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Biomedical subjects

G S Williams

Publications and source records attributed to G S Williams.

27 records · Page 2Linked to original sources
PubMed1980

Treatment of drug-resistant hypertension with minoxidil or angiotensin-converting enzyme inhibitor: blood pressure, renin, aldosterone, and electrolyte responses.

The effects of minoxidil and the angiotensin-converting enzyme inhibitor SQ 14,225 on blood pressure, sodium balance, plasma renin activity, plasma aldosterone concentration, aldosterone excretion rate, and renal function were studied in 11 drug-resistant hypertensive patients under controlled diets of sodium and potassium intake. Minoxidil treatment lowered blood pressure from 178/112 +/- 8/5 mm Hg (means +/- SEM) to 14/95 +/- 6/3 mm Hg. Plasma renin activity rose from 4.8 +/- 1.7 ng/ml/hr to 9.9 +/- 2.4; plasma aldosterone rose from 32.6 +/- 7.4 to 50.5 +/- 9.8 ng/dl; and aldosterone excretion rate rose from 7.6 +/- 1.3 to 15.2 +/- 3.5 micrograms/24 hr. Sodium retention could be controlled by increasing doses of diuretics, but a 10 mEq/day sodium intake in two patients resulted in significant increases of serum creatinine, and hyperkalemia was reversed by sodium loading. In five minoxidil-treated patients, substitution with the angiotensin-converting enzyme inhibitor SQ 14,225 lowered plasma and urinary aldosterone levels in two normal and high-renin patients but not significantly in three low-renin patients. Sodium excretion increased when aldosterone decreased, but blood pressure were more consistently controlled with minoxidil than with oral SQ 14,225.

Adult↗
PubMed1977

Detection of renovascular hypertension with angiotensin II blockade.

Angiotensin II blockade with sarcosine 1-alanine 8-angiotensin II (saralasin, P-113) was done in 40 studies of 20 hypertensive patients. Eleven of 12 patients with a depressor response to angiotensin II blockade had significant renovascular or renal disease, and nine of 10 had renal vein renin measurements that lateralized to the abnormal kidney. In contrast, none of the patients without a depressor response had renovascular abnormalities. Plasma renin activity was usually high in responders to saralasin (18 ng/ml-h) when compared with nonresponders (0.5 ng/ml-h). In these studies a correlation between the fall in blood pressure and the rise in plasma renin activity during angiotensin II blockade was observed while renin was unchanged in the absence of depressor responses. In two renovascular renin-dependent hypertensive patients, treatment with diuretics induced severe hyperreninemia and a rise in blood pressure that was reversed by sodium loading.

Angiotensin II↗
PubMed1976

Renal vein thrombosis, nephrotic syndrome, and systemic lupus erythematosus: an association in four cases.

We report here four cases of systemic lupus erythematosus associated with the nephrotic syndrome and renal vein thrombosis and review six familiar cases previously noted in the literature. Renal biopsy in each of our cases showed changes consistent with the membranous type of lupus nephropathy. We discuss the exclusive appearance of this pattern in relation to renal vein thrombosis in other forms of renal disease. The occurance of renal vein thrombosis in patients with systemic lupus erythematosus and the nephrotic syndrome supports the evidence that the thrombosis is a complication rather than a cause of the nephrotic syndrome. The presence of pleuritic pain in a patient with systemic lupus erythematosus and the nephrotic syndrome should alert the clinician to the possibility of renal vein thrombosis and pulmonary emboli. With appropriate diagnosis and anticoagulation therapy, our patients had a benign course during 7 to 48 months of follow-up.

Adult↗