Drugs online research references
Clin Exp Hypertens A. 1989;11(5-6):1075-83.
Alpha blockers and vasodilating beta blockers--influence on factors involved in the pathogenesis of vascular disease in patients with hypertension.
Louis WJ, Drummer OH, Howes LG.
Department of Clinical Pharmacology & Therapeutics, Austin Hospital, Heidelberg, Vic, Australia.
Antihypertensive drugs that interact with adrenoceptors have certain advantages and disadvantages (on the treatment of hypertension). Alpha-1 antagonists such as prazosin have favorable effects on plasma lipids but may produce excessive postural falls in blood pressure, particularly following the initial dose. Recently developed alpha-1 antagonists (doxazosin, terazosin) have longer durations of action than prazosin, allowing less frequent administration. Beta blockers may be cardioprotective but in contrast to alpha-1 antagonists tend to have adverse effects on plasma lipids. Drugs with combined beta and alpha-1 blocking activity such as labetalol have favorable metabolic effects but postural hypotension remains a problem. Recently developed drugs with different alpha-1/beta blocking ratios that differ from labetalol may prove to be more popular clinically. Several beta blockers with vasodilator activity which is not due to alpha-1 blockade have also been developed. These drugs appear to have favorable metabolic effects similar to drugs with alpha-1 blocking activity, but do not cause postural hypotension.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2571433&dopt=Abstract
Am J Hypertens. 1989 Nov;2(11 Pt 1):834-9.
Hemodynamic and endocrinological effects of a new selective alpha 1-blocking agent, terazosin, in patients with essential hypertension. Results of long-term treatment.
Tomoda F, Takata M, Yoshida K, Yasumoto K, Mikawa M, Sasayama S.
Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
Thirteen patients with essential hypertension were treated with an alpha 1-adrenoceptor antagonist, terazosin (1 to 4 mg/day) for 12 months. To assess the mechanism of its antihypertensive effect, the hemodynamic and endocrinological responses to terazosin were determined before, 3, and 12 months after the administration of terazosin. Blood pressure significantly decreased within 2 weeks after the start of terazosin and its effect was sustained throughout the 12 month period. Pulse rate did not change except slight increase in the third month. The hemodynamic studies revealed that total peripheral resistance significantly decreased and cardiac output slightly increased, indicating that the antihypertensive effect of terazosin is mainly produced by its vasodilation. Blood volume and plasma volume did not change. Although plasma renin activity remained the same, plasma aldosterone significantly decreased in response to terazosin. Plasma noradrenaline increased in the third month, but returned to the baseline level in the twelfth month. Thus, terazosin monotherapy lowered blood pressure throughout one year without drug tolerance including volume expansion and/or accentuation of renin-angiotensin-aldosterone system or sympathetic function.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2574044&dopt=Abstract
J Hum Hypertens. 1989 Dec;3 Suppl 2:69-73; discussion 74.
Metabolic changes during antihypertensive therapies.
Krone W, Nagele H.
Medizinische Kernklinik und Poliklinik, Universitats-Krankenhaus Eppendorf, Hamburg, West Germany.
There is controversy whether various classes of antihypertensive drugs can reduce significantly cardiovascular morbidity and mortality in primary prevention. A failure to show this in many studies was attributed, at least in part, to deleterious effects of these drugs on lipid metabolism. Especially adrenergic antihypertensives cause marked effects on lipoprotein levels in plasma. A review of the literature revealed that beta-blockers increase triglycerides and VLDL (very low density lipoprotein)-cholesterol and may lower plasma HDL (high density lipoprotein) levels. In contrast alpha 1-adrenergic inhibitors like prazosin, doxazosin and terazosin lower triglycerides, total cholesterol, LDL (low density lipoprotein)- and VLDL-cholesterol and increase plasma HDL levels. The mechanisms by which alpha- and beta-blockers may produce the observed effects on plasma lipids and lipoproteins are not well understood. It has been shown in our laboratory that the activity of the LDL receptor of peripheral cells, a major determinant of cholesterol levels in plasma, is regulated by catecholamines via alpha 2- and beta 2-adrenergic receptors. Accordingly, blockade of these adrenoceptors with alpha- and beta-adrenergic antagonists can reverse the catecholamine effect. In addition these agents may affect lipoprotein lipase, lecithin cholesteryl acyltransferase and cholesterol ester hydrolase. These data may explain, at least in part, the plasma effects. However, long-term studies are needed to clarify the clinical value of antihypertensives with different metabolic profiles.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2575177&dopt=Abstract
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