PubMed · 11028313
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K Kimura. 2000. [Water, electrolytes abnormalities].. https://pubmed.ncbi.nlm.nih.gov/11028313/
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Carvedilol, an antihypertensive agent, has been in clinical use for several years. In addition to its function as a beta-blocker, carvedilol has been shown to act as an antioxidant. However, there is some controversy as to how carvedilol achieves its antioxidative ability: by radical scavenging or ion chelation? We therefore used a method of radical generation independent of metal ions to investigate the antioxidative properties of carvedilol. We showed that carvedilol decreased low-density lipoprotein (LDL) oxidation induced by a peroxyl radical-generating system [2,2'-azobis(2-amidinopropane)hydrochloride]. Formation of thiobarbituric acid-reactive substances, lipid hydroperoxides, and newly generated epitopes on oxidised LDL was used to monitor LDL oxidation. We further showed that carvedilol was consumed during reaction with peroxyl radicals. However, carvedilol showed no reaction with nitrogen-centered radicals (1,1-diphenyl-2-picrylhydrazyl and 2,2'-azino-di-[3-ethylbenzthiazoline sulphonate]), which are often used in assays for determining antioxidative properties. On the other hand, we found that carvedilol acted as a chelator of ferric ions. Using mass spectrometry and NMR spectroscopy, we observed complex formation with free and acetylacetonate-complexed ferric ions. The binding constant with Fe(3+) was in the range of 10(5) L/mol. From our data, we concluded that carvedilol acts as both a metal chelator and a radical scavenger in vitro. However, it is selective in reacting with different radicals and is not an electron-donating radical scavenger as is alpha-tocopherol. Therefore, taking into account the low physiological concentration, the antioxidative properties reported earlier may not solely be explained by its radical-scavenging activity.
The National High Blood Pressure Education Program's Working Group on High Blood Pressure in Pregnancy recently issued a report implicating hypertension as a complication in 6 to 8 percent of pregnancies. Hypertension in pregnancy is related to one of four conditions: (1) chronic hypertension that predates pregnancy; (2) preeclampsia-eclampsia, a serious, systemic syndrome of elevated blood pressure, proteinuria and other findings; (3) chronic hypertension with superimposed preeclampsia; and (4) gestational hypertension, or nonproteinuric hypertension of pregnancy. Edema is no longer a criterion for preeclampsia, and the definition of blood pressure elevation is 140/90 mm Hg or higher. Patients with gestational hypertension have previously unrecognized chronic hypertension, emerging preeclampsia or transient hypertension of pregnancy, an obstetrically benign condition. Because distinguishing among these conditions can be done only in retrospect, clinical management of gestational hypertension consists of repeated evaluations to look for signs of emerging preeclampsia. Women with chronic hypertension should be followed for evidence of fetal growth restriction or superimposed preeclampsia. Management options for chronic hypertension in most women include discontinuing antihypertensive medications during pregnancy, switching to methyldopa or continuing previous antihypertensive therapy.