Biomedical subjects

P E Pool

Publications and source records attributed to P E Pool.

4 recordsLinked to original sources

PubMed1991

Metabolic consequences of treating hypertension.

Reduction of morbidity and mortality has been the aim of drug treatment for hypertension since its beginning in the 1950s. Its efficacy has been tested in many trials. An outstanding result of these trials has been their clear success in preventing stroke and stroke-related deaths and in decreasing the incidence of congestive heart failure (CHF) and renal disease. A similar success has not been achieved in reducing coronary heart disease endpoints. Diuretics and beta-blockers played a central role in these studies; however, their adverse effects on lipid metabolism have been cited as a possible explanation for the failure of antihypertensive therapy to affect coronary heart disease (CHD). Recently, the extent and significance of these lipid changes has been put into perspective, and new insights into the role of carbohydrate metabolism and insulin resistance in hypertension have emerged. The same drugs which adversely affect lipid metabolism also adversely affect carbohydrate metabolism, and more is becoming known about these mechanisms and their role in hypertension and its sequelae. Other classes of antihypertensive drugs such as the calcium antagonists, angiotensin converting enzyme (ACE) inhibitors, and alpha 1-antagonists do not share these adverse effects. It has become increasingly clear that effective antihypertensive therapy includes both the lowering of blood pressure and containment of the abnormalities that accompany the hypertensive state.

Adrenergic beta-Antagonists↗

PubMed1990

Antihypertensive monotherapy with tablet (prompt-release) diltiazem: multicenter controlled trials.

The tablet formulation of diltiazem has been available for the treatment of angina pectoris but has not been comprehensively evaluated in hypertension. This study's aim was to evaluate the efficacy, dose-response characteristics, and duration of action of tablet (prompt-release) diltiazem in mild to moderate hypertension. Three placebo-controlled trials were designed. The first (trial #1) evaluated the dose response of 120, 240, and 360 mg/day (q12h regimen) of diltiazem in parallel fixed-dose fashion using hourly blood pressures. The second (trial #2) evaluated a q12h titration from 240 to 360 mg/day, which could be switched to q8h. The third (trial #3) evaluated a q8h titration from 180 to 270 to 360 mg/day, followed by conversion to a q12h regimen. The goal was a supine diastolic blood pressure of less than 90 mmHg and 10 mmHg less than baseline. With doses of diltiazem increasing from 120 to 240 to 360 mg/day, there was a progressive decrease in the average mean arterial pressure, describing a dose response with 120 mg/day as the ineffective dose. The peak effect for each dose regimen was found at 6 hours, with significant reductions lasting over 10 hours in the 240 mg/day and 360 mg/day groups. Peak plasma concentrations occurred at 3 hours. The residual effect at the trough of the 240 mg/day and 360 mg/day doses was 48% and 53% of the peak effect, respectively. When titration was carried out on a q8h regimen, both systolic and diastolic blood pressures were significantly decreased. When the regimen was switched from q8h to q12h, the effect was not maintained.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1976

Augmented right ventricular function in systemic hypertension-induced hypertrophy.

The contractile properties of right ventricular papillary muscles from the hearts of 15 rats which had developed hypertension 6 weeks following renal artery ligation were compared with those from 14 normal litter-mates. In the experimental group, the heart weight-body weight ratio was increased by 39%, while the right ventricular weight-body weight ratio increased 20%. Right ventricular papillary muscles from the hypertensive rats demonstrated increased tension development at the apex of the length-active tension curve (P less than 0 X 0001), elevated maximal rate of tension development (P less than 0 X 001), and increased maximal velocity of contraction at muscle lengths corresponding to both a light preload and at Lmax (P less than 0 X 05). Resting tension and time-to-peak tension in the muscles from the hypertensive group were not significantly different from the normal group. Thus, improved right ventricular performance, in the presence of increased left ventricular afterload, may indicate the existence of a stimulus to increased function in hypertrophied muscle not yet negated by the adverse effects of direct exposure to stress.

Animals↗

PubMed1976

Influence of hyperthyroidism on glycerol-extracted cardiac muscle from rabbits.

The mechanism responsible for the enhancement of myocardial contractility in hyperthyroidism is unclear. The possibility that this mechanism may involve a direct effect on the contractile proteins was investigated using the glycerol-extracted muscle strip from right ventricular papillary muscles of euthyroid rabbits and rabbits made hyperthyroid by the intraperitoneal injection of 0.25 mg/kg 1-thyroxine for 10 d. Intact papillary muscles from the hyperthyroid rabbits had an enhanced rate of tension development, a decreased time to peak tension, and a slight though insignificant increase in active tension compared to control animals. Maximal isometric contractions were induced in glycerol-extracted cardiac muscle strips from the two animal groups by the addition of 5 mmol/litre ATP and 5 mmol/litre MgCl in a buffer solution containing 0.15 mol/litre Tris-HCl (pH 7.1) at 26 degrees C. Peak isometric tension was increased in glycerinated muscle strips from hyperthyroid rabbits (1.52+/-0.10 vs 1.26 +/-0.13g/mm2), but the differences did not reach statistical significance. However, there was a marked increase in the rate of tension development in the hyperthyroid group (62.5+/-5.4 vs 41.8+/-4.7 mg/mm-2/s, P less than 0.01). This increase in the rate of isometric tension development in both intact and glycerinated muscles from hyperthyroid rabbits may be related to changes in the intrinsic turnover of actomyosin cross-bridge links in this condition. Thus, these findings suggest that thyroid hormone may influence cardiac muscle function by a direct effect on the contractile proteins.

Adenosine Triphosphate↗