Effects of prazosin on forearm resistance and capacitance vessels

Awan, Najam A.; Miller, Richard R.; Maxwell, Kevin S.; Mason, Dean T.

doi:10.1002/cpt197722179

Cited by 60 publications

(8 citation statements)

References 9 publications

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“…Volume depletion and venodilation reduce the venous return to the right side of the heart, and may cause postural hypotension (Weissler et al, 1957). Prazosin dilates human veins in vitro (Jauernig, Moulds & Shaw, 1978), and in vivo (Awan et al, 1977). Prazosin is at least five times more potent at venous than at arterial sites in normal man (Collier, Lorge & Robinson, 1978).…”

Section: Discussionmentioning

confidence: 99%

Acute and Chronic Cardiovascular Effects of Indoramin and Prazosin in Normal Man

Nicholls¹,

Harron²,

Shanks³

1981

Brit J Clinical Pharma

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The effect of single and repeated oral doses of indoramin 25 mg, prazosin 1 mg and placebo on arterial pressure and heart rate supine, standing and after exercise was studied in five normal volunteers. Each study period lasted four days. Observations were made before, and at 1, 2, 3, 4 and 6 h after drug administration on days 1 and 4. On days 2 and 3, the drugs were administered 8‐hourly, and observations made before and 2 h after the morning dose on each day. Neither drug changed arterial pressure or heart rate in the supine position, or after exercise. Neither drug reduced standing diastolic arterial pressure. On day 1, indoramin reduced standing systolic arterial pressure from 119.0 ± 3.4 mm Hg (mean ± s.e. mean) to 100.0 ± 10.3 mm Hg at 2 h (P<0.01) and 99.4 ± 7.6 mm Hg at 4 h (P<0.01). This reduction was accompanied by a slight increase in heart rate, which was not significant (P>0.05). The effects of indoramin on arterial pressure and heart rate observed on day 4, after repeated drug administration, were similar. On day 1, prazosin produced a slight reduction in standing systolic arterial pressure which was not significant (P>0.05). This reduction was accompanied by a marked increase in standing heart rate, from 85.0 ± 3.9 beats min−1 to 108.8 ± 3.6 beats min−1 at 2 h (P<0.01) and 101.6 ± 5.9 beats min_1at 4 h (P<0.05). On day 4, prazosin reduced standing systolic arterial pressure to the same extent as indoramin, with no increase in heart rate. The effects of the two drugs were similar on day 4, but different on day 1. One subject became syncopal after the first dose of prazosin, and another subject after both prazosin and indoramin. Plasma renin activity (PRA) was reduced by placebo on day 4 (P<0.02), and increased by prazosin on day 1 (P<0.05). Indoramin had no effect on PRA. The difference in effects observed after indoramin and prazosin administration may be related to their relative potency at arterial and venous sites. Indoramin may be less likely than prazosin to produce a first‐dose effect in normal subjects.

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Section: Discussionmentioning

confidence: 99%

Acute and Chronic Cardiovascular Effects of Indoramin and Prazosin in Normal Man

Nicholls¹,

Harron²,

Shanks³

1981

Brit J Clinical Pharma

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“…Our data do not allow conclusions to be drawn about the mechanism of the observed changes but permit us to suggest a relevant hypothesis. t1f2 is related to the blood clearance (CI) of a drug and its extent of tissue distribution (Vd) and can be expressed as shown in Equation 1. t1f2 = ~~ x 0.693 (1) Area under the curve is a function of the fraction of drug absorbed (bioavailability or F), the clearance, and the extent of tissue distribution, as shown in Equation 2.…”

