Angiotensin II contents in plasma, and cardiac and renal tissues of sinoaortic denervated rats.
- Author:
Zheng-Zheng SHAN
1
;
Sheng-Ming DAI
;
Feng FANG
;
Ding-Feng SU
Author Information
1. Department of Pediatrics, Changhai Hospital and Department of Pharmacology, Faculty of Basic Medicine, Second Military Medical University, Shanghai 200433.
- Publication Type:Journal Article
- MeSH:
Angiotensin II;
blood;
metabolism;
Animals;
Aorta;
innervation;
metabolism;
Autonomic Denervation;
Baroreflex;
physiology;
Blood Pressure;
physiology;
Carotid Sinus;
innervation;
metabolism;
Hypertension;
metabolism;
physiopathology;
Kidney;
metabolism;
Male;
Myocardium;
metabolism;
Rats;
Rats, Sprague-Dawley
- From:
Acta Physiologica Sinica
2003;55(1):75-78
- CountryChina
- Language:Chinese
-
Abstract:
Our previous data demonstrate that impairment of arterial baroreceptor reflex (ABR) plays an independent role in hypertension target organ damage. To elucidate the mechanisms responsible for the dysfunction of ABR associated organ damage, sinoaortic denervated (SAD) rats were used as an animal model of ABR dysfunction. Twenty-four-hour continuous blood pressure (SBP and DBP), blood pressure variability (BPV), heart rate (HR) and HR variability (HRV) were measured in conscious and unrestrained rats. Angiotensin II (Ang II) in plasma, heart and kidney was assayed by raio-immunological assay (RIA) 1 or 18 weeks after denervation. In short-term SAD rats, twenty-four-hour mean SBP and DBP increased compared with that of sham-operated rats and long-term SAD rats. No significant difference in SBP, DBP or HR was found between long-term SAD rats and sham-operated ones. Compared with the sham-operated rats, long-term SAD rats had elevated BPV. No significant change in Ang II levels of caridiac and renal tissues was found in short-term SAD rats. In long-term SAD rats, Ang II level of plasma was not increased while the Ang II content in the heart and kidney increased. Ang II contents of plasma and tissues in long-term SAD rats exposed to chronic stress were higher than those in the control rats. These results show (1) in short-term SAD rats blood pressure increased, while in long-term SAD rats 24 h mean blood pressure did not increase, although BPV elevated in long-term SAD rats; (2) in long-term SAD rats, secretion of Ang II in cardiac and renal tissues was enhanced and more Ang II released when the animals were exposed to chronic stress. These results suggest that elevated BPV and secretion of Ang II may be related to the development of organ damage induced by ABR dysfunction.
