sensitivity to heart rate control (BRSHR)] and blood pressure [expressed as baroreceptor sensitivity to blood pressure control (BRSBP)] in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) that were used as controls, both at the age of 50–52 wk. Rats were also instrumented to record BP, HR, and BP variability (BPV) in the conscious, unrestrained state. In SHR compared with WKY, BP and BPV were significantly increased, whereas BRSHR and BRSBP were significantly decreased. SHR had remarkable EOD when compared with WKY (EOD score: 6.3 ± 2.5 vs. 2.9 ± 0.8, P < 0.01). Univariate regressive analysis demonstrated that EOD score was increased with BP and BPV and decreased with BRS. In multivariate analysis, EOD score was predicted by greater systolic BP and lower BRS and HR variability. These results indicate that BRS is negatively related to BPV and EOD score, and impaired BRS might be one of the major causes for hypertensive EOD.


1994 ◽  
Vol 267 (6) ◽  
pp. R1467-R1471 ◽  
Author(s):  
H. Okada ◽  
H. Suzuki ◽  
Y. Kanno ◽  
Y. Yamamura ◽  
T. Saruta

Chronic effects of orally available, nonpeptide vasopressin V1 and V2 receptor antagonists on conscious spontaneously hypertensive rats (SHR) were investigated. SHR and Wistar rats were divided into four groups, groups S-1 to S-4 and W-1 to W-4, respectively. Groups S-1 and W-1 were untreated as control. Groups S-2 and W-2 were treated with V1 antagonist, groups S-3 and W-3 received V2 antagonist, and groups S-4 and W-4 were treated with both of V1 and V2 antagonists. V1 and/or V2 antagonists did not affect degree of blood pressure of W-2, W-3, and W-4 rats, and V1 antagonist, alone or combined with V2 antagonist, slightly reduced increases in blood pressure of S-2 and S-4 rats without significance. However, V2 antagonist induced significantly massive and hyposmolar urine in W-3 rats compared with that in S-3 rats. In conclusion, in SHR, circulating vasopressin contributes to increases in blood pressure via either V1 or V2 receptors less than expected from previous studies with antibodies or peptide antagonists.


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