Effects of nisoldipine on atrial natriuretic peptides, blood pressure and cardiac hypertrophy in Dahl rats

• Published in: Clinical and experimental hypertension. Part A, Theory and practice Vol. 12; no. 8; p. 1419
• Main Authors: Stasch, J P, Kazda, S, Hirth-Dietrich, C, Neuser, D
• Format: Journal Article
• Language: English
• Published: United States 1990
• Subjects: Animals; Atrial Natriuretic Factor - blood; Blood Pressure - drug effects; Cardiomegaly - blood; Cardiomegaly - drug therapy; Cardiomegaly - prevention & control; Male; Minoxidil - pharmacology; Nisoldipine - pharmacology; Rats; Renin - blood; Sodium, Dietary - administration & dosage
• ISSN: 0730-0077
• DOI: 10.3109/10641969009073528

The role of the calcium antagonist nisoldipine and the arteriolar vasodilator minoxidil on plasma levels of atrial natriuretic peptides (ANP), systolic blood pressure and heart weight was estimated in inbred Dahl salt sensitive (S) rats and inbred Dahl resistant (R) rats in long-term experiments. S rats develop quickly malignant hypertension, cardiac hypertrophy and have increased ANP plasma levels when fed a high salt diet (8% NaCl), while R rats on a high salt stay normotensive. In S rats 5 weeks on a high salt diet, therapeutic treatment with nisoldipine for 5 weeks not only decreased blood pressure but also produced a regression in cardiac hypertrophy and a reduction in elevated ANP plasma levels in comparison to the untreated salt-loaded S controls. Similar results were achieved in a preventive trial. In contrast with nisoldipine, therapeutic treatment with minoxidil in salt-loaded S rats lead to no reduction in cardiac hypertrophy and produced an additional increase in plasma ANP despite a reduction in blood pressure. The increase in plasma ANP level in this model of hypertension and its modulation by antihypertensive treatment with a calcium antagonist or an arteriolar vasodilator show that the changes in ANP plasma levels are probably secondary to hypertensive disease and the associated cardiac volume overload.