Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of protein associated with pregnancy (placental specific beta 1 glycoprotein, SP1, and pregnancy associated -alpha 2- globulin, alpha 2-PAG), immune function (complement, C3c) and inflammation (ceruloplasmin, C), were studied at term in groups of patients with normal and complicated primigravid and multigravid pregnancy. The levels of SP1 and C3c were similar in all the groups studied. In patients matched for parity, the levels of alpha 2-PAG were significantly lower than normal in preeclamptic primigravidas and in multigravidas with a history of preeclampsia in their first pregnancy. Ceruloplasmin levels were significantly elevated in preeclampsia patients and in patients with essential hypertension. It is suggested that reduced plasma alpha 2-PAG may be of prognostic value and have a role in the aetiology of preeclampsia whereas increased ceruloplasmin levels may be no more than an acute phase reactant resulting from pathological changes due to hypertension.
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PMID:Pregnancy-associated plasma protein levels at term in normal pregnancy, preeclampsia and essential hypertension. 657 51

The urinary excretion of prostaglandins (PG) E2 and F2 alpha was measured by radioimmunoassay in 15 patients with essential hypertension, before and after 2 and 4 weeks of treatment with the selective beta 1-adrenergic blocker, atenolol. Systolic and diastolic blood pressure, pulse rate and plasma renin activity decreased significantly during the treatment. No change was observed in renal function and electrolyte balance. The 24-hour excretion of PGE2 and PGF2 alpha was also unaffected by the antihypertensive treatment. The above findings, in contrast with those previously observed with another beta-blocker, propranolol, suggest that tubular beta-receptors are not involved in the synthesis of PGs. The different hemodynamic effects of the two drugs are the most likely explanation for the different responses in prostaglandin excretion.
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PMID:Effect of atenolol treatment on urinary prostaglandins E2 and F2 alpha in essential hypertension. 658 55

The possibility that hemodynamic and biohumoral factors may help predict the antihypertensive effectiveness of selective beta 1 blockers was investigated. The effects of 3 wk of treatment with two selective beta 1 blockers, metoprolol and atenolol, were observed in 54 patients with mild or moderate essential hypertension. No significant difference between the hemodynamic effects of the two drugs was found. The percent fall in systolic blood pressure induced by the two correlated strongly with the pretreatment values of the chronotropic response to isoproterenol and with the pretreatment values of cardiac output, heart rate, and plasma renin activity (PRA). There was no correlation between the decrease in systolic blood pressure induced and initial 24-hr urinary catecholamine output, total peripheral resistance, and plasma aldosterone. Percent fall in diastolic blood pressure correlated only with the pretreatment levels of PRA. Our results support the view that the hypotensive effect of beta 1 blockers are predictable on the basis of the pretreatment values of chronotropic response to isoproterenol, PRA, heart rate, and cardiac output.
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PMID:Predictability of antihypertensive efficacy of selective beta 1 blockers. 664 Oct 91

The behaviour of active (AR) and inactive (IR) renin was studied in 48 hypertensive patients (37 with uncomplicated essential hypertension and 11 with reno-vascular hypertension) treated with indomethacin alone or with AR stimulating (bumetanide, tienilic acid, captopril) and inhibiting (atenolol) drugs before and after indomethacin addition. In 10 pts indomethacin (50mg q.i.d./3 days) reduced (p less than 0.05) AR and to a lesser extent IR. In 6 pts bumetanide (1 mg) increased (p less than 0.05) only AR and this effect was abolished by indomethacin. In 6 pts tienilic acid (250 mg) increased (p less than 0.05) only AR and this action was unchanged by indomethacin. In 11 renovascular pts captopril (100mg) increased AR (p less than 0.01) and lesser IR and both these effects were uninfluenced by indomethacin. In 11 essential hypertensive pts captopril (25mg b.i.d./3 days) increased only AR (p less than 0.02), but after 1 year both AR and IR were increased (p less than 0.05) and these effects were abolished by indomethacin. In all the above reported protocols we did never find any inverse correlation between either AR and IR values or their induced changes. These data suggest that prostaglandins stimulate, even if not to a similar extent, both AR and IR and that drugs, which stimulate renin either through or independently of PGs, did not cause any apparent interconversion of plasma IR into AR. In 6 pts atenolol (100 mg daily/6 days) reduced AR (p less than 0.05) and tended to increase IR. Indomethacin addition further decreased AR and reduced IR (both p less than 0.05 vs atenolol alone): however the proportion (% of total) of IR was still reduced. These findings suggest that beta 1-adrenoreceptors blockade exerts a divergent effect on active and inactive renin and that this action is not influenced by PGs synthesis inhibition.
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PMID:Effects of prostaglandins inhibition on changes in active and inactive renin induced by antihypertensive drugs. 675 7

Thirty-two patients with primary hypertension were studied in a double-blind cross-over comparison between the cardioselective beta 1-blocking agent atenolol and the combined alpha- and beta-blocking agent labetalol. The doses used were atenolol 50--150 mg twice daily and labetalol 200--600 mg twice daily. Both drugs effectively reduced blood pressure and heart rate. Dose increments every second week resulted in a higher proportion of patients with normal blood pressure (les than or equal to 150/90 mm Hg) with both drugs. Labetalol was somewhat more effective in lowering upright blood pressure while atenolol caused a more pronounced heart-rate reduction. Both agents decreased plasma renin activity and urinary aldosterone excretion. Scalp tingling on labetalol (2 patients) and cold fingers with atenolol (1 patient) caused withdrawal of the drugs. Cold fingers were reported in another four patients during treatment with atenolol and in one when on labetalol. Tiredness and postural symptoms were more common during intake of labetalol.
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PMID:Antihypertensive and metabolic effects of increasing doses of atenolol and labetalol. A comparative study in primary hypertension. 676 Jun 79

Inappropriate vascular smooth-muscle cell (VSMC) growth is the hallmark of vascular pathology in essential hypertension and diabetic macroangiopathy, whereas platelets constitute an important regulator of vessel wall homeostasis because of their content of various growth factors. Numerous abnormalities exist in platelet functions in diabetes and hypertension, such as enhanced activity and altered adhesion and aggregation. Increased thromboxane (TX2) production is characteristic of diabetes, and an elevation of intracellular free Ca2+ is found in platelets of hypertensive patients. By studying the growth patterns of VSMC from spontaneously hypertensive rats (SHRs) vs. those obtained from their normotensive counterparts, Wistar-Kyoto (WKY) rats, we have demonstrated that VSMC from SHRs exhibited a higher specific growth rate, abnormal contact inhibition, and accelerated entry into the S phase of the cell cycle. Moreover, they were hyperresponsive to many growth factors such as calf serum, epidermal growth factor (EGF), platelet-derived growth factor (PDGF), transforming growth factor beta 1 (TGF beta 1), and insulin. Additive effects were observed for EGF and PDGF or EGF and insulin. These intrinsic growth anomalies in cells of hypertensive origin persist in culture indicating their putative primary role in the pathogenesis of hypertension. Endogenous TGF beta 1 revealed an augmented expression of its message levels in SHR VSMC, the difference in mRNA between both strains being more pronounced at high cell density. Further, TGF beta 1 protein synthesis and secretion in VSMC culture were confirmed by immunoprecipitation of de novo labeled TGF beta 1. At high cell density, which most likely represents the physiological state of VSMC, plasmin, an activator of TGF beta 1, significantly stimulated DNA synthesis of VSMC in both strains. The reverse effect was obtained at low cell density. Yet, the fold stimulation was higher in WKY rats, suggesting that TGF beta 1 may be partially activated in SHR VSMC. This is supported by the inhibition of baseline DNA synthesis by TGF beta 1 neutralizing antibody in VSMC of hypertensive origin and not of normotensive controls. TGF beta 1 antisense oligodeoxynucleotide (ODN) nearly normalized the increased proliferation of SHR VSMC in culture. On the other hand, growth-promoting activity (GPA) in platelets of either diabetic or hypertensive patients was higher than in platelets of healthy controls and was found to be normalized by intensive insulin therapy in insulin-dependent diabetic patients. In hypertensive patients, however, hydrochlorothiazide (HCTZ)--even in low doses (25 mg/day)--enhanced the GPA in platelets, whereas other antihypertensive agents such as indapamide, atenolol, and captopril, had neutral effects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Platelets, growth factors, and vascular smooth-muscle cells in hypertension and diabetes. 750 64

We compared the beta 1-selective adrenoceptor antagonists bisoprolol and atenolol in a double-blind, randomized crossover study. After 4 weeks placebo phase, 59 patients with essential hypertension received either 10 mg bisoprolol or 50 mg atenolol once daily for 8 weeks, increased if necessary (target BP < or = 150/90 mmHg) to 20 and 100 mg, respectively, after 4 weeks. After a second placebo phase, crossover occurred to the alternative drug. We measured resting systolic and diastolic blood pressures and heart rate at 24 h post-dose baseline and after 4 and 8 weeks treatment. Both drugs significantly lowered systolic and diastolic blood pressures and heart rate at 8 weeks compared to baseline (all p < 0.05). Bisoprolol reduced heart rate significantly more than atenolol (p < 0.01), but systolic and diastolic blood pressure changes were not different between the two drugs. There was no difference in patient acceptability of the drugs as assessed by visual analogue scale. Despite theoretical and circumstantial evidence to suggest superiority of bisoprolol over atenolol, no significant difference between the two was found except for greater heart rate reduction with bisoprolol.
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PMID:A double-blind comparison of bisoprolol and atenolol in patients with essential hypertension. 764 43

Untreated essential hypertension leads to cardiovascular and renal disease and stroke, but antihypertensive drug therapy effectively reduces these consequences of hypertension. Several studies indicate that hypertension can negatively impact on cognitive function, especially on learning and memory, but the ability of antihypertensive drugs to ameliorate these cognitive dysfunctions is less clear. None of the recent studies convincingly demonstrates that any of the antihypertensive drugs currently in use has a major deleterious effect on cognition in hypertensive patients, but some of the drugs more reliably benefit cognitive function in the hypertensive patient. As a class, the angiotensin-converting enzyme inhibitors most consistently lead to cognitive improvement in the overall hypertensive population, but beta 1-adrenergic receptor blockers and a subset of calcium channel blockers appear to have very similar effects. Animal studies and clinical studies in demented patients suggest that angiotensin-converting enzyme in the cerebral cortex plays a role in normal learning and memory, a finding that provides a theoretic foundation to the beneficial actions of this class of drugs on cognitive function in hypertensive individuals.
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PMID:Neurologic consequences of hypertension and antihypertensive drug therapy. 784 74

The nocturnal production of melatonin synthesis has been associated with circadian mechanisms of the organization of sleep. It is well known that the synthesis of melatonin is under the control of pineal beta 1-adrenoreceptors. In this study the effect of ten weeks treatment with the beta