Cardiovascular end-organ damage in Ren-2 transgenic rats compared to spontaneously hypertensive rats

1997 ◽  
Vol 75 (5) ◽  
pp. 371-377 ◽  
Author(s):  
Yigal M. Pinto ◽  
Hendrik Buikema ◽  
Wiek H. van Gilst ◽  
Egbert Scholtens ◽  
Peter-Paul van Geel ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Organ Damage ◽  
Hypertensive Rats ◽  
Transgenic Rats ◽  
Spontaneously Hypertensive ◽  
End Organ Damage

Angiotensin-(1–7) prevents development of severe hypertension and end-organ damage in spontaneously hypertensive rats treated with l-NAME

2006 ◽  
Vol 290 (2) ◽  
pp. H684-H691 ◽  
Author(s):  
Ibrahim F. Benter ◽  
Mariam H. M. Yousif ◽  
J. T. Anim ◽  
C. Cojocel ◽  
D. I. Diz
Keyword(s):  
Nitric Oxide ◽  
Spontaneously Hypertensive Rats ◽  
Severe Hypertension ◽  
Organ Damage ◽  
Left Ventricular ◽  
Protective Effects ◽  
Additive Effects ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
End Organ Damage

We examined the influence of chronic treatment with ANG-(1–7) on development of hypertension and end-organ damage in spontaneously hypertensive rats (SHR) chronically treated with the nitric oxide synthesis inhibitor l-NAME (SHR-l-NAME). l-NAME administered orally (80 mg/l) for 4 wk significantly elevated mean arterial pressure (MAP) compared with SHR controls drinking regular water (269 ± 10 vs. 196 ± 6 mmHg). ANG-(1–7) (24 μg·kg−1·h−1) or captopril (300 mg/l) significantly attenuated the elevation in MAP due to l-NAME (213 ± 7 and 228 ± 8 mmHg, respectively), and ANG-(1–7) + captopril completely reversed the l-NAME-dependent increase in MAP (193 ± 5 mmHg). l-NAME-induced increases in urinary protein were significantly lower in ANG-(1–7)-treated animals (226 ± 6 vs. 145 ± 12 mg/day). Captopril was more effective (96 ± 12 mg/day), and there was no additional effect of captopril + ANG-(1–7) (87 ± 5 mg/day). The abnormal vascular responsiveness to endothelin-1, carbachol, and sodium nitroprusside in perfused mesenteric vascular bed of SHR-l-NAME was improved by ANG-(1–7) or captopril, with no additive effect of ANG-(1–7) + captopril. In isolated perfused hearts, recovery of left ventricular function from 40 min of global ischemia was significantly better in ANG-(1–7)- or captopril-treated SHR-l-NAME, with additive effects of combined treatment. The beneficial effects of ANG-(1–7) on MAP and cardiac function were inhibited when indomethacin was administered with ANG-(1–7), but indomethacin did not reverse the protective effects on proteinuria or vascular reactivity. The protective effects of the ANG-(1–7) analog AVE-0991 were qualitatively comparable to those of ANG-(1–7) but were not improved over those of captopril alone. Thus, during reduced nitric oxide availability, ANG-(1–7) attenuates development of severe hypertension and end-organ damage; prostaglandins participate in the MAP-lowering and cardioprotective effects of ANG-(1–7); and additive effects of captopril + ANG-(1–7) on MAP, but not proteinuria or endothelial function, suggest common, as well as different, mechanisms of action for the two treatments. Together, the results provide further evidence of a role for ANG-(1–7) in protective effects of angiotensin-converting enzyme inhibition and suggest dissociation of factors influencing MAP and those influencing end-organ damage.

Relationship between baroreceptor reflex function and end-organ damage in spontaneously hypertensive rats

1999 ◽  
Vol 277 (3) ◽  
pp. H1200-H1206 ◽  
Author(s):  
Zheng-Zheng Shan ◽  
Sheng-Ming Dai ◽  
Ding-Feng Su
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Spontaneously Hypertensive Rats ◽  
Organ Damage ◽  
Baroreceptor Reflex ◽  
Hypertensive Rats ◽  
Baroreceptor Sensitivity ◽  
Spontaneously Hypertensive ◽  
End Organ Damage ◽  
Wistar Kyoto

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.

Sign in / Sign up

Export Citation Format

Share Document