| pubmed-article:1781768 | pubmed:abstractText | Light and electron microscopic stereological studies were performed on the myocardium of spontaneously hypertensive rats (SHR) before and after treatment with nifedipine (27 mg/kg b.w./day) and the sympatholytic agent moxonidine (8 mg/kg b.w./day). The treated groups were compared with nontreated SHR and normotensive WKY (n = 10 in each group). When the therapy was started in 6-month old male SHR, blood pressure was increased and left ventricular hypertrophy had developed. On the other hand, pathologic changes of myocardial structure were not observed. After 3 months, the nontreated hypertensive rats showed cardiac fibrosis (volume density of fibrosis + 45%), activation and proliferation of interstitial cells (volume density of nonvascular interstitium + 240%), media hypertrophy of small arteries (total volume of arterial media in the left ventricle + 180%), reduced capillarization (length density of capillaries--11%), as well as focal degeneration of myocytes at the ultrastructural level. Both treatments showed similar effects on blood pressure, degree of hypertrophy, and cardiac structure. Blood pressure as well as degree of hypertrophy were significantly reduced (relative left ventricular weights: --25% and --16%). As far as myocardial fibrosis, capillarization, and regressive changes of myocytes are concerned a complete normalization was observed. Microarteriopathy and activation of nonvascular interstitial cells (first step in development of interstitial myocardial fibrosis) were significantly suppressed by therapy (total media volume --40%, volume density of nonvascular interstitium --38%), but the normal level of the normotensive control could not be maintained (+ 70%, + 111% vs WKY). This may be due to the slightly elevated systolic blood pressure despite therapy (+ 25%, vs WKY) or to hormonal factors in SHR which are independent of blood pressure. Since nifedipine and moxonidine are pharmacologically different drugs with different effects on sympathetic activity, one may cautiously conclude that increase in blood pressure itself is an important determinant of arterial, interstitial as well as myocellular alterations which are related to the pathogenesis of hypertensive heart muscle disease. | lld:pubmed |
