Drugs online research references
J Cardiovasc Pharmacol. 1985;7 Suppl 2:S56-61.
Regression of cardiac hypertrophy after therapy in animal hypertension.
Motz W, Strauer BE.
Studies on spontaneously hypertensive rats (SHR), which represent a model of genetically determined arterial hypertension, revealed that cardiac hypertrophy can be controlled by blood pressure normalization by use of various antihypertensive drugs such as hydralazine, captopril, metoprolol, guanethidine, and alpha-methyldopa. Adrenergic influences seem to play a part except for left ventricular (LV) systolic unloading on cardiac hypertrophy, because LV hypertrophy was quantitatively less expressed after a combined therapy with both metoprolol and hydralazine than after a single hydralazine treatment, although blood pressure was not different between the groups. To study whether nifedipine can cause an already existing cardiac hypertrophy to regress, 20-week-old SHR were treated with nifedipine for a period of 20 weeks. After nifedipine treatment, LV muscle mass/body weight ratio was significantly less than before therapy (2.13 +/- 0.18 vs. 2.37 +/- 0.30 mg/g; p less than 0.05). Mass to volume ratio, i.e., quotient of LV muscle mass and LV end-diastolic volume, dropped from 3.40 +/- 0.66 to 3.07 +/- 0.30 mg/microliters (p less than 0.05) after therapy. Accordingly, an antihypertensive treatment with the calcium channel blocker nifedipine can cause an already existing LV hypertrophy in SHR to regress. Because blood pressure reduction resulting from therapy with beta-receptor-blockers, vasodilators, sympatholytic drugs, angiotensin converting enzyme inhibitors, and calcium channel blockers has qualitatively similar effects with respect to causing regression of hypertrophy, reversal of cardiac hypertrophy seems to be mainly related to the reduced LV systolic load. Specific pharmacodynamic effects may only modulate the extent of LV mass reduction along with blood pressure normalization.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2409372&dopt=Abstract
J Cardiovasc Pharmacol. 1987;10 Suppl 6:S148-52.
Regression of cardiac hypertrophy: experimental and clinical results.
Motz W, Klepzig M, Strauer BE.
Department of Medicine, University of Dusseldorf, F.R.G.
Since left ventricular hypertrophy is considered to be a precursor of later hypertensive heart failure, a treatment that can prevent or even reverse myocardial hypertrophy is a highly desirable goal. In order to evaluate which type of antihypertensive treatment is able to induce regression of hypertensive hypertrophy, experimental and clinical studies were performed. Experimental studies were performed in spontaneously hypertensive rats (SHRs). Left ventricular hypertrophy and pumping function were studied after antihypertensive treatment with a beta-receptor blocker (metoprolol), an arteriolar vasodilator (hydralazine), and a calcium channel blocker (nifedipine) had been instituted for a period of 20-40 weeks. Patients with hemodynamically compensated hypertensive heart disease were treated with a calcium channel blocker (nifedipine), an angiotensin-converting enzyme (ACE) inhibitor (enalapril), an antisympathetic agent (clonidine), and prazosin. Comparing the amount of blood pressure reduction with the extent of hypertrophy reversal, nifedipine, prazosin, and enalapril were equipotent, whereas clonidine was most efficient in this respect. Muscle mass was overproportionally reduced in relation to blood pressure reduction following treatment with clonidine. It is likely that this was caused by lowered catecholamine levels secondary to clonidine therapy. Left ventricular pumping function was enhanced as a result of a reduction in left ventricular afterload, whereas myocardial contractility was found to be unchanged.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2485021&dopt=Abstract
Hypertension. 1991 Dec;18(6):722-7.
Reducing pulse pressure in hypertension may normalize small artery structure.
Christensen KL.
Biophysics Institute, University of Aarhus, Denmark.
To investigate the relation between the small artery structure and different blood pressure parameters, spontaneously hypertensive rats were treated from 4 to 24 weeks of age (20 weeks in total) with five different antihypertensive therapies: two angiotensin converting enzyme inhibitors (perindopril and captopril), a calcium antagonist (isradipine), a beta-blocker (metoprolol), and a vasodilator (hydralazine). At 24 weeks of age, 24-hour blood pressure was measured, and two mesenteric resistance vessels were taken from each animal. Blood pressure was 227/135 mm Hg (systolic/diastolic) and 161/106 mm Hg in untreated hypertensive and normotensive control rats, respectively. Heart rates were 376 min-1 and 295 min-1 for the two strains. All treatments reduced all blood pressure parameters except for metoprolol, which did not reduce pulse pressure. In the small arteries, the media cross-sectional area was unaffected by the treatments. When a simple correlation analysis was made, pulse pressure was found to correlate more closely (r = 0.64, p less than 0.001) to the resistance vessel media/lumen ratio than any of the other pressure parameters studied: systolic (r = 0.51, p = 0.011), mean (r = 0.41, p = 0.05), or diastolic (r = 0.28, p = 0.19). When an analysis of covariance was performed that included pulse pressure, mean blood pressure, and heart rate, which also correlated significantly to the media/lumen ratio, 81% of the variation in the media/lumen ratio could be accounted for by the variation in the three covariates (p less than 10(-5)), pulse pressure being the major factor.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1835958&dopt=Abstract
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