Acute Blood Pressure Reduction Research Articles

The use of short-acting (SA) nifedipine in acute blood pressure reduction in hospitalized hypertensive children

The use of short-acting (SA) nifedipine in acute blood pressure reduction in hospitalized hypertensive children

Acute and chronic reduction of blood pressure by CPAP in patients with refractory hypertension and obstructive sleep apnea

Acute and chronic reduction of blood pressure by CPAP in patients with refractory hypertension and obstructive sleep apnea

Effect of acute blood pressure reduction on vascular responses in the brachial arteries of essential hypertensive patients

Effect of acute blood pressure reduction on vascular responses in the brachial arteries of essential hypertensive patients

Sympathoexcitatory responses to the acute blood pressure fall induced by central or peripheral antihypertensive drugs

This study was designed to evaluate the effects of an acute blood pressure reduction brought about by a peripheral vasodilator agent (prazosin) or by a drug combining central and peripheral modes of action (urapidil), on three markers of adrenergic tone such as muscle sympathetic nerve traffic (MSNA), venous plasma norepinephrine (NE), and heart rate (HR). In 12 untreated essential hypertensives (age, 50.7 ± 1.9 years; mean ± SEM), we evaluated in two experimental sessions, according to a double-blind crossover design, the effects of acute oral administration of 2 mg prazosin or 30 mg urapidil on beat-to-beat finger blood pressure (Finapres), HR (electrocardiogram), NE (high-performance liquid chromatography), and MSNA (microneurography at a peroneal nerve). In each session measurements were performed in the no-drug control state and repeated throughout a 3-h period after drug administration. For similar blood pressure reductions, the two drugs caused similar increases in NE and MSNA (peak effects: NE = +1.1 ± 0.2 vs 0.9 ± 0.2 nmol/L and MSNA = +10.9 ± 1.8 vs +10.1 ± 1.6 bursts/min for prazosin and urapidil respectively, P = ns between drugs), whereas HR increased more markedly after prazosin administration (+6.1 ± 1.1 vs +2.4 ± 0.8 beats/min, P < 0.05). These data provide evidence that acute blood pressure reductions induced by antihypertensive drugs with central or peripheral modes of action activate the sympathetic nervous system to a similar extent. Thus adrenergic activation is not peculiar to vasodilators but rather generalized to any drug-induced acute blood pressure fall, presumably because of the lack of a baroreflex resetting, which occurs during chronic but not during acute antihypertensive treatment.

Resetting of renal blood autoregulation during acute blood pressure reduction in hypertensive rats.

Decrease in systemic blood pressure, duration of pressure decrease, and change in the activity of the renin or the sympathetic nervous system may represent mechanisms involved in resetting the renal blood flow (RBF) autoregulation found in hypertensive rats. Autoregulation of RBF, plasma renin concentration (PRC), and the time needed for resetting to take place were studied in the nonclipped kidney before and after removal of the clipped kidney of two- kidney, one-clip (2K1C) hypertensive rats and before and after mechanical reduction of the renal arterial pressure (RAP) for 10 min in the spontaneously hypertensive rat (SHR) and in the nonclipped kidney of 2K1C hypertensive rats with and without renal denervation. Mean arterial pressure (MAP) fell from 147 to 107 mmHg 30 min after removal of the clipped kidney, and the lower pressure limit of RBF autoregulation decreased from 113 to 90 mmHg (P < 0.01); PRC fell. Mechanical reductions of RAP from 161 to 120 mmHg in the nonclipped kidney for 10 min did not change RBF, but at 120 mmHg, the lower pressure limit of RBF autoregulation was reduced from 115 mmHg before pressure reduction to 96 mmHg afterwards (P < 0.02). In SHR, similar pressure reduction for 10 min decreased the lower pressure limit of RBF autoregulation from 106 to 86 mmHg (P < 0.01). PRC was unchanged in both models, and denervation did not change RBF autoregulation. When RAP was reduced below the lower pressure limit of RBF autoregulation, RBF decreased approximately 20%; the lower pressure limit of RBF autoregulation remained unchanged. In normotensive Wistar-Kyoto rats, pressure reduction did not change the range of RBF autoregulation. These results indicate that acute normalization of the pressure range of RBF autoregulation in hypertensive rats is dependent on the degree of pressure reduction of RAP, whereas renal innervation and PRC do not play a major role. We propose that the mechanism of resetting is due to afterstretch of noncontractile elements of the vessel wall or is caused by pure myogenic mechanisms. An effect of intrarenal angiotensin cannot be excluded.

