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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium-entry blockade produced by verapamil was studied in 13 subjects with sustained essential hypertension. Noninvasive echo-Doppler methods were used to evaluate cardiac structure and function, maximum aortic acceleration (used as an indirect index of cardiac performance), and carotid-femoral pulse-wave velocity. Measurements were performed in baseline conditions, following 12 weeks of active treatment, and 4 weeks of placebo. Following verapamil, blood pressure (BP) significantly decreased (p less than 0.001) with a slight reduction in cardiac output (p less than 0.05) and a more substantial decrease in heart rate (p less than 0.002). No significant change occurred in maximum acceleration and in the curve relating percent fractional shortening to end-systolic stress, suggesting that verapamil decreased BP with minor changes in cardiac performance. Cardiac mass decreased by approximately 6.3% whereas pulse-wave velocity did not change, suggesting that the small decrease in cardiac mass could be related to the lack of improvement in the capacitative component of vascular impedance, as judged from the determination of pulse-wave velocity. The study provides evidence that calcium blockade due to verapamil results in a dissociation between the antihypertensive effect and the absence of significant changes in cardiac and arterial structure and function.
J Cardiovasc Pharmacol 1991
PMID:Cardiac mass and aortic distensibility following calcium blockade in hypertension. 171 91

Serotonin (5-HT) released from activated blood platelets plays a pivotal role in the development of thromboembolic complications. Essential hypertension, elevated plasma cholesterol, older age, and smoking are predisposing factors for these vascular events, and they all lead to platelet activation. In hypertensive patients, platelet 5-HT uptake is reduced with increasing age and blood pressure. This uptake inhibition is paralleled by an exaggerated platelet shape change and aggregation response. As a consequence, periplatelet 5-HT plasma concentrations are increased and promote further platelet aggregation and vasoconstriction. Low-density lipoproteins (LDL) induce a platelet shape change reaction and amplify the aggregatory response to serotonin. This effect is enhanced in smokers and even greater in hypertensive patients. LDL also inhibit endothelium-dependent relaxations to serotonin thereby unmasking the vasoconstrictor effect. 5-HT2-Receptor blockade with ketanserin interferes with this chain of events at several sites. Ketanserin inhibits platelet 5-HT release and 5-HT-induced platelet aggregation. It exerts a beneficial influence on the lipid profile. Blockade of 5-HT2 receptors leads to direct vascular smooth muscle dilatation as well as unopposed activation of endothelial 5-HT1-like receptors with the subsequent release of endothelium-derived relaxing factor. Taken together, the antihypertensive agent ketanserin may provide a new approach for multiple risk factor intervention therapy, eventually to prevent thromboembolic complications.
J Cardiovasc Pharmacol 1991
PMID:Platelet serotonin-LDL interaction in essential hypertension. 171 71

Ambulatory blood pressure (ABP) monitoring was used to evaluate the 24-h antihypertensive efficacy of single- and repeat-dose administrations of the nonsulfhydryl-converting enzyme inhibitor cilazapril, 2.5 and 5 mg, versus placebo in patients with mild to moderate essential hypertension. After a 2-week placebo run-in period, patients were randomized to receive, in a double-blind procedure, either 2.5 mg cilazapril (n = 14), 5 mg cilazapril (n = 14), or placebo (n = 14) for 4 weeks. In calculating the systolic/diastolic blood pressure (BP) trough-to-peak (T/P) ratio after subtraction of the placebo effect, 5 mg cilazapril appeared to be more effective than 2.5 mg cilazapril following single- (59/54% vs. 21/48%) and repeat-dose administration (47/76% vs. 31/49%). There were significant differences in 24-h and awake ABP for both 2.5 and 5 mg cilazapril as compared to placebo after single- and repeat-dose administrations. However, there were no significant differences in 24-h and awake ABP reduction between 2.5 and 5 mg cilazapril after single- and repeat-dose administrations. Furthermore, the percentages of "BP load" were identical with both regimens after the first dose (46 vs. 43%) and at steady-state (37 vs. 29%). These data demonstrate that 2.5 and 5 mg doses of cilazapril have equivalent antihypertensive efficacy using ABP and that 24-h ABP monitoring should also be performed in dose-response studies.
J Cardiovasc Pharmacol 1991 Aug
PMID:Antihypertensive effects of cilazapril, 2.5 and 5 mg, once daily versus placebo on ambulatory blood pressure following single- and repeat-dose administration. 171 82

