Blood pressure variability, cardiac baroreflex sensitivity and organ damage in experimentally hypertensive rats.
1. The present study was designed to investigate the haemodynamic features and morphological changes in experimentally hypertensive rat models. 2. Sprague-Dawley rats were used to prepare the experimentally hypertensive models, including two-kidney, one-clip renovascular hypertensive (2K1C) rats, deoxycorticosterone acetate salt hypertensive (DOCA) rats and N(G)-nitro-l-arginine methyl ester-induced hypertensive (l-NAME) rats. Six weeks after the induction of hypertension, 24 h blood pressure was recorded and blood pressure variability (BPV) expressed by 24 h (or 12 h in the daytime and night-time study) standard deviation of the variables was calculated. Then, cardiac baroreflex sensitivity (BRS) was determined and four endogenous factors (tumour necrosis factor-alpha, interleukin-1beta, angiotensin II and endothelin-1) were measured. Finally, morphological changes were examined. 3. It was found that an increase in BPV and a decrease in BRS were accompanied by an elevation of blood pressure in all three hypertensive models. The DOCA rats had the highest BPV, whereas the l-NAME rats had the lowest BRS. 4. Morphological changes were similar in DOCA and l-NAME rats and the cardiac changes were relatively slight in 2K1C rats. Tumour necrosis factor-alpha was increased in all the three models, especially in DOCA rats. Endothelin-1 was higher in DOCA rats and angiotensin II was increased in 2K1C rats and decreased in DOCA rats. 5. In conclusion, increased BPV and decreased BRS accompanied the elevation of blood pressure in all three hypertensive models. The DOCA rats had the highest BPV and the l-NAME rats had the lowest BRS. Obvious organ damage was seen in all three hypertensive models 6 weeks after the induction of hypertension.
Wang
Di-Song
DS
Department of Pharmacology, Second Military Medical University, Shanghai, China.
Xie
He-Hui
HH
Shen
Fu-Ming
FM
Cai
Guo-Jun
GJ
Su
Ding-Feng
DF
D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology*; D001795:Blood Pressure Determination / Q000379:methods; D003900:Desoxycorticosterone / Q000008:administration & dosage / Q000633:toxicity; D004195:Disease Models, Animal; D019332:Endothelin-1 / Q000378:metabolism; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology*; D006978:Hypertension, Renovascular / Q000378:metabolism / Q000503:physiopathology*; D007375:Interleukin-1 / Q000378:metabolism; D007678:Kidney Glomerulus / Q000473:pathology*; D008297:Male; D009206:Myocardium / Q000473:pathology; D019331:NG-Nitroarginine Methyl Ester / Q000008:administration & dosage / Q000633:toxicity; D009929:Organ Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D019332:Endothelin-1; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D000804:Angiotensin II; D003900:Desoxycorticosterone; D019331:NG-Nitroarginine Methyl Ester