Blood pressure control after acute stroke

Although long-term blood pressure control is known to prevent stroke, acute blood pressure reduction after stroke is associated with worse neurological and functional outcome. Chronic blood pressure reduction for secondary prevention of stroke is presently being tested within the PROGRESS trial. This study uses angiotensin-converting enzyme (ACE) inhibitor-based treatment (perindopril) versus placebo. ACE inhibitors may reduce blood pressure without adversely affecting cerebral blood flow. We have recently reported elsewhere that perindopril 4 mg once daily, initiated within 2-7 days of acute ischaemic stroke, reduces blood pressure without adverse effects on cerebral blood flow as measured by Doppler ultrasound. Nevertheless, the optimal policy with regard to blood pressure management in the first 48 h after acute stroke remains uncertain. A clinical trial is proposed to establish whether it is better to maintain pre-existing antihypertensive therapy or to discontinue this temporarily.

Relationship between mechanical properties of the carotid artery wall and baroreflex function in acutely treated hypertensive patients.

To evaluate the relationship between the mechanical properties of the carotid artery wall and baroreflex function after acute reduction of blood pressure with lacidipine in essential hypertension. After 15 days of placebo washout, the hypertensive patients underwent a single-blind haemodynamic study before and 90 min after administration of 4 mg lacidipine (a dihydropyridine calcium antagonist). Brachial intra-arterial blood pressure was recorded in eight mild-to-moderate essential hypertensive patients aged 40-53 years (mean +/- SEM 46.8 +/- 4.7 years). The carotid pulse diameter was recorded simultaneously by an echo-tracking technique. The mechanical properties of the carotid artery wall were evaluated by calculating Peterson's incremental elastic modulus (Ep) both as an averaged value of 10 heart cycles with stable blood pressure and was the dynamic correlation, on a beat-to-beat basis, of Ep and the systolic blood pressure during a 20 mmHg increase in blood pressure following a bolus injection of phenylephrine. The elastic properties of the carotid artery were investigated further by determining the correlation between the systolic pressure and systolic diameter, beat by beat, during a ramped increase of blood pressure after phenylephrine administration. The baroreceptor reflex sensitivity was measured simultaneously by the Oxford method and by correlating Ep and the electrocardiographic R-R' interval on a beat-to-beat basis during phenylephrine injections. After lacidipine administration Peterson's elastic modulus, measured under resting steady-state conditions, was reduced (18.7 +/- 7.4 versus 16.4 +/- 6 x 10(5) dyne/cm2), whereas the baroreflex sensitivity was unchanged (6.6 +/- 3.3 versus 6.3 +/- 0.2 ms/mmHg) and resetting of the baroreflex had occurred. At the same time, the correlations between the systolic blood pressure and Ep and between the systolic blood pressure and carotid systolic diameter over a 20 mmHg increase in blood pressure were unchanged. Moreover, the correlations between the systolic blood pressure and the R-R' interval and between Ep and R-R' interval during the phenylephrine-induced blood pressure increase did not differ statistically. The results suggest that the resetting of the baroreflex after the acute reduction in blood pressure caused by lacidipine is dissociated from mechanical changes in the carotid artery wall.

Platelet Lipoxygenase in Spontaneously Hypertensive Rats

We have previously reported that the nonselective lipoxygenase inhibitor phenidone is a potent hypotensive agent in the spontaneously hypertensive rat (SHR). In the present study, we examined the relationship between production of platelet 12-hydroxyeicosatetraenoic acid (12-HETE) and intra-arterial blood pressure in SHR and Wistar-Kyoto rats (WKY) using both a cross-sectional analysis and an acute pharmacological intervention. Basal generation rate of 12-HETE by platelets collected from the SHR was approximately 3.7-fold higher than in the WKY (0.86 +/- 0.24 versus 0.23 +/- 0.05 nmol/mL per 10 minutes, respectively; P < .01). Systolic arterial pressure was positively related to platelet 12-HETE formation rate when the entire rat population was considered (r = .70, P < .001). The specific 12-lipoxygenase inhibitor cinnamyl-3,4-dihydroxycyanocinnamate induced lowering of both arterial blood pressure and platelet 12-lipoxygenase activity in SHR. At 15 mg/kg, cinnamyl-3,4-dihydroxycyanocinnamate elicited a marked hypotensive effect in SHR but not in WKY. This reduction in arterial pressure was accompanied by an approximate 70% inhibition in platelet 12-HETE production rate. The return of high blood pressure to basal levels was associated with a significant rise in the production of platelet 12-HETE toward control values (baseline, 0.97 +/- 0.33 nmol/mL per 10 minutes; nadir of blood pressure, 0.19 +/- 0.03; resumption of basal pressure, 0.42 +/- 0.14). In contrast, captopril (15 mg/kg) induced a quantitatively similar decrease in blood pressure but had no effect on platelet 12-HETE generation rate. Thus, hypertension in SHR is linked to increased production rate of platelet 12-HETE. Acute blood pressure reduction attained during lipoxygenase inhibition but not by angiotensin converting enzyme inhibition leads to a concomitant reduction in the production of platelet 12-HETE. We speculate that since rat arterial tissue produces 12-HETE, increased 12-lipoxygenase activity in SHR may contribute to the maintenance of elevated arterial pressure in this strain.

