Disease relevance of urapidil

• Intraventricular urapidil administration (40 to 100 micrograms) produced a transient depressor response followed by a pressor response coupled with tachycardia [1].
• These results suggest that urapidil produces hypotension by an action on the peripheral vasculature and in the hindbrain [2].
• Acute effects of increasing doses of urapidil in patients with hypertension [3].
• The acute haemodynamic and myocardial metabolic effects of intravenous urapidil were evaluated in 12 patients with severe congestive heart failure due to coronary heart disease [4].
• This study shows that intravenous urapidil produces beneficial haemodynamic effects without a deleterious effect on myocardial metabolism in patients with heart failure due to coronary heart disease [4].

Psychiatry related information on urapidil

• Urapidil and enuresis [5].
• Urapidil, a postsynaptic alpha 1 -adrenergic antagonist, has been reported to improve intraoperative hemodynamic stability, although it has never been used to prevent the hemodynamic response of electroconvulsive therapy (ECT) [6].
• We have performed a double-blind cross over trial in 40 patients with erectile dysfunction of mixed etiology comparing SIN-1, SIN-1 plus the alpha-blocker Urapidil, and prostaglandin E1 (PGE1) in order to determine the effectiveness of SIN-1 [7].

High impact information on urapidil

• Phentolamine and urapidil increased thickening to 36+/-17% and 41+/-14% in IRA and to 48+/-11% and 49+/-17% in non-IRA myocardium respectively, and TIMI frame count decreased to 16+/-6 and to 17+/-5, respectively [8].
• The administration of 1 mg intracisternally of urapidil decreased blood pressure and heart rate in normotensive dogs, whereas 2 and 4 mg decreased heart rate and returned blood pressure to the control level [9].
• The central effect of urapidil on mean arterial blood pressure, heart rate, and reflex tachycardia was studied in anesthetized normotensive and Goldblatt hypertensive dogs and anesthetized cats [9].
• With urapidil treatment, the decrease in vascular resistance was distributed throughout all circulations, with no change in heart rate or cardiac index [10].
• Prazosin increased heart rate, whereas no change was found with urapidil [1].

Chemical compound and disease context of urapidil

• Reflex tachycardia evoked by the intravenous administration of bradykinin was suppressed in a dose-dependent manner by urapidil [9].
• Since both normotensive and hypertensive animals exhibited similar hypotensive responses after both urapidil and prazosin, the degree of alpha-receptor blockade achieved did not reveal greater sympathetic tone in renal hypertension [11].
• Comparison of urapidil and atenolol in hypertension [12].
• Effects of sodium nitroprusside and urapidil on gas exchange and ventilation: perfusion ratios in patients with congestive heart failure [13].
• Comparison between the effects of urapidil and methyldopa on left ventricular hypertrophy and haemodynamics in humans [14].

Biological context of urapidil

• In the anesthetized cat, urapidil was administered intracisternally (50 to 400 micrograms) and had no effect on heart rate [9].
• Both drugs induced dose-dependent reductions in total peripheral resistance, which resulted in reduction in left ventricular end-systolic wall stress and increases in heart rate (limited at +10 bpm with urapidil), fractional shortening, cardiac output, and the (dZ/dt)/RZ index [15].
• Following urapidil administration, cardiac index increased by 29%, mean pulmonary artery wedge pressure fell by 35% and systemic vascular resistance by 33% [4].
• Acute haemodynamic and myocardial metabolic effects of intravenous urapidil in severe heart failure [4].
• With each drug, diastolic blood pressure fell by 5 mm Hg, the corrected preejection period shortened (dihydralazine greater than urapidil), the corrected electromechanical systole did not change, and mean electrical thorax impedance rose with urapidil [15].

Anatomical context of urapidil

• Administration of urapidil (129 micrograms) into the cerebroventricles of cats revealed no effect after lateral ventricle injection, a decrease of 9.7 +/- 3.0 mm Hg after fourth ventricle injection, and an increase of 10.8 +/- 2.2 mm Hg after restriction of the drug in the forebrain ventricles [2].
• In another set of experiments (15 WKY rats and 15 SHR), the carotid compliance (microliters/mm Hg) was determined from the arterial volume-pressure relation under control conditions, after local incubation with Urapidil, and after total abolition of the vascular smooth muscle by KCN [16].
• Urapidil given either intracerebroventricularly or into the cisterna magna had no influence on baroreceptor responses [17].
• The major purpose of our study was to determine whether urapidil acts in the central nervous system (CNS) to lower arterial blood pressure [18].
• Urapidil does not impair the cardiovascular control exerted by arterial baroreceptors and cardiopulmonary receptors [19].

Associations of urapidil with other chemical compounds

• We inhibited the vascular response to the sympathetic vasomotor activity with a peripheral alpha-blocker (urapidil) and maintained mean blood pressure at control levels with angiotensin II [20].
• There was no change in heart rate in the urapidil group, but a marked reduction occurred in the atenolol group, with significant differences from placebo and urapidil (p less than 0.001) [12].
• Several potent antihypertensive drugs, such as sodium nitroprusside, labetalol and urapidil, are available to produce an immediate fall in blood pressure [21].
• On the other hand, aldosterone was less suppressed while atrial natriuretic peptide was less stimulated following the saline load when patients had been treated with urapidil [22].
• The frequency rates of responders (DBP less than 95 mm Hg) on urapidil and methyldopa were 54% and 62%, respectively, after 12 weeks [14].

Gene context of urapidil

• Our results show that urapidil derivatives bind to the 5-HT1A recognition site and that [3H]5-methylurapidil is a valuable tool for the investigation of this receptor subtype [23].
• Instead, the inhibition by urapidil of stimulation-evoked tachycardia could be accounted for by its beta 1-adrenoreceptor antagonistic effect [24].
• In a randomised double-blind study the effects on left ventricular mass (LV mass) and cardiac haemodynamics of urapidil, an antihypertensive agent with a vascular postsynaptic alpha 1-blocking action and a central antihypertensive effect, were compared with those of methyldopa in 29 patients with essential hypertension [14].
• Responses of renin, angiotensin II and catecholamines were not modified by urapidil [22].
• Urapidil increased plasma renin activity in the normotensives, but not in the hypertensives, whereas heart rate was increased and renal vascular resistance was decreased in both groups [25].

Analytical, diagnostic and therapeutic context of urapidil

• The central effects of urapidil were investigated in conscious rats with sinoaortic denervation [1].
• Intravenous injection (1 mg/kg) of Urapidil, a selective alpha 1-adrenergic antagonist, induced a significant decrease in arterial pressure (-26%, p less than 0.01 and -37%, p less than 0.001 in WKY rats and SHR, respectively) without significant changes in cardiac output [16].
• It is concluded that urapidil, given intravenously, has an immediate blood pressure lowering effect associated with a fall in renal vascular tone and an increase in renal perfusion [26].
• In order to evaluate the acute effects of urapidil on renal vascular tone and on pressor systems we performed a randomised placebo-controlled crossover study in 8 patients with uncomplicated essential hypertension [26].
• In clinical trials urapidil therapy resulted in significant reductions in blood pressure in patients with mild to severe essential hypertension, with little influence on heart rate [27].

References