Atrial‐specific granule number and plasma atrial natriuretic peptide in rats: Effects of beta‐adrenoceptor blockade and sodium intake

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 ± 8.7 vs. 42.3 ± 5.7; left atria 47.7 ± 7.7 vs. 30.6 ± 3.4 granules/unit area) and plasma renin activity (28 ± 3.7 vs. 5.4 ± 0.8 ng Al/ml/hr). Plasma ANP levels were lower in the low‐sodium animals (98 ± 34 vs. 345 ± 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 already‐suppressed 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.