Role of nitric oxide in the control of blood pressure in young and adult spontaneously hypertensive rats.

1. The depressor response to sodium nitroprusside (SNP) and the pressor response to Nomega-nitro-L-arginine methyl ester (L-NAME) were investigated in anaesthetized and ganglion-blocked 6 week old (young) and 20 week old (adult) spontaneously hypertensive rats (SHR), and the results were compared with those in age-matched normotensive Wistar-Kyoto (WKY) rats. 2. SNP produced a dose-dependent decrease of the mean blood pressure (BP) in both strains, and no differences in vascular sensitivity to SNP were observed between the strains. 3. L-NAME caused dose-dependent pressor responses in both strains. The sensitivity and the maximal response to L-NAME in SHR were significantly greater than those in age-matched WKY (P< 0.05 or 0.01; t-test, 13 d.f. in both ages). However, there were no significant differences in the responses between ages in each strain. 4. Acute reduction of BP induced by 7-O-ethylfangchinoline did not affect the responses to SNP and L-NAME in the adult SHR. 5. These results indicate that a greater amount of NO is tonically released in SHR and that its contribution to BP control is greater in SHR than in WKY, whereas vascular sensitivity to NO does not differ between the strains. In addition, acute changes in BP do not affect the degree of dependency on NO for BP control.

Nifedipine and Mortality

When an approved treatment is considered for an unapproved indication, the physician must evaluate the safety of the medication, its value in related conditions, and the individual patient. What is asked is that he make a prudent decision based upon full knowledge of the available evidence.”1 Furberg and his colleagues2 entitle their article “Nifedipine: Dose-Related Increase in Mortality in Patients With Coronary Heart Disease.” They provide a valuable service by making us think more carefully about the benefit/risk ratio of the calcium antagonists as a group. However, by touting calcium antagonists as being unsafe and possibly lethal, they also create a great deal of uncertainty and anxiety among physicians and patients. We feel that they overstate their case. The following is an attempt to show that (1) the allegations focus on short-acting nifedipine, so that even if correct, they cannot be applied to other calcium antagonists; (2) the accusation of a dose-related increase in mortality rests on a biased selection of data chosen for the meta-analysis; and (3) several of the mechanisms suggested for the proposed adverse effects are unlikely. Finally, we shall argue that pharmaceutical companies have been remiss in not obtaining outcome studies for short-acting nifedipine and for other calcium antagonists, especially in the case of ischemic heart disease. Several aspects of the Furberg paper suggest that calcium antagonists in general are accused; for example, the statement that “the literature reviews strongly suggest that the problem may go beyond short-acting nifedipine. Troubling and major adverse cardiovascular events have been linked to other calcium antagonists, primarily dihydropyridines.” It should be clearly and unequivocally stated that Furberg et al2 provide no evidence whatsoever for any adverse effect on mortality or morbidity for any other agent, with one important exception. That exception is nimodipine, approved for use in …

Hemodynamic Effects of Dilevalol Following Acute and Long-Term Administration in Normal and Hypertensive Subjects.

