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

The reduction of increased platelet aggregation in essential hypertension is one of the aims of modern antihypertensive therapy. Twenty-one hospitalized patients with non-treated essential hypertension were examined. The platelet function measurements were made before the therapy and after 1 week of celiprolol administration (300 mg/day). Fifteen essentially hypertensive patients were investigated before and after 1 week of placebo administration. Plasma beta-thromboglobulin was assayed, and the whole blood platelet aggregation (initial and total-induced by adrenaline and ADP) was measured. A significant decrease in adrenaline-induced (from 19 to 13%, p < 0.02) and ADP-induced aggregation (from 15 to 13%, p < 0.05) was observed after celiprolol administration. This reduction of adrenaline-induced platelet aggregation may be explained by the stimulation effect of celiprolol on platelet beta 2-receptors. Thus, some inhibitory effect of celiprolol on platelet aggregation is one of the further advantages of this drug in the therapy of essential hypertension.
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PMID:The effect of short-term celiprolol therapy on platelet function in essential hypertension. 840 62

The aim of this study was to evaluate the substrate (ATP) kinetics of erythrocyte membrane Na, K-ATPase in children with borderline or essential hypertension. Although the activity of Na, K-ATPase in the presence of in vivo concentrations of ATP was not significantly altered, kinetic studies showed an obvious inhibition of enzyme activity in the erythrocyte membrane of children with borderline or essential hypertension. Hanes plot analysis revealed a decrease of V(max) from 7.19 in erythrocytes from control subjects to 4.93 and 3.33 in those from children with borderline or essential hypertension, respectively. A mean value of the K(m) decreased from 0.10 in the control to 0.08 and 0.02 in children with borderline or essential hypertension, respectively. The energy status of erythrocytes, estimated by ATP, ADP and AMP levels, ATP/ADP ratio, and adenylate energy charge (AEC) was not significantly changed in the cells from hypertensive children. The use of a free radical-generating system (FeSO4/ascorbate) in vitro significantly reduced enzyme activity in the control erythrocytes while in those from hypertensive children it was abolished completely. The level of lipid peroxides was considerably higher (+ 37 per cent) in the plasma, while that of reduced glutathione was significantly lower both in the erythrocytes and the plasma of children with essential hypertension than in healthy children. These results indicate significant alterations of the antioxidant status which could be the cause of the inhibited Na, K-ATPase activity in erythrocyte membranes from hypertensive children.
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PMID:Alteration of erythrocyte membrane Na, K-ATPase in children with borderline or essential hypertension. 864 Sep 56

Anticoagulant and antiplatelet function of NICM is weak, thereby presenting a hazard of coronary thrombus growth in patients subjected to coronary angiography. Similar antiplatelet effect was demonstrated for verapamil (V). The present study was designed to determine iopromide induced modifications in blood platelet membrane structure and aggregation in patients with primary hypertension and ischaemic heart disease receiving V compared to non-receivers of V. The blood for examinations was collected by Judkins' catheter placed in the vicinity of the coronary vessel ostium, and next centrifuged to obtain platelet-rich plasma. The ADP- and ristocetin (R)-induced blood platelet aggregation was determined by means of an aggregometer while their membrane structure was studied by electron paramagnetic resonance. The spin-label used, 4-maleimide-2, 2, 6, 6-tetramethyl-piperidine-1-oxyl (MSL) binds covalently to the -SH and -NH2 groups of platelet membrane proteins. The modifications in various spectral components, examined by means of a spectrometer, reflect conformational changes in these proteins. In non-receivers of V, iopromide diminished the aggregation, significantly in the case of ADP (p = 0.05), whereas in the receivers of V the iopromide-induced platelet aggregation examined with ADP did not change while with R was even enhanced (p = 0.05, Fig. 2). The platelet membrane protein conformation also changed due to iopromide: in non-receivers of V the accessibility of the above named groups for MSL was significantly reduced, p < 0.05, but in the receivers of V--inversely--significantly increased, p < 0.05. The results obtained confirm that in non-receivers of V, iopromide modifies the conformation of platelet membrane proteins which, in turn, may result in the lessening of the aggregation rate, favourable as regards the conditions of coronary thrombus growth. The tendency in the receivers of V was reverse and, however its nature remains obscure, this effect should be an indication for discontinuing the use of V several days before subjection the patient to coronary angiography.
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PMID:Verapamil influences the effect of nonionic contrast agent on platelet membrane structure and aggregation. 872 70

To assess platelet changes in pregnant women with chronic glomerulonephritis (CGN) and essential hypertension (EH) we estimated platelet lactic dehydrogenase activity (LDH), beta-thromboglobulin and thromboxane B2 (TxB2) plasma levels and ADP-stimulated platelet aggregability. Five groups of gravidae (26-40 weeks of gestation) were studied: with EH (n = 20), with CGN and hypertension (n = 31), with CGN without hypertension (n = 29), with late toxemia (n = 11), nonpregnant CGN women (n = 10) and healthy pregnant women (n = 20). Activation of platelet function was found in gravidae with CGN and EH. Platelet disorders were especially pronounced in pregnant women with CGN and with EH, but they were less pronounced than in control group with late toxemia. We believe that hypertension is more important stimulating factor for platelet activation than renal disease. We suggest that platelet disorders in outpatients are brought about by endothelium damage caused by elevated blood pressure.
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PMID:[Thrombocytic disorders in pregnant women with chronic glomerulonephritis and hypertension]. 902 46

