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Biomedical subjects

M L Overturf

Publications and source records attributed to M L Overturf.

25 records · Page 2Linked to original sources
PubMed1978

Prazosin and clonidine for moderately severe hypertension.

In a single-blind comparative study of the cases of 30 moderately hypertensive patients, clonidine hydrochloride and prazosin hydrochloride had similar effectiveness in lowering blood pressure. Neither agent had significant effects on the renin-aldosterone axis. Addition of polythiazide to prazosin and chlorthalidone to clonidine notably increased the antihypertensive effect of both drugs. Serum cholesterol levels were observed to decrease when prazosin and clonidine were given and to rise when the diuretics were added to the regimen. The patients treated with clonidine were troubled by side effects, particularly drowsiness and dry mouth. Prazosin was better tolerated, with side effects tending to diminish with time. The "first-dose" effect was seen in two patients given prazosin, but it did not limit treatment. Both diuretics induced notable hypokalemia.

Adult↗
PubMedDate not supplied

Renin as a risk factor for atherogenesis. Effects of hypercholesterolemia and two-kidney--one-clip hypertension in the rabbit.

Four groups of New Zealand rabbits were used to study the effect of plasma renin activity (PRA) on atherogenesis. Control groups were fed normal rabbit chow (Group I) or chow supplemented with 0.25% cholesterol and 0.75% corn oil (Group II). The two-kidney--one-clip (2K-1C) hypertensive model was produced in 2 additional groups; Group III (normal diet) and Group IV (atherogenic diet). The latter 2 groups were subgrouped according to PRA levels. Each group was examined over a 7-month period. Group II became hyperlipidemic and developed extensive lipoidal vascular lesions. Mean arterial pressure remained normal throughout the experimental period; PRA fell below normal. Group III and Group IV rabbits developed sustained hypertension irrespective of circulating PRA. The atheromas of Group III were predominantly microscopic and fibromuscular; the extent of aortic and coronary artery involvement was independent of renin response. The most extensive and complicated atheromas were seen in the 2K-1C rabbits consuming the atherogenic diet (Group IV). The lesions were mostly lipoidal, although some were fibromuscular. These results demonstrated that cardiovascular lesions and atherogenesis were exacerbated in the 2K-1C rabbits on a high cholesterol diet; however, PRA was excluded as the cause.

Adrenal Glands↗
PubMedDate not supplied

Renin as a risk factor for atherogenesis. Part 2. Effects of hypercholesterolemia and hyporeninemia in the rabbit.

Four groups of New Zealand rabbits were used to study the effect of suppressed plasma renin activity (PRA) on atherogenesis. Control groups were fed normal rabbit chow (Group I) or normal chow supplemented with 0.25% cholesterol--0.75% corn oil (Group III). Group II animals were fed normal chow and received periodic injections of 11-desoxycorticosterone (DOC)pivalate and 0.5% saline to drink, while Group IV animals were treated similarly except that they were also fed the atherogenic diet. Blood pressure and blood chemistry measurements were performed monthly over a 7-month period. The blood pressure was unaffected by either the diet or the DOC-saline treatment, however, the PRA was greatly reduced in the animals receiving DOC-saline (Groups II and IV). Similarly, plasma aldosterone was significantly (P less than 0.05) reduced in the DOC-saline-treated animals. No atheromata were observed in the animals consuming the regular diet, regardless of DOC-saline treatment. All of the animals fed the atherogenic diet showed extensive aortic atheromata. However, there was no difference in the lesion index between the animals with normal PRA levels (Group III) and those with suppressed PRA levels (Group IV). Likewise, microscopic evaluation of the aorta, coronary arteries, and renal arteries failed to show a consistent difference in the vascular involvement between animals of Groups III and IV. We therefore conclude that the suppression of PRA does not have a protective effect on atherogenesis in the cholesterol-fed normotensive rabbit.

Animals↗
PubMedDate not supplied

Evidence against acetone-soluble renin inhibitors in normal human plasma.

The presence of acetone-soluble renin inhibitors in normal plasma has been proposed to explain the variation of plasma reactivity (PRR) in samples from normotensive and hypertensive subjects. In our experience, acetone extraction decreased PRR in relation to unextracted control values, an observation which is not consistent with the circulating lipid-renin inhibitor hypothesis. Exposure to acetone at -40 degrees C for 1 minute invariably denatured some endogenous angiotensinogen. The PRR in extracted and unextracted plasma was positively correlated with the concentration of available angiotensinogen, r = 0.955 (p < 0.05), and r = 0.964 (p < 0.01), respectively, but the addition of exogenous substrate did not uniformly increase PRR in acetone-treated plasma above control values. These data argue against the use of acetone extraction to demonstrate the existence of circulating lipid-renin inhibitors. Acetone removed 14% to 25% of the normal plasma lipids and although the extract contained most of the major lipid classes, neutral lipids were the most abundant (73% by weight). The presence of acetone-soluble phospholipids appeared to increase angiotensin I formation in the partially purified renin-angiotensinogen system, but phospholipids interfered with the radioimmunoassay and resulted in an overestimation of angiotensin I. Plasma neutral lipids decreased in vitro renin activity by 13% (p < 0.025) but this degree of inhibition suggests that lipid-renin interactions may have minimal in vivo physiological significance. In contrast to previous reports, we found the correlation between PRR and endogenous angiotensinogen in normotensive and hypertensive plasmas to be statistically significant (r = 0.643, p < 0.01). Inactivated human angiotensinogen was also shown to be an inhibitor of renin in vitro. This effect could have possibly influenced PRR values that were determined by others in the presence of inactivated angiotensinogen.

Acetone↗