Forearm hemodynamics using pulsed Doppler flowmetry were studied in 12 healthy volunteers and 20 patients with mild to moderate hypertension before and after acute and long-term oral administration of the beta-blocking agent dilevalol. The study was performed using a double-blind design versus placebo. Both 200-mg and 400-mg dosages produced a significant acute blood pressure reduction in normotensive and hypertensive subjects. In hypertensive subjects, forearm vascular resistance was poorly modified, brachial artery diameter decreased significantly but only with long-term administration of the 400-mg dosage. A significant reduction in brachial artery tangential tension was consequently observed. The study provides evidence that Dilevalol produced a significant decrease in blood pressure in normotensive and hypertensive subjects in association with a decrease in brachial artery tangential tension.

The effect of acute volume expansion and vasodilatation with verapamil on uterine and umbilical artery Doppler indices in severe preeclampsia

Preeclampsia is associated with increased peripheral, uterine, and umbilical artery resistance. Acute blood pressure reduction may result in shunting of blood and sudden fetal distress. We therefore investigated the effects of volume expansion and verapamil therapy on uteroplacental and umbilical resistance during treatment of preeclampsia. Five severe preeclamptics underwent volume expansion and subsequent vasodilatation with an infusion of verapamil. Invasive hemodynamic monitoring and Doppler ultrasonography were used to study changes in maternal, uterine, and umbilical hemodynamics. Volume expansion and subsequent verapamil therapy was associated with significant changes in maternal hemodynamics without significant change in uteroplacental or umbilical resistance. Uterine artery waveform changes were noted, with disappearance of notching in some cases. Volume expansion and verapamil therapy effectively reduces maternal blood pressure in preeclampsia, without adversely affecting uteroplacental or umbilical artery resistance. Uterine artery waveform changes may be associated with improved fetal outcome.

Renin Responses in Patients with Orthostatic Hypotension: Case Reports

In orthostatic hypotensive patients renin is reported to increase in response to head-up tilt unless the lesion involves postganglionic sympathetic efferent nerves. The authors examined responses of plasma renin activity (PRA) to acute blood pressure reduction in 4 patients with orthostatic hypotension. When the coexistence of normal plasma norepinephrine (PNE) and normal or high-normal pressor response to alpha stimulant is considered to be a sign of preserved function of postganglionic fibers, 2 of the patients had sympathetic lesions mainly confined to central and/or preganglionic fibers. They were diagnosed as having multiple system atrophy (MSA). The other 2 were diagnosed as having idiopathic orthostatic hypotension with possible postganglionic lesions. Although 1 MSA patient showed an increase in PRA from 2.0 to 4.7 ng/mL/hr in response to the tilt, the other MSA patient showed no PRA response to the tilt. The head-up tilt did not provoke an apparent PRA response in patients with idiopathic orthostatic hypotension. The authors infused sodium nitroprusside (SNP) in the 3 patients whose PRA did not respond to the head-up tilt. The infusion decreased blood pressure by 40 mmHg or more, but PRA responses were inappropriately small or suppressed. In all cases, PNE did not respond at all to the head-up tilt and to the infusion of SNP. These findings suggest that possible preservation of postganglionic fibers does not necessarily indicate an intact responsiveness of PRA. The PRA profiling may not be an accurate predictor for the site of the fiber degeneration in orthostatic hypotension.

Electrocardiographic Changes During Acute Treatment of Hypertensive Emergencies With Sodium Nitroprusside or Fenoldopam

Electrocardiograms are routinely obtained before and during the acute treatment of hypertensive emergencies, usually to rule out "ischemic changes." Despite a few anecdotal reports of electrocardiographic changes, little is known about the incidence and significance of such changes, or their relationship to the treatment used. We prospectively analyzed 12-lead electrocardiograms from 21 patients admitted for hypertensive emergencies (average blood pressure, 222 +/- 4/140 +/- 3 mm Hg). Patients were randomly assigned to treatment with sodium nitroprusside (n = 11) or the dopamine receptor agonist fenoldopam mesylate (n = 10). Electrocardiograms were obtained at baseline and within 30 minutes of reaching goal blood pressure (diastolic blood pressure, 100 to 110 mm Hg). There was no significant effect of either drug treatment on PR interval, QRS duration, QT interval, or R-wave amplitude, and no major ST-segment changes were noted. During treatment with either drug, the average T-wave amplitude decreased in all leads except aVR. New T-wave inversions in lead V4 occurred in two and four patients after fenoldopam and nitroprusside treatment, respectively. There were no clinically apparent episodes of myocardial ischemia in any patient. Even in the absence of obvious myocardial ischemia, a decrease in T-wave amplitude, including T-wave inversion, occurs commonly during acute blood pressure reduction in hypertensive emergencies, an observation that may be explained by the accompanying acute changes in cardiac chamber volumes.

