Drugs online research references
Cardiovasc Res. 1989 Nov;23(11):934-40.
Delayed recovery of homogeneous perfusion distribution in isolated rat heart after vasodilatation induced by alpha 1 adrenoceptor blockade during postischaemic reperfusion.
Mohanlal RW, Mauve I, van der Valk L, Bruschke AV, van der Laarse A.
Department of Cardiology, University Hospital, Leiden, The Netherlands.
The purpose of this study was to investigate whether vasodilatation induced by doxazosin, an alpha 1 adrenoceptor blocker, during postischaemic reperfusion was able to accelerate reflow in unperfused myocardium. Isolated isovolumetrically beating rat hearts were exposed to global ischaemia by perfusion at 15 mm Hg for 2 h, resulting in an end ischaemic coronary flow rate of 2.3 (SD 1.7)% of preischaemic value, and an unperfused myocardial volume of 71.8(4.3)% of total myocardial volume. Subsequent reperfusion at 80 mm Hg for 2 h produced a partial recovery of coronary flow rate of 41(6)% in the absence of doxazosin and a complete recovery [97(28)%] in the presence of doxazosin 2 mumol.litre-1. Surprisingly, doxazosin induced vasodilatation retarded the disappearance of "no reflow" during reperfusion: after 3 h of reperfusion the volume of unperfused myocardium was 14.3(5.5)% v 1.5(1.7)% in the control group (p less than 0.005). Assessed histologically the regions of "no-reflow" were localised predominantly in the subendocardium. In the presence of doxazosin, left ventricular end diastolic pressure during reperfusion was twice as high as in the control group, indicating pronounced subendocardial compression. The mechanism underlying prolonged subendocardial "no-reflow" in the presence of doxazosin during postischaemic reperfusion is a compressive action of dilated (sub)epicardial vessels on the vasculature in the unperfused subendocardial regions ("hydraulic" or "erectile" effect of increased vascular volume). Thus coronary vasodilatation induced by alpha 1 adrenergic receptor blockade during postischaemic reperfusion delays the recovery of homogeneous transmural perfusion distribution.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2532956&dopt=Abstract
Life Sci. 1989;44(15):1013-7.
Inhibition of hepatic cholesterol synthesis by the alpha 1-adrenoceptor blocker doxazosin in the hypercholesterolemic golden hamster.
Jansen H, Lammers R, Baggen MG, Penders JM, Birkenhager JC.
Department of Biochemistry I, Medical Faculty, Erasmus University Rotterdam, The Netherlands.
The effect of treatment with the alpha 1-specific adrenoceptor blocker, Doxazosin, on lipid parameters was studied in male Golden hamsters fed a cholesterol-enriched diet. Within 1 week the Doxazosin-treated animals had a lower plasma (-12%) and hepatic (-30%) cholesterol content than the cholesterol-fed controls. De novo cholesterol synthesis in the liver was lowered by 39% in the Doxazosin-treated animals. These data indicate that the reported beneficial effect of alpha 1-blockade on plasma cholesterol levels may be due to lowering of the hepatic cholesterol synthesis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2564614&dopt=Abstract
Clin Exp Hypertens A. 1989;11 Suppl 1:247-56.
Pressor responsiveness in essential hypertension and the effects of treatment with an alpha blocker, calcium antagonist or ACE inhibitor.
Reid JL, Donnelly R, Meredith PA, Elliott HL.
Department of Materia Medica and Therapeutics, University of Glasgow, Stobhill General Hospital, Scotland.
We have studied the contribution of neurohumoral and structural factors to pressor responsiveness and peripheral resistance in mild/moderate hypertension. Pressor responses to intravenous infusions of phenylephrine (an alpha1 agonist) and angiotensin II were studied in groups of patients with essential hypertension before and after treatment, for 6 weeks with either nifedipine (20 mg bid), enalapril (20 mg daily) or doxazosin (2 mg daily). All drugs lowered blood pressure to a similar extent. Pressor responsiveness to both phenylephrine and angiotensin II showed wide intersubject variation when expressed as the dose of agonist required to raise mean arterial pressure by 20 mmHg (PD20). A group of age-matched normotensive controls showed a similar PD20 for phenylephrine to hypertensives. Angiotensin 11 sensitivity was greater in hypertensives. Drug treatment had different effects in hypertensive patients. Doxazosin, an alpha blocker, reduced the responsiveness to phenylephrine but had no effect on responses to angiotensin II. Nifedipine attenuated responses to both agonists while treatment with enalapril increased responsiveness to both phenylephrine and angiotensin II. We have not found evidence of systematic differences in alpha 1 receptor responses in hypertensives and different "vasodilator" drugs can lower blood pressure with widely different effects on adrenergic and non-adrenergic vascular responses.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2568200&dopt=Abstract
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