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Biomedical subjects

H M Wilson

Publications and source records attributed to H M Wilson.

31 records · Page 2Linked to original sources
PubMed1992

The isolation and characterization of high-density-lipoprotein subfractions containing apolipoprotein E from human plasma.

1. Plasma high-density lipoprotein (HDL) was separated by heparin-Sepharose affinity chromatography into a non-bound, apolipoprotein E-poor, and a bound, apolipoprotein E-rich, fraction through the binding effect of Mn2+ in the column buffer. 2. The application of a series of elution buffers in which the concentration of Mn2+ was progressively replaced by Mg2+ resulted in the separation of the bound HDL into five subfractions. 3. Each subfraction migrated a different distance on gradient-gel electrophoresis. Three of the subfractions had RF (relative migration compared with BSA) values within the range of HDL2b. One subfraction contained largely HDL2a, with some material in the regions of HDL2b and HDL3a, and one subfraction spanned the RF regions of HDL2a, HDL3a and HDL3b. 4. The number of molecules, per HDL particle, of cholesteryl ester, non-esterified cholesterol and phospholipid increased with particle size, whereas triacylglycerol passed through a maximum and the number of amino acid residues remained approximately the same. 5. Apolipoprotein (apo) A-I was the major apoprotein in all five subfractions, but the latter differed appreciably in their contents of apo A-II and apo E. 6. The major fatty acid component of each subfraction was linoleic acid, with moderate amounts of C16:0 and C18:1 fatty acids and a smaller content of C18:0, C20:4,n-6 and C22:6,n-3, with no significant difference in composition between the subfractions. 7. This paper provides the first description of a method for the isolation of three subfractions of HDL2b together with other subfractions in quantities that are sufficient for further analytical or metabolic studies.

Adult↗
PubMed1977

Saralasin infusion in the recognition of renovascular hypertension.

Saralasin, an angiotensin II antagonist, was infused into 49 patients with renal artery stenosis, 10 patients with essential hypertension and normal renal arteriograms, and five patients with "low-renin essential hypertension." Renal venous renin and differential renal function studies were used to assess the functional significance of arterial stenoses. "Response" to saralasin, evidenced by a fall in blood pressure during infusion, occurred in no patients with "low renin" hypertension and in only 20% of patients with normal renal arteriograms. In contrast, saralasin "response" occurred in more than 80% of patients with renal artery stenosis and lateralizing functional studies and 100% of cases of "proven" renovascular hypertension (cure or improvement of hypertension after operative treatment). We suggest that saralasin infusion might be a valuable screening test for the recognition of renovascular hypertension.

Angiotensin II↗
PubMed1977

Are there unknown mineralocorticoids in low-renin essential hypertension?

The blood pressure elevation of primary aldosteronism is caused by excessive production of the known mineralocorticoid, aldosterone. The blood pressure elevation of low-renin essential hypertension may also be caused by mineralocorticoid excess, but which which mineralocorticoid is responsible is uncertain. Normal levels of aldosterone, found in this disorder despite suppressed plasma renin, and the presence of an unknown mineralocorticoid have been hypothesized to explain low-renin essential hypertension. We contrasted the blood pressure responses and changes in aldosterone seen in patients with low-renin essential hypertension and primary aldosteronism during treatment with two adrenal enzyme inhibitors. The results demonstrate the similarity between decrease in blood pressure and in aldosterone during early adrenal inhibition in both primary aldosteronism and in low-renin essential hypertension. During treatment with a distal adrenal blocker, patients with primary aldosteronism demonstrated decreases in both aldosterone and blood pressure, whereas patients with low-renin essential hypertension showed a decrease in aldosterone without significant change in blood pressure. This suggested that aldosterone was not the major mineralocorticoid responsible for low-renin essential hypertension. Unknown mineralocorticoid excretion decreased (along with blood pressure) during early inhibition but failed to decrease (along with blood pressure) during late inhibition at a time when aldosterone excretion decreased. This suggests that unknown mineralocorticoids play significant roles in the blood pressure elevation of low-renin essential hypertension.

Aminoglutethimide↗
PubMedDate not supplied

Effect of transforming growth factor-beta 1 on plasminogen activators and plasminogen activator inhibitor-1 in renal glomerular cells.

Recent evidence suggests that the balance between serine proteases and their inhibitors is central to the maintenance of the glomerular extracellular matrix. We have characterised the urokinase type and the tissue type plasminogen activators (PA) and their inhibitor, PAI-1, secreted from glomerular epithelial and mesangial cells as well as their co-cultures and have investigated the effect of transforming growth factor-beta 1 (TGF-beta 1) on the production of such species. Similar data were derived from whole glomeruli suspensions. TGF-beta 1 increased PAI-1 production significantly in epithelial and mesangial cells as well as in whole glomeruli, while PA production was decreased; platelet-derived growth factor had no effect. These effects are consistent with a possible decrease in matrix proteolysis, suggesting a mechanism by which TGF-beta 1 may enhance mesangial matrix accumulation, a characteristic of many forms of glomerular disease.

Epithelial Cells↗
PubMedDate not supplied

Opposing effects of interleukin-1 and transforming growth factor-beta on the regulation of tissue-type plasminogen activator and plasminogen activator inhibitor type-1 expression by human mesangial cells.

Several proteases have been implicated in regulating the turnover of mesangial matrix within the glomerulus. One such group, the plasminogen activators (PAs) and their inhibitor, PA inhibitor type-1 (PAI-1), is produced by glomerular cells with altered expression during nephritis. We report the effect of IL-1 and transforming growth factor-beta (TGF-beta) and a combination of the two cytokines on the secretion of tissue-type PA (t-PA) and PAI-1 from human mesangial cells. IL-1 significantly downregulates PAI-1 production and upregulates t-PA over a range of concentrations (1-10 U/ml), while TGF-beta (0.5-10 ng/ml) has the opposite effect. The combined effect of these factors is that TGF-beta attenuates the increase in t-PA and decrease in PAI-1 expression caused by IL-1, and has a dominant effect upon their secretion, thus decreasing t-PA and increasing PAI-1. These findings contribute to our understanding of fibrinolysis and tissue remodelling within the glomerular mesangium during the course of nephritis.

Base Sequence↗