In this study of the efficacy and safety of isradipine as first-line therapy in hypertension, 1,647 patients enrolled; 1,472 completed the 4-week placebo run-in period and began treatment with isradipine at 2.5 mg twice daily for 4 weeks. During placebo, 11% (n = 175) of the 1,647 patients withdrew because of normalization of blood pressure, side effects, noncompliance, violation of the study protocol, side effects from concomitant therapy, or other reasons. During isradipine therapy (n = 1,376), blood pressure decreased from 168 +/- 18/102 +/- 8 mm Hg at the end of the placebo period to 155 +/- 17/94 +/- 9 mm Hg after 2 weeks (p less than 0.001) and 151 +/- 16/92 +/- 9 mm Hg after 4 weeks (p less than 0.001). During active treatment, 6.4% (n = 94) were withdrawn because of flushing, headache, edema, palpitations, gastrointestinal side effects, skin rashes, or other side effects, and two patients because of lack of efficacy. The side effect score in the remaining patients worsened for flushing, remained unchanged for edema, but significantly improved for palpitations, fatigue, dizziness, headache, and nervousness. After 4 weeks, 60% of patients had diastolic blood pressures of less than or equal to 90 mm Hg. Thus, isradipine is effective and safe as first-line therapy in patients with primary hypertension as seen in general practice.
J Cardiovasc Pharmacol 1991
PMID:Calcium antagonists as first-line therapy in hypertension: results of the Swiss Isradipine Study. Swiss Hypertension Society. 172 Apr 76

The effect of the calcium antagonist isradipine on serotonin metabolism and platelet aggregation was studied in 17 patients with essential hypertension. Platelet serotonin content, plasma serotonin, 5-hydroxyindoleacetic acid levels, and platelet aggregation [induced ex vivo by serotonin and low-density lipoprotein (LDL)] were measured after a 4-week placebo period and after 12 weeks of oral treatment with isradipine. Isradipine treatment significantly inhibited platelet aggregation induced by LDL and serotonin; the amplifying effect of LDL on serotonin-induced aggregation seen with placebo was not observed after 12 weeks of treatment with isradipine. Platelet serotonin content increased significantly during isradipine treatment; this increase was inversely related to the pretreatment content of serotonin in platelets. The results indicate that treatment with isradipine restores the impaired handling of platelet serotonin as well as the platelet response to serotonin and LDL in hypertensive patients. This effect of isradipine may be regarded as one of the cellular mechanisms of thrombovascular protection and may be of clinical significance in terms of platelet and vessel wall interaction.
J Cardiovasc Pharmacol 1991
PMID:Serotonin and platelet activation during treatment with isradipine. 172 Apr 82

The efficacy and safety of isradipine and nifedipine retard were compared in 51 patients with mild-to-moderate essential hypertension. A 4-week placebo run-in period was followed by an 8-week course of treatment. Patients were randomly allocated to either isradipine 1.25 mg twice daily (n = 24) or nifedipine 20 mg twice daily (n = 826); dosages were doubled if blood pressure was not normalized [diastolic blood pressure greater than or equal to 90 mm Hg) after 4 weeks of active treatment. Systolic/diastolic blood pressures were significantly reduced (p less than 0.01/p less than 0.01) by isradipine from 162/103 to 145/89 mm Hg, and by nifedipine from 162/104 to 143/88 mm Hg. Normalization rates were 79% with isradipine and 67% with nifedipine. It was necessary to double the dosage in seven of the patients taking isradipine and in three of those taking nifedipine; the mean final dosages were 1.63 mg and 22.4 mg twice daily, respectively. Heart rate did not change significantly with either treatment. There were drug-related adverse events in five patients (21%) taking isradipine (2 edema, 2 headache, 2 palpitations, 1 flushing) and in eight (30%) of those taking nifedipine (5 edema, 2 headache, 1 palpitations). Therapy was withdrawn in one patient in the isradipine group (1 headache) and two patients in the nifedipine group (1 edema, 1 headache). We conclude that isradipine is a highly effective and well tolerated antihypertensive agent.
J Cardiovasc Pharmacol 1991
PMID:First clinical experience with isradipine in the treatment of hypertension in Portugal. 172 Apr 85

