Compared myocardial and vascular effects of captopril and dihydralazine during hypertension development in spontaneously hypertensive rats

• Published in: British journal of pharmacology 1983-11, Vol.80 (3), p.533-543
• Main Authors: Freslon, J.L., Giudicelli, J.F.
• Format: Article
• Language: English
• Subjects: Animals; Antihypertensive agents; Biological and medical sciences; Blood Pressure - drug effects; Blood Vessels - drug effects; Captopril - pharmacology; Cardiovascular system; Dihydralazine - pharmacology; Heart - drug effects; Hydralazine - analogs & derivatives; Hypertension - physiopathology; Hypertension - prevention & control; Male; Medical sciences; Organ Size - drug effects; Pharmacology. Drug treatments; Proline - analogs & derivatives; Rats; Rats, Inbred Strains
• ISSN: 0007-1188; 1476-5381
• DOI: 10.1111/j.1476-5381.1983.tb10726.x

1 When administered to young spontaneously hypertensive rats (SHRs), dihydralazine (25 mg kg−1, daily) and captopril (100 mg kg−1, daily) prevent with the same efficacy genetic hypertension development (GHD). 2 Dihydralazine treatment increased vascular mesenteric compliance, as shown by a significant decrease in the stiffness of the vessels (‐27%), and induced slight reductions in contractility (‐12%) and in wall to lumen (W/L) ratio (‐15%). After treatment withdrawal, all these parameters returned to control values within 7 weeks, as did blood pressure. 3 Captopril treatment also strongly increased the mesenteric vessels compliance, vessel stiffness being decreased by 16%, and reduced their contractility (‐15%) and their W/L ratio (—30%). These effects as well as those exerted on blood pressure persisted up to 7 weeks after treatment ceased although there was a slight trend to a progressive reduction in the intensity of both phenomena. 4 These experiments show that captopril but not dihydralazine has a long‐lasting effect in opposing the functional and morphological vascular alterations occurring during GHD in SHRs and this phenomenon probably contributes to a large extent to the sustained preventive effects of the drug against GHD.