Pressor and non-pressor effects of sodium loading on stroke in stroke-prone spontaneously hypertensive rats.
1. Aetiological studies have shown that sodium loading increases both blood pressure and death from stroke. The present study was designed to investigate the pressor and non-pressor effects of sodium loading on stroke in stroke-prone spontaneously hypertensive rats (SHRSP). 2. Eighty-five female SHRSP were used. Forty-nine SHRSP, aged 5 months, were randomly divided into two groups with or without sodium loading and their survival times were recorded. Thirty-six SHRSP, aged 3 months, were randomly divided into two groups and were instrumented to determine blood pressure, heart period and baroreflex sensitivity (BRS) after 4 months of sodium loading or normal rat chow. After determination of BRS, blood samples were collected for the measurement of tumour necrosis factor (TNF), interleukin (IL)-1beta, IL-6 and angiotensin (Ang) II and brains were dissected for light microscopic examination. 3. Over the 15 month period, the mortality of control SHRSP was 37.5%, which reached 80.0% in the sodium loading group. Compared with the control group, blood pressure was increased but BRS was significantly decreased (P < 0.001) in sodium-loaded rats. Levels of IL-1beta, IL-6 and AngII were all significantly increased (P < 0.05) in the sodium-loaded rats. Sodium loading also markedly increased the number of cerebral aneurysms. Multivariate regression analysis showed that IL-6 was the most significant factor related to aneurysm formation. 4. Sodium loading increases death from stroke in SHRSP. The increased blood pressure, impaired BRS, inflammatory reaction and the formation of cerebral aneurysms may contribute to the development of stroke.
Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai, China.
Wei
W
Zhang
Ai-Jun
AJ
Liu
Wuliya
W
Yi-Ming
Jian-Guo
JG
Liu
Fu-Ming
FM
Shen
Ding-Feng
DF
Su
D000804:Angiotensin II / Q000097:blood; D000818:Animals; D017704:Baroreflex / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects*; D001921:Brain / Q000187:drug effects / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D006339:Heart Rate / Q000187:drug effects*; D006973:Hypertension / Q000097:blood / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D002532:Intracranial Aneurysm / Q000097:blood / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D011918:Rats, Inbred SHR; D012044:Regression Analysis; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*; D020521:Stroke / Q000097:blood / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D053583:Interleukin-1beta; D015850:Interleukin-6; D017673:Sodium Chloride, Dietary; D014409:Tumor Necrosis Factor-alpha; D000804:Angiotensin II