Exercise Performance in Patients with Uncomplicated Essential Hypertension: Effects of Nifedipine-induced Acute Blood Pressure Reduction

In untreated patients with uncomplicated essential hypertension, exercise induces an abnormal increase in blood pressure; the influences of this increase on exercise were evaluated by a cardiopulmonary exercise test (CPX) performed in control conditions (step 1) and during acute blood pressure reduction (step 2). Patients were classified as (1) normotensive (resting diastolic blood pressure [BPd] less than 90 mm Hg; n = 14), (2) mildly hypertensive (BPd of 90 to 104 mm Hg; n = 9), and (3) moderately to severely hypertensive (BPd greater than or equal to 105 mm Hg; n = 16). For the three groups, peak mean blood pressure during exercise was 125 +/- 5 mm Hg (mean +/- SEM), 144 +/- 3 mm Hg (p less than 0.01 vs normotensive), and 161 +/- 4 mm Hg (p less than 0.01 vs normotensive and p less than 0.01 vs mild hypertension), respectively. Oxygen consumption (VO2) at peak exercise and at ventilatory anaerobic threshold was 26.1 +/- 1.1 and 17.2 +/- 0.5 ml/min/kg, 25.4 +/- 1.1 and 16.9 +/- 0.8 ml/min/kg, and 26.4 +/- 1.3 and 17.5 +/- 1.2 ml/min/kg in normotensive subjects, those with mild hypertension, and those with moderate to severe hypertension, respectively. Fourteen normotensive subjects, six with mild hypertension, and nine with moderate to severe hypertension participated to step 2 (nifedipine vs placebo, double-blind crossover). Nifedipine reduced blood pressure at rest and at peak exercise in those with hypertension. Peak exercise VO2 was unaffected by nifedipine in both normotensive subjects and those with hypertension. With nifedipine, ventilatory anaerobic threshold occurred earlier and at a lower VO2 in mild and in moderate to severe hypertension (delta VO2 = -1.9 and -2.4 ml/min/kg, respectively). These findings might be due to nifedipine-induced redistribution of blood flow during exercise and might be the reason for the complaint of weakness after blood pressure reduction in hypertensive subjects.

The effect of acute and chronic antihypertensive therapy on maternal and fetoplacental Doppler velocimetry

Maternal and feto-placental Doppler flow velocity waveforms were studied during acute and chronic antihypertensive therapy in patients with pregnancy-induced hypertension. Eight primigravidae were acutely treated with oral nicardipine. Diastolic blood pressure fell at 30, 45 and 60 min after nicardipine. The uteroplacental systolic/diastolic ratio rose significantly at 30 min, but this change was no longer apparent at 60 min. Umbilical artery and maternal brachial artery systolic/diastolic ratios were unchanged. Fifteen patients with mild pre-eclampsia were chronically treated with oral pindolol. Diastolic blood pressure fell significantly within 24 h. The uteroplacental systolic/diastolic ratio rose 3 days after pindolol. Brachial artery or umbilical artery systolic/diastolic ratios were unchanged. A control group of 15 patients with untreated mild pre-eclampsia showed a significant rise in uteroplacental and umbilical artery systolic/diastolic ratios within 7 days of starting recordings. In patients with pregnancy-induced hypertension, acute and chronic blood pressure reduction was associated with no change in umbilical artery or maternal brachial artery Doppler systolic/diastolic ratios and a transient rise in the uteroplacental systolic/diastolic ratio.

Severe hypertension induces disturbances of renal autoregulation.

To study if the severity of hypertension could be associated with disturbances of the autoregulation of renal blood flow and glomerular filtration, we compared the renal hemodynamic and functional responses to acute blood pressure reductions of a group of patients with moderate essential hypertension (n = 10) with those of a group of patients with severe hypertension (n = 10). Blood pressure was reduced to normal levels by a stepwise infusion of sodium nitroprusside, and effective renal blood flow (by 131I-hippuran), glomerular filtration rate (by endogenous creatinine clearance), and filtration fraction were determined. After acute blood pressure normalization, effective renal blood flow and glomerular filtration rate were significantly reduced in patients with severe hypertension (-41.6 +/- 8.3% and -44.7 +/- 6.8%, respectively; p less than 0.01 for both) but not in those with moderate hypertension (+4.9 +/- 9.1% and +6.2 +/- 13.3%, respectively; NS). Filtration fraction remained unchanged in both groups. These results show that severe but not moderate essential hypertensive patients have a displacement to the right of the lower limit of the renal autoregulation curve due to impaired vasodilation to maintain adequate renal blood flow during acute reductions of blood pressure. This impairment may be due to anatomic or functional defects of preglomerular vessels, or to both. Furthermore, the inability to maintain adequate glomerular filtration in these circumstances shows that patients with severe hypertension also have an impaired ability to adjust postglomerular vasomotor tone in the face of reductions in glomerular blood flow.

