Drugs online research references
Exp Hematol. 1988 Sep;16(8):674-80.
Suppression of in vitro granulocytopoiesis by captopril and penicillamine.
Hammond WP, Miller JE, Starkebaum G, Zweerink HJ, Rosenthal AS, Dale DC.
Department of Medicine, University of Washington School of Medicine, Seattle 98195.
The mechanisms underlying drug-induced neutropenia are poorly characterized. We have examined the mechanism of suppression of granulocytopoiesis by captopril and penicillamine using human and canine bone marrow cells in an in vitro culture system. Addition of captopril caused no significant change in granulocyte-macrophage colony formation at concentrations up to 30 micrograms/ml. In the presence of CuSO4 (1-3 micrograms/ml), however, captopril caused significant inhibition of colony growth (p less than 0.05). Penicillamine, another agent associated with neutropenia and, like captopril, having a reactive thiol group, also inhibited colony formation in the presence of copper. Chemical congeners of captopril lacking a reactive thiol group and enalaprilic acid, an alternative angiotensin-converting enzyme (ACE) inhibitor, failed to show inhibition, suggesting that the thiol group and not ACE inhibition was responsible. Analysis of day-7 colonies (98% neutrophilic) and day-21 colonies (37% neutrophilic, 30% macrophagic, 27% eosinophilic, and 6% mixed) showed that neutrophil-containing colonies, but not nonneutrophilic colonies were inhibited by the addition of captopril plus copper. Catalase totally reversed the inhibition of colony formation caused by these agents. Direct measurement of oxygen consumption in the presence of captopril showed marked enhancement with the addition of CuSO4 and a 48% reduction in the presence of added catalase. These data indicate that drugs with a reactive thiol group can interact with copper to generate H2O2, which can be toxic to neutrophilic progenitor cells. We postulate that this may be an important mechanism for drug-associated neutropenia and a general mechanism for drug-induced marrow cell injury.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2841147&dopt=Abstract
J Hypertens Suppl. 1984 Dec;2(2):S89-92.
Contrasting renal haemodynamic responses to the angiotensin converting enzyme inhibitor enalapril and the beta-adrenergic antagonist metoprolol in essential hypertension.
O'Connor DT, Mosley CA, Cervenka J, Bernstein KN.
The individual target organ response to blood pressure reduction is an important criterion in the selection of appropriate antihypertensive therapy. We assessed both the renal and the systemic haemodynamic responses to antihypertensive monotherapy (five to seven weeks) with the angiotensin converting enzyme (ACE) inhibitor enalapril (n = 12), in contrast to the cardioselective beta-adrenergic blocker metoprolol (n = 11) in subjects with essential hypertension. Enalapril lowered systolic and diastolic blood pressure, and the fall in blood pressure was mediated haemodynamically by a 34% fall in systemic vascular resistance. In the kidney, glomerular filtration rate, renal plasma flow and renal blood flow were maintained by a 23% fall in renal vascular resistance. The disproportionate fall in systemic resistance versus renal resistance actually reduced the renal fraction of cardiac output. By contrast, metoprolol lowered predominantly diastolic blood pressure, with an associated 25% fall in cardiac output, without significant changes in overall systemic vascular resistance. In the renal circulation, renal perfusion was well maintained by a 20% fall in renal vascular resistance, perhaps at the efferent arteriole, without change in the renal fraction of cardiac output. Neither drug altered weight, plasma volume or total blood volume. Thus, each drug represents effective antihypertensive monotherapy, with a generally favourable, though different, renal haemodynamic profile, characterized by effective autoregulation of renal perfusion even in the face of a fall in perfusion pressure.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6100882&dopt=Abstract
Scand J Urol Nephrol Suppl. 1984;79:81-5.
Acute and subacute haemodynamic effects of enalapril. Non-invasive studies of a new converting enzyme inhibitor for antihypertensive treatment.
Wikstrand J, Herlitz H, Berglund G.
After a run-in period on placebo, 15 patients with primary hypertension got antihypertensive treatment with enalapril in single therapy during six weeks. Before and four hours after drug administration simultaneous non-invasive recordings of ECG, phonocardiogram and carotid pulse tracing or apexcardiogram or impedance cardiogram were made. After six weeks' therapy the recordings were repeated 12 hours and four hours after dose intake. The results showed enalapril to be a potent antihypertensive agent with considerable effect already four hours after the first dose intake. The blood pressure reduction was explained by a decrease in total peripheral resistance, semiquantitatively measured with impedance cardiography. Cardiac output was significantly higher during long-term treatment than before therapy started, due to a significant increase in stroke volume. Lef ventricular (LV) diastolic function was not altered but a considerable improvement in LV systolic function was achieved as judged from the systolic time intervals. Open questioning regarding side effects indicated good tolerance.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6089322&dopt=Abstract
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