Hyposecretion of atrial natriuretic factor by prehypertensive Dahl salt-sensitive rat.

Abstract

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 afterload-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.