Effects of long-term verapamil treatment on blood pressure, cardiac hypertrophy and collagen metabolism in spontaneously hypertensive rats

• Published in: Cardiovascular research Vol. 19; no. 6; pp. 355 - 362
• Main Authors: RUSKOAHO, HEIKKI J, SAVOLAINEN, EEVA-RIITTA
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.06.1985
• Subjects: Animals; Antihypertensive agents; antihypertensive drugs; Aorta - metabolism; Biological and medical sciences; Blood Pressure - drug effects; Cardiomegaly - drug therapy; Cardiovascular system; collagen; Collagen - metabolism; Female; Heart - drug effects; Hydroxyproline - metabolism; hypertension; Hypertension - drug therapy; Hypertension - metabolism; left ventricular hypertrophy; Male; Medical sciences; Minoxidil - pharmacology; Myocardium - metabolism; Pharmacology. Drug treatments; Pregnancy; Procollagen-Proline Dioxygenase - metabolism; prolyl hydroxylase; Rats; Rats, Inbred SHR; regression of hypertrophy; spontaneously hypertensive rats; Time Factors; verapamil; Verapamil - administration & dosage; Heart; Hypertension; Rat; Rodentia; Calcium antagonist; Cardiovascular disease; Administration schedule; Hereditary; Metabolism; Long term; Vertebrata; Chemotherapy; Mammalia; Animal; Collagen; Blood pressure; Hypertrophy
• DOI: 10.1093/cvr/19.6.355
• ISSN: 0008-6363

The effects of long-term treatment with verapamil on blood pressure, cardiac hypertrophy and collagen content, collagen concentration and prolyl hydroxylase activity were studied in spontaneously hypertensive rats (SHR). Verapamil administration (0.75 mg·ml−1in drinking water) was commenced: (1) to pregnant SHR 3 to 5 days before delivery and continued to the mothers and offspring during the nursing period; or (2) to SHR at 10 weeks of age. Both groups were maintained on verapamil treatment up to the age of 45 weeks. Verapamil treatment significantly decreased blood pressure, heart rate and the ratio of ventricular weight to body weight in treated SHR. Verapamil did not significantly change the cardiac collagen concentration and prolyl hydroxylase activity. Since, however, the cardiac muscle mass was diminished by verapamil administration, treatment actually slightly reduced the collagen content of the heart. In the aorta collagen concentration was increased by verapamil treatment. Contrary to these results, minoxidil treatment was observed to increase the cardiac collagen concentration, content and prolyl hydroxylase activity in SHR. These results suggest that the factors governing myocardial connective tissue proliferation and regression may be independent of those governing muscle fibre hypertrophy and that particular drug actions on myocardial collagen metabolism must be taken into account.