Section: Discussionmentioning

confidence: 99%

Influence of congestive heart failure on prazosin kinetics

Jaillon

Rubin

Yee

et al. 1979

Clin Pharma and Therapeutics

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The kinetics of oral prazosin was studied in 10 healthy normal subjects (NS) and in 9 patients with congestive heart failure (CHF). NS received a single 5-mg dose, and blood concentrations of prazosin (CB) were measured, using a specific HPLC assay, during an 8-hr period. CHF patients received a 2-mg dose after which CB was measured for 10 hr. These patients then received 2 to 5 mg prazosin every 8 hr for 48 hr. After the last dose of prazosin, CB was measured for 24 hr. After the initial dose, time to peak CB did not differ significantly between that of the NS (123 +/- 19 SEM min) and of patients with CHF (132 +/- 31.3 min). AUC/mg prazosin was greater (p less than 0.001) in patients with CHF (3,385 +/- 380 Ng x min/ml) than in NS (1,603 +/- 208 ng x min/ml). Elimination of prazosin from blood was slower in CHF patients (t1/2 = 374 +/- 33.4 min) than in NS (t1/2 = 144.5 +/- 4.3 min) (p less than 0.001). These data suggest that in patients with CHF the elimination of prazosin is substantially slower than in NS and therefore higher steady-state prazosin concentrations can be expected in CHF patients than in NS.

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“…Basal plasma renin activity and plasma aldosterone were decreased by prazosin as well as by propranolol. However its mechanism has not been elucidated: it is postulated that prazosin (1) is a specific blocker of al-receptors (Brogden et al, 1977;Cambridge et al, 1977;Cavero et al, 1978); (2) has a combined action of reducing vascular tone in both resistance and capacitance vessels (Awan et al, 1977), and (3) may cause fluid retention (Ibsen et al, 1978;Koshy ef al., 1977).…”

Section: Discussionmentioning

confidence: 99%

Haemodynamic and Hormonal Effects of Prazosin on Head‐up Tilt in Essential Hypertensive Patients: Comparison With Those of Propranolol

Kida

Morotomi

Higa

et al. 1984

Clin Exp Pharma Physio

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To evaluate the haemodynamic and hormonal effects of prazosin, head-up tilt was performed in 10 essential hypertensive patients, and these effects of prazosin on the tilt were compared with those of propranolol. The tilts were performed in control phase and the last days of treatment for two weeks with propranolol (90 mg/day) or prazosin (3-6 mg/day). Each drug significantly lowered the mean blood pressure at rest, and also suppressed its rise on the tilt. Heart rates were significantly increased by the tilt in the control phase, in the propranolol phase and in the prazosin phase. Cardiac index was significantly reduced by the tilt from 2.66 (s.e.m. = 0.22) 1/min per m2 to 2.08 (s.e.m. = 0.20) in the propranolol phase. However, there were not significant changes in other phases. Total peripheral resistance indices were significantly increased by the tilt in all three phases. Plasma renin activity and plasma aldosterone were significantly increased by the tilt from 2.14 (s.e.m. = 0.47) ng/ml per h to 2.46 (s.e.m. = 0.54) and from 50.6 (s.e.m. = 12.9) pg/ml to 74.9 (s.e.m. = 14.9) respectively, in the control phase. And they were also significantly increased from 1.06 (s.e.m. = 0.29) to 1.65 (s.e.m. = 0.45) and from 41.4 (s.e.m. = 16.3) to 54.0 (s.e.m. = 17.4) in the prazosin phase. There were no significant increases during the administration of propranolol. We observed that prazosin did not alter heart rate and cardiac index, but suppressed the renin-angiotensin system at rest. It is suggested that prazosin did not influence haemodynamic and hormonal responses to the tilt.

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Effects of prazosin on forearm resistance and capacitance vessels

Cited by 60 publications

References 9 publications

Acute and Chronic Cardiovascular Effects of Indoramin and Prazosin in Normal Man

Acute and Chronic Cardiovascular Effects of Indoramin and Prazosin in Normal Man

Influence of congestive heart failure on prazosin kinetics

Haemodynamic and Hormonal Effects of Prazosin on Head‐up Tilt in Essential Hypertensive Patients: Comparison With Those of Propranolol

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