Hyposecretion of Atrial Natriuretic Factor by Prehypertensive Dahl Salt‐Sensitive Rat
作者:
Michael Onwochei,
John Rapp,
期刊:
Hypertension
(OVID Available online 1989)
卷期:
Volume 13,
issue 5
页码: 440-448
ISSN:0194-911X
年代: 1989
出版商: OVID
关键词: genetic hypertension;atnal natnuretic factor;cardiac output;isolated heart-lung preparation
数据来源: OVID
摘要:
Studies were carried out to determine if the release of atrial natriuretic factor (ANF) is altered in the inbred Dahl salt-sensitive (SS/Jr) rat. Isolated heart-lung preparations of prehypertensive young SS/Jr rats (6–8 weeks of age) and age-matched inbred Dahl salt-resistant (SR/Jr) rats were used. At this relatively young age the blood pressure difference between strains (SS/Jr, 108±3 mm Hg; SR/Jr, 103±2 mm Hg) was minor. ANF release was stimulated with preload-induced or afterload-induced atrial stretch. Increased preload produced increases in right and left atrial pressures that were equivalent between young SS/Jr and SR/Jr rats; increased afterload produced increases only in left atrial pressures, which again were equivalent for young rats of the two strains. At any preload-induced change in atrial pressure SS/Jr rat hearts released less ANF than those of SR/Jr rats. Similarly, at any afterioad-induced increase in left atrial pressure, SS/Jr rat hearts released less ANF than those of SR/Jr rats. In contrast to the above results in young rats, the strain differences were dramatically reversed when older rats (5–6 months of age) were used; at this age SS/Jr rats were markedly hypertensive (SS/Jr, 211±8 mm Hg; SR/Jr 130±4 mm Hg). Hearts from adult hypertensive SS/Jr rats released more ANF than hearts from adult normotensive SR/Jr rats at any left atrial pressure as afterload was increased. This reversal of SS/Jr rats from hyposecreters to hypersecreters of ANF is probably a consequence of hypertension-induced changes such as cardiac hypertrophy and recruitment of the ventricles to produce ANF. It is concluded that the hyposecretion of ANF by prehypertensive SS/Jr rats may represent a genetic trait relevant to the pathogenesis of genetic hypertension and that this is obscured by adaptive changes in the heart as hypertension progresses.
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