This was a double-blind multicenter study to compare the efficacy, tolerability and effects on the quality of life with isradipine and atenolol in the treatment of essential hypertension. Of 588 patients entering the 6-week placebo run-in period, 549 were eligible for randomization to receive either isradipine or atenolol for 8 weeks. If, at the end of this period, diastolic blood pressure (DBP) remained greater than 90 mm Hg, then both agents were given in combination for a further 10 weeks. Tolerability and quality of life were assessed repeatedly during the placebo and active-treatment phases. A subgroup of 30 patients were followed by 24-h ambulatory blood pressure monitoring, and their results are now being analyzed. In another subgroup of 26 patients, maximum exercise capacity, as determined by ergometer bicycle-testing, was measured once during placebo and twice during active treatment. At the end of the 24-week study period, both isradipine and atenolol as monotherapy had produced significant decreases in blood pressure. There were no significant differences overall between the compounds in quality-of-life and side-effect profiles, although there was a relative absence of ankle edema and headache with isradipine. Furthermore, patients receiving isradipine had no change in performance on exercise testing whereas patients on atenolol had a significant decrease (p less than 0.01).
J Cardiovasc Pharmacol 1991
PMID:Swedish Isradipine Study in Hypertension: evaluation of quality of life, safety, and efficacy. SWISH Group. 172 Apr 87

The antihypertensive effect of isradipine compared with placebo was assessed in 28 male patients (aged 40-64 years) with mild-to-moderate essential hypertension. After withdrawal of all previous antihypertensive treatment, these patients were entered into a 4-week placebo period followed by randomization to receive double-blind, for 8 weeks, either placebo (n = 14) or isradipine at 1.25-2.5 mg twice daily (n = 14). Twenty-four-hour ambulatory blood pressure was measured by Accutracker at the end of the placebo period and at the end of active treatment. In the isradipine group, both systolic and diastolic blood pressures decreased significantly (p less than 0.0001) whereas blood pressure increased in those taking placebo. In addition, isradipine as monotherapy controlled blood pressure throughout the day and night, and especially during the early morning, in these patients.
J Cardiovasc Pharmacol 1991
PMID:The antihypertensive action of isradipine in mild essential hypertension. 172 Apr 88

The hemodynamic disturbances in essential hypertension depend on the age of the subjects and the severity of the hypertensive state. In a 20-year follow-up study, we demonstrated a shift in the hemodynamic characteristics from a high output/normal resistance pattern in the early phase toward a low-flow/high-resistance pattern in the later period. The arteriovenous oxygen difference increased, particularly during exercise, and the oxygen reserve in venous blood decreased. Treatment with conventional drugs (beta-blockers and/or diuretics) for 20 years with satisfactory control of diastolic blood pressure did not prevent a marked increase in total peripheral resistance and a reduction in stroke index and cardiac index. In recent years, beta-blockers with vasodilating activity have been introduced in the treatment of hypertension (labetalol, acebutolol, dilevalol, celiprolol, and carvedilol). The hemodynamic effects of these compounds clearly differ from the changes induced during acute and chronic conventional beta-blocking treatment. In contrast to the usual beta-blockers, these drugs reduce total peripheral resistance acutely, and reduce cardiac index considerably less; arteriovenous oxygen difference is more normal. In an acute study of carvedilol in 18 patients with essential hypertension, total peripheral resistance was reduced 8% at rest (supine) and 6% during exercise. Exercise heart rate was reduced 12%, but due to an increase in stroke index, the reduction in cardiac index was only 6%-considerably less than what is seen during treatment with conventional beta-blockers.
J Cardiovasc Pharmacol 1991
PMID:Essential hypertension: hemodynamic and therapeutic changes over 20 years. 172 71

Carvedilol is a novel treatment for hypertension, having a balanced pharmacology of vasodilation and beta-receptor blockade. We present here the results of a three-way, multicenter, comparative study on the use of carvedilol, slow-release nifedipine, and atenolol in the management of essential hypertension. A total of 311 patients was entered into the study, of which 293 were randomized to one of the three treatment regimens. Full data are available on 255 patients. Systolic and diastolic blood pressure measurements, in both sitting and standing positions, were taken, together with the heart rate. There was no consistently significant difference between treatments with respect to blood pressure control. Differences in heart rate were more pronounced, with the reduction due to carvedilol being generally intermediate between nifedipine and atenolol. Further studies of carvedilol in hypertension, as well as other indications, are warranted.
J Cardiovasc Pharmacol 1991
PMID:A comparative study of carvedilol, slow-release nifedipine, and atenolol in the management of essential hypertension. 172 77


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