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OBJECTIVE: Sodium depletion stimulates the renin-angiotensin and sympathetic nervous systems, which may affect the role of each of these systems in the regulation of vascular tone. We investigated the influence of sodium depletion on the roles of the angiotensin II type 1 receptor and the alpha1- and alpha2-adrenergic receptors, and on nitric oxide generation, in the regulation of human forearm vascular tone. SUBJECTS AND METHODS: We studied the effects of the angiotensin II type 1 receptor antagonist losartan (0.1-3 microg/kg per min), angiotensin II (0.01-10 ng/kg per min), the alpha1- and alpha2-adrenoceptor antagonists doxazosin (3-100 ng/kg per min) and yohimbine (0.5-4 microg/kg per min) and the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA; 7.5-60 microg/kg per min) on forearm blood flow in control subjects (n = 12) and sodium-depleted subjects (n = 11). Sodium depletion was achieved by 3 days of pretreatment with 40 mg furosemide twice a day and a sodium-restricted diet. Forearm blood flow was measured by venous occlusion plethysmography. RESULTS: Sodium depletion resulted in activation of the renin-angiotensin and sympathetic nervous systems, as indicated by increased levels of plasma renin, aldosterone and heart rate (P < 0.05). Blood pressure remained unchanged. Losartan at the highest dose increased forearm blood flow in the sodium-depleted group by 42 +/- 9%, but had no effect in controls (P < 0.05). Both doxazosin and yohimbine caused an increased vasodilatory effect in the sodium-depleted versus the control group (228 +/- 42 versus 83 +/- 13% and 192 +/- 24 versus 95 +/- 8%, respectively; P < 0.05). The constrictor effects by angiotensin II and L-NMMA of -65 +/- 6% and -79 +/- 4%, respectively, in controls were unchanged by sodium depletion. CONCLUSIONS: In sodium-depleted subjects, endogenous angiotensin II appears to play a role in the regulation of forearm vascular tone, in contrast to sodium-replete conditions. Furthermore, in these subjects the role of alpha1- and alpha2-adrenoceptors in the regulation of forearm vascular tone was enhanced compared with control conditions. Neither the forearm vascular effects of exogenously infused angiotensin II nor those of baseline nitric oxide production were influenced by sodium depletion.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10067792&dopt=Abstract
J Hypertens Suppl. 1990 Sep;8(5):S41-6.
Selective alpha 1 inhibition with doxazosin in hypertensive smokers and non-smokers: haemodynamic and metabolic effects.
Westheim A, Daae LN, Kierulf P, Brusletto B, Holme I, Syvertsen JO.
Department of Internal Medicine, Ullevaal University Hospital, Oslo, Norway.
Hypertensive cigarette smokers have an especially high risk of coronary heart disease. Doxazosin, which has beneficial effects on haemodynamic factors and lipid metabolism, may be suitable for treating these patients. The haemodynamic and metabolic effects of doxazosin were investigated in a 16-week open, parallel, comparative study of 64 heavy cigarette smokers and 69 non-smokers after a 4-week placebo period. Of the 133 patients who entered, six patients (one smoker and five non-smokers) withdrew due to adverse events. Doxazosin significantly reduced blood pressure without reflex tachycardia in both the smokers and the non-smokers. The therapeutic success rates (reduction in sitting diastolic blood pressure to less than or equal to 90 mmHg and greater than or equal to 5 mmHg reduction, or greater than or equal to 10 mmHg reduction from baseline) were similar for the smokers (93.3%) and the non-smokers (92.5%). Doxazosin significantly decreased total cholesterol and low-density lipoprotein (LDL) cholesterol, but increased high-density lipoprotein (HDL) cholesterol and the HDL:total cholesterol ratio in both smokers and non-smokers. Doxazosin corrected the reduction in HDL cholesterol caused by smoking; compared with baseline, doxazosin increased HDL cholesterol by 19% in hypertensive smokers. The beneficial effects of doxazosin on blood pressure and the lipid profile were apparent in the change in the 10-year probability of developing coronary heart disease as calculated by the Framingham equation; the calculated risk of coronary heart disease decreased by 39% in smokers and by 33% in non-smokers. Plasma fibrinogen and plasminogen activator inhibitor, which independently contribute to atherosclerosis, were significantly reduced by doxazosin in the non-smokers but not in the smokers.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1981076&dopt=Abstract
Br J Clin Pharmacol. 1990 Apr;29(4):417-22.
The pharmacokinetics of doxazosin in patients with hypertension and renal impairment.
Oliver RM, Upward JW, Dewhurst AG, Honeywell R, Renwick AG, Waller DG.
University of Southampton, Southampton General Hospital, Hampshire.
1. The pharmacokinetics of doxazosin, following a single oral dose (1 mg) and chronic oral dosing (doubling doses up to a maximum of 16 mg day-1), were studied in 18 patients with mild to moderate hypertension and stable renal function varying from normal to severely impaired. In addition, the effect of chronic administration of doxazosin on renal haemodynamics was evaluated. 2. Significant accumulation of doxazosin occurred with chronic dosing, but comparison of dose-adjusted AUC after single and chronic dosing suggested that there was no change in clearance or bioavailability during chronic administration. 3. There was no significant relationship between plasma elimination half-life or the AUC for doxazosin and the degree of renal impairment. 4. Symptomatic postural hypotension occurred in six patients following the initial dose of 1 mg doxazosin. Systolic and diastolic blood pressure measured 24 h after the previous dose were significantly reduced during chronic administration of doxazosin by a mean of 12/6 mm Hg supine and 10/7 mm Hg on standing. 5. During chronic administration of doxazosin, there was a significant reduction of 13% in glomerular filtration rate compared with pre-treatment, but no change in effective renal plasma flow.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2139337&dopt=Abstract
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