Coronary microvascular disease in hypertensives.

Arterial hypertension can badly affect coronary circulation through several mechanisms that are not mutually exclusive, namely, coronary artery disease, left ventricular hypertrophy, and microvascular disease. Theoretical and experimental data suggest that coronary microvascular disease may exist in hypertensives, in whom it can cause both a reduction of coronary flow reserve and a shift to the right of the coronary flow autoregulation curve. To address this issue, we used dipyridamole- echocardiography test, which causes ischemic-like ST segment depression with no detectable changes in left ventricular function in different subsets of patients with microvascular disease (Syndrome X; Hypertrophic cardiomyopathy; acute heart rejection). We found that dipyridamole infusion can cause a similar pattern of response (i.e., echocardiographically silent ST segment depression) in mild-moderate essential hypertensives with normal epicardial coronary arteries, without left ventricular hypertrophy, with increased forearm minimal vascular resistances and with a reduced coronary reserve. This pattern of response identifies hypertensives with higher risk of ventricular arrhythmias, is amplified by acute reduction of diastolic blood pressure and can be reversed, together with the reduction of forearm vascular resistances by chronic antihypertensive treatment. Taken together these findings suggest that microvascular coronary disease can exist in hypertensives with two adverse consequences, consistent with the experimental background: the reduction of coronary flow reserve as well as a shift to the right of the coronary flow autoregulation curve.

Acute and chronic hemodynamic effects of drugs with different actions on adrenergic receptors: A comparison between alpha blockers and different types of beta blockers with and without vasodilating effect

The regulation of vascular resistance, cardiac output, and thus blood pressure can be influenced by antihypertensive drugs acting at central and peripheral adrenergic receptors. The results presented here are from acute or chronic studies in 205 patients with mild or moderately severe essential hypertension: beta blockers (N = 101); alpha blockers (N = 36); a separate alpha- + beta-blocker combination or the combination agent labetalol (N = 37); prizidilol, a beta-blocker/vasodilator (N = 14); and dilevalol, a beta blocker/beta 2-stimulator (N = 17). Beta blockers without strong intrinsic sympathomimetic activity reduce heart rate and cardiac output immediately, but due to a reflex increase in total peripheral resistance index, blood pressure is unchanged or only slightly reduced. During chronic use, total peripheral resistance drops towards pretreatment level and pressure falls. Beta blockers with strong intrinsic sympathomimetic activity do not reduce heart rate or cardiac output at rest when sympathetic tone is low. During exercise, heart rate and cardiac output are reduced, but less than with conventional beta blockers, and resistance is unchanged or slightly reduced. An acute and chronic reduction in blood pressure can be produced by alpha-adrenergic receptor blockers (prazosin, doxazosin, trimazosin), and in these cases the fall occurs via a reduction in total peripheral resistance index without reflex tachycardia. These drugs tend to increase exercise stroke volume and cardiac output during chronic treatment. Free combinations of beta and alpha blockers or the use of the fixed combination drug, labetalol, induce marked reductions in blood pressure at rest and during exercise, mainly through a reduction in total peripheral resistance index. During chronic treatment, exercise stroke volume and cardiac output are well maintained. In acute studies with dilevalol, systolic blood pressure, diastolic blood pressure, and mean arterial pressure were reduced (p less than 0.001) within 1 hour in 17 males with essential hypertension (WHO stage I) who received 200-400 mg oral dilevalol. The reduction in MAP was around 16-17% and was associated with an immediate fall in the total peripheral resistance index of the same magnitude (14%, p less than 0.001) after 1 hour at rest. There were no significant changes in heart rate or cardiac index.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute blood pressure reduction causes left ventricular functional impairment in hypertensive patients with coronary heart disease and left ventricular hypertrophy

Acute blood pressure reduction causes left ventricular functional impairment in hypertensive patients with coronary heart disease and left ventricular hypertrophy