Angiotensin II enhances platelet aggregation through activation of the G protein-linked pathway present in platelets. Studies of several angiotensin-converting enzyme (ACE) inhibitors have demonstrated marked differences on platelets. Therefore this prospective, randomized, double-blind, crossover study compared the ex vivo effects of equivalent antihypertensive doses of captopril, enalapril, and fosinopril on platelet aggregation and thromboxane B2 (TxB2) formation in subjects with stage I-II essential hypertension. Nineteen male subjects with a baseline mean seated blood pressure of 141 +/- 3/100 +/- 1 mm Hg were enrolled. The decline in mean arterial pressure after 4 weeks of stable dosing was 10 +/- 1, 12 +/- 1, and 11 +/- 1 mm Hg for captopril, enalapril, and fosinopril, respectively (p = NS). There was no significant change in adenosine diphosphate (ADP)-, epinephrine-, or thrombin-stimulated platelet aggregation from baseline or between ACE inhibitors. Compared with baseline, fosinopril decreased TxB2 concentrations 27.5-67.6% with all stimuli after 1 and 5 min. Captopril also decreased TxB2 formation, but this effect was stimulus and time dependent. Enalapril consistently increased TxB2 concentrations, independent of stimuli or time. We conclude that different ACE inhibitors have distinct effects on platelet TxB2 formation without significant effects on platelet aggregation. Fosinopril may be a direct antagonist ofTxA2 synthase, suggesting benefit in syndromes of platelet activation or vascular occlusion.
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PMID:ACE inhibitor effects on platelet function in stages I-II hypertension. 933 5

The effects of a novel calcium antagonist, benidipine hydrochloride, on responses of platelets to mental stress were evaluated in nine patients with essential hypertension. Before and 12 weeks after the monotherapy with benidipine (2-4 mg/day), platelet aggregability and plasma beta-thromboglobulin were determined during rest and after a 10-min arithmetic stress. Before the treatment, arithmetic stress significantly increased platelet aggregability in response to adenosine diphosphate (ADP) and plasma beta-thromboglobulin level. Blood pressure, pulse rate, and plasma catecholamines also increased during arithmetic stress. The treatment with benidipine did not affect resting values of platelet functions, but attenuated significantly stress-induced alterations in primary aggregation to 1.0 microM ADP (34 +/- 4% to 40 +/- 3% before treatment vs. 32 +/- 2% to 34 +/- 3% after benidipine), ADP threshold for biphasic aggregation (2.2 +/- 0.4 to 1.8 +/- 0.3 microM before treatment vs. 2.2 +/- 0.3 to 2.2 +/- 0.4 microM after benidipine) and plasma beta-thromboglobulin level (74 +/- 16 to 104 +/- 15 ng/ml before treatment vs. 60 +/- 10 to 52 +/- 8 ng/ml after benidipine; p < 0.05 for Stress x Treatment interactions in all values). The pretreatment elevations in blood pressure and sympathetic activity with stress were not modified by benidipine treatment. In conclusion, the monotherapy with benidipine did not affect platelet function during the resting condition, but significantly suppressed the platelet activation induced by arithmetic stress in patients with essential hypertension.
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PMID:Effects of a novel calcium antagonist, benidipine hydrochloride, on platelet responsiveness to mental stress in patients with essential hypertension. 1044 76

The contents of adenine nucleotides (ATP, ADP, AMP), phosphocreatine (PCr) and creatine (Cr) in the heart, skeletal muscle, liver and spleen in spontaneously hypertensive (SHR) and normotensive (WKY) rats. The ATP/ADP ratio in cardiac tissue was lower in SHR compared with WKY, while myocardial contents of adenine nucleotides, PCr and Cr did not differ significantly between the groups. A lower ATP/ADP ratio in the skeletal muscle SHR of was accompanied by a reduction of PCr content comparing with these indices in WKY rats. The liver and spleen of SHR exhibited lower ATP contents and higher ADP and AMP levels compared with those ones in WKY rats, despite of the close values of adenine nucleotide pools (sigma AN = ATP + ADP + AMP). This redistribution of tissue adenine nucleotides was corresponded to lower energy charges (EC = (ATP + 0.5 ADP)/sigma AN) and ATP/ADP ratios in SHR group. The reduction of the energy state of tissues in SHR rats increased in the following rank: heart > skeletal muscle > liver > spleen, thus, reflecting progressive decrease of intensity of oxidative metabolism. The results suggest changes in the balance of rates of ATP formation and hydrolysis occur at the system level in primary hypertension. Probably, consequences of such rearrangement in energy metabolism are functional disturbances of plasma membrane and sacroplasmic reticulum well-documented in a number of experimental and clinical studies.
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PMID:[Changes in the energy state of tissues in spontaneously hypertensive rats]. 1051 1

To determine whether platelet response to mental stress is altered in essential hypertension, platelet aggregability and plasma beta-thromboglobulin were determined in 24 patients with essential hypertension (11 patients with World Health Organization (WHO) stage I and 13 patients with stage II) and 14 normotensive controls before and after a 10-min arithmetic stress (serial subtraction of 7 from 1000). In normotensive subjects, arithmetic stress did not affect primary aggregations to 1.0 micromol/L adenosine diphosphate (ADP) and to 2.5 micromol/L 5-hydroxytryptamine (5-HT), ADP threshold for biphasic aggregation and plasma beta-thromboglobulin level. In hypertensive patients with WHO stage I, these parameters were similar to those in normotensives before arithmetic stress, but the arithmetic stress test significantly increased primary aggregation to reagents and beta-thromboglobulin level, and decreased threshold of ADP for biphasic aggregation. In WHO stage II patients, platelet aggregability to reagents and beta-thromboglobulin level were already enhanced as compared with WHO stage I patients and normotensive subjects before arithmetic stress. However, the stress-induced changes in platelet function were less pronounced in WHO stage II patients compared with stage I patients. In conclusion, platelet aggregability and proaggregatory effect of mental stress differed depending on the severity of hypertension in patients with essential hypertension; the transient activation of platelet function during stress with no enhancement under the resting condition in the early phase of hypertension and the continuous activation of platelet function in the advanced phase with hypertensive organ damage.
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PMID:Different platelet aggregability during mental stress in two stages of essential hypertension. 1060 81

Patients with peripheral vascular disease or diabetes mellitus tend to have elevated circulating levels of naturally occurring platelet agonists like serotonin (5 hydroxytryptamine; 5-HT). This bioamine can induce platelet shape change (PSC) an early phase of platelet activation, which is essentially aspirin resistant. In addition, 5-HT exerts other harmful effects (eg stimulating vascular smooth muscle proliferation and inducing vasoconstriction in atheromatous coronary vessels). The aim of this study was to determine whether doxazosin inhibits 5-HT-induced PSC. Doxazosin is a long acting alpha(1)-adrenoceptor antagonist, used in the treatment of essential hypertension and/or benign prostatic hyperplasia (BPH). Platelet rich plasma (PRP) was prepared from healthy volunteers (n = 8; five males and three females with a median age of 32 years, range: 26-57). Agonists (5-HT, 0.06-0.5; ADP, 0.1-0.2 micromol/l or U46619, a TXA(2)analogue, 0.025-0.05 micromol/l) were added to PRP and aliquots were removed at specific time points for median platelet volume (MPV) measurement (using a high-resolution channelyser). The MPV was used as an indicator of PSC. PRP was also incubated with doxazosin (final concentration: 0.33 microM, a concentration similar to therapeutic plasma levels) prior to the addition of each of the above-mentioned agonists. Doxazosin significantly inhibited (P = 0.007 and P = 0.008, at 30 sec and 60 sec, respectively) the 5-HT-induced increase in MPV. Doxazosin did not significantly inhibit ADP- or U46619-induced PSC. The inhibitory effect of doxazosin seems to be specific to platelet 5-HT(2) receptors, since there was no effect on ADP- or U46619-induced PSC. This inhibition of platelet activation may be an additional, clinically relevant, advantage. Future in vivo studies should consider assessing the effect of doxazosin on 5-HT-induced platelet activation.
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PMID:Doxazosin, an alpha1-adrenoceptor antagonist, inhibits serotonin-induced shape change in human platelets. 1131 6

The angiotensin II receptor, losartan, has been found to inhibit platelet aggregability to some extent in in vitro experiments. There have been conflicting results about the in vivo effects of losartan. We sought to clarify the in vivo effect of losartan on platelet aggregation. Forty patients with grade I essential hypertension were treated with losartan for 3 weeks. Platelet aggregation tests with adenosine diphosphate (ADP) and ristocetin were analyzed and compared before and at the end of the study. Losartan effectively decreased systolic (SBP) and diastolic (DBP) blood pressure. Mean SBP before and after treatment was 159.6 +/- 12.8 and 149.2 +/- 17.3 mmHg, respectively. Mean DBP decreased from 93.7 +/- 8.2 to 87.7 +/- 10.3 mmHg after treatment. The results of the platelet aggregation tests with ADP and ristocetin were not significantly different when both rate and amplitude of maximal aggregation were included. Peak platelet aggregation with ADP regarding the lowest light transmission in the aggregometer was 59.8% +/- 24.3% before and 58.3% +/- 18.1% after the treatment. The same variables with ristocetin were 66.8% +/- 21.6% and 60.8% +/- 23.3%, respectively. In vivo effects of losartan on platelet aggregation with ADP and ristocetin were insignificant.
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PMID:In vivo effect of losartan on platelet aggregation in patients with hypertension. 1527 89


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