Biomedical subjects

M Leitschuh

Publications and source records attributed to M Leitschuh.

4 recordsLinked to original sources

PubMed1991

Aortic ornithine decarboxylase activity in deoxycorticosterone/salt hypertensive rats.

Previous studies from our own and other laboratories have shown that hypertension induces changes in the growth of arterial smooth muscle cells (SMC). The purpose of this study was to examine the role of ornithine decarboxylase (OrnDCase) in this process. OrnDCase, the rate limiting enzyme in polyamine biosynthesis, increases in activity early in the cell cycle, and has been used as a marker of cell growth or proliferation. Deoxycorticosterone (DOC)/salt hypertension was induced in male Wistar rats. At 1-3 day intervals of DOC/salt treatment, the aortas were removed and OrnDCase activity and DNA content were determined. The results indicated that OrnDCase activity increased as early as day 2 of DOC/salt administration, reached a peak at day 10, and fell to a baseline by day 16. DNA content increased after day 10 to levels approximately 25% greater than in controls. Significant increases in blood pressure were not observed until after day 8. The findings indicate that OrnDCase activity is stimulated by DOC/salt even before the rise in blood pressure and that factors other than blood pressure per se may be important in stimulating aortic smooth muscle cell growth in the development of hypertension.

Animals↗

PubMed1991

High-normal blood pressure progression to hypertension in the Framingham Heart Study.

This study sought to determine if individuals with high-normal blood pressure (diastolic blood pressure of 85-89 mm Hg) progress to hypertension more frequently than those with normal blood pressure (diastolic blood pressure less than 85 mm Hg), thus advancing to a higher cardiovascular risk category. Individuals from the Framingham Heart Study were placed in normal and high-normal blood pressure categories and followed for 26 years for the development of hypertension. With hypertension defined as a diastolic blood pressure of 95 mm Hg or greater or the initiation of antihypertensive therapy, 23.6% of men and 36.2% of women with normal blood pressure developed hypertension compared with 54.2% of men and 60.6% of women with high-normal blood pressure. The relative risk for the development of hypertension associated with high-normal blood pressure was 2.25 for men (95% confidence interval [CI], 1.8-2.8; p less than 0.0001) and 1.89 for women (95% CI, 1.5-2.3; p less than 0.0001). The age-adjusted relative risks estimated by the proportional hazards model were 3.36 for men and 3.37 for women (p less than 0.001). Among those risk factors examined, baseline systolic and diastolic blood pressure, Metropolitan relative weight, and change in weight over time were significant predictors of future hypertension in men and women whose initial blood pressure was normal. For men with high-normal blood pressure, systolic blood pressure and change in weight were identified as risk factors for future hypertension. These results indicate that the probability of individuals with blood pressure in the high-normal range developing hypertension is twofold to threefold higher than in those with normal blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Vascular changes in hypertension.

Hypertension can directly damage blood vessels, and leads to renal failure, intracranial bleeds, and lacunar infarctions. Of equal importance is the effect of hypertension on the development of atherosclerosis. Specific changes in both the microvasculature and macrovasculature vary depending on the degree and rapidity of blood pressure elevation. Changes in the intima and media can lead to significant narrowing of vessels and ischemia in various tissues. In addition, changes in small-resistance vessels contribute to changes in peripheral-vasculature resistance and thus affect blood pressure regulation. Treatment of moderate to severe elevation in blood pressure clearly results in a decrease in the incidence of stroke. However, evidence that treating mild hypertension reduces coronary events is less convincing. Antihypertensive therapy may result in partial regression of vascular changes, especially fibrinoid necrosis seen in malignant hypertension, but more work needs to be done to clearly define the roles of specific drugs in preventing or regressing hypertensive vascular disease.

Animals↗

PubMed1987

Inhibition of nuclear polyploidy by propranolol in aortic smooth muscle cells of hypertensive rats.

The ability of propranolol to inhibit the development of polyploidy in aortic vascular smooth muscle cells associated with hypertension was studied in deoxycorticosterone (DOC)-salt treated rats. Six-week treatment with DOC-salt resulted in significant increases in systolic blood pressure, heart weight, and aortic weight in treated animals compared to increases in uninephrectomized controls. Additionally, the percentage of tetraploid nuclei in aortic smooth muscle cells increased to 17.0 +/- 0.2% in DOC-salt treated rats versus 7.8 +/- 0.3% in normotensive controls. Administration of propranolol (500 mg/L in drinking water) did not inhibit the development of hypertension for up to 4 weeks or the associated increase in cardiac or aortic weight in DOC-salt-treated rats, but did prevent the increase in polyploidy of aortic smooth muscle cell nuclei (8.9 +/- 0.9% in propranolol-treated rats compared to 7.8 +/- 0.3% in normotensive controls). These results indicate that propranolol inhibits the development of hypertension-induced polyploidy in aortic smooth muscle cells of DOC-salt-treated rats and that factors other than blood pressure may be important in this change.

Animals↗