Article: PDF OnlyKazda S.; Stasch, J.-P.; Hirth, C.Journal of Cardiovascular Pharmacology: 1987 - p S90-S95 Free Abstract Summary In spontaneously hypertensive rats (SHR), chronic treatment with nitrendipine provided normotension for nearly the entire life span and prevented cardiac hypertrophy. In 60-week-old control SHR, heart failure developed, as documented by a progressive decrease of systolic blood pressure and a drastic increase in plasma concentration of atrial natriuretie peptides (ANP)(470 ± 38 vs. 80 ± 23 pg/ml in age-matched normotensive Wistar Kyoto control rats) measured by radioimmunoassay. In SHR chronically treated with nitrendipine, the increase in plasma ANP was not observed (155 ± 36 pg/ml). Plasma levels of ANP were also elevated in young SHR with established hypertension, suggesting an early impairment of cardiac function by volume load in SHR. Therapeutic treatment of these 5-month-old SHR with nitrendipine for 11 weeks resulted in a decrease of systolic blood pressure, a regression of cardiac hypertrophy, and a reduction of the elevated plasma ANP levels (287 ± 31 vs. 226 ± 15 pg/ml). These effects could not be achieved by a simple peripheral vasodilation since the decrease of blood pressure induced by minoxidil treatment resulted in an aggravation of cardiac hypertrophy. In addition to the decreased afterload, nitrendipine obviously normalized the impaired volume homeostasis by improving renal function in hypertension. and thus reduced the need for activation of the ANP system. This complex effect is further evidence for a pathogenetically oriented mode of antihypertensive action of nitrendipine. © Lippincott-Raven Publishers.