Atrial-specific granule number and plasma atrial natriuretic peptide in rats: Effects of beta-adrenoceptor blockade and sodium intake
✍ Scribed by Penner, S. Brian ;Thliveris, James A. ;McKenzie, John K. ;Smyth, Donald D.
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 924 KB
- Volume
- 228
- Category
- Article
- ISSN
- 0003-276X
No coin nor oath required. For personal study only.
✦ Synopsis
An interrelationship between atrial natriuretic peptide (ANP) and the renin-angiotensin system has been established. Both of these hormonal systems are modulated by sodium balance. The role of the beta-adrenoceptor in the regulation of release of ANP is not clear. We therefore undertook a study to examine changes in atrial-specific granule number and plasma ANP level following beta-adrenoceptor blockade in rats on low and high sodium intakes. A low-sodium diet, as compared with a high-sodium diet, elevated right and left atrial-specific granule number (right atria 54.6 2 8.7 vs. 42.3 t 5.7; left atria 47.7 2 7.7 vs. 30.6 2 3.4 granuledunit area) and plasma renin activity (28 k 3.7 vs. 5.4 2 0.8 ng AI/ml/hr). Plasma ANP levels were lower in the low-sodium animals (98 ? 34 vs. 345 2 38 pg/ml). When treated with the nonspecific beta-adrenoceptor blocker propranolol, the elevated plasma renin activity and atrial-specific granule number in rats on a low sodium intake were significantly less. Neither of these parameters changed in rats on a high sodium intake. Conversely, propranolol treatment resulted in lower plasma ANP levels in rats with high sodium intake. The alreadysuppressed plasma ANP level in rats on a low-sodium diet was unaltered with beta-adrenoceptor blockade. The results suggest that dietary sodium intake is an important determinant of the response of atrial-specific granule number and plasma ANP levels following beta-adrenoceptor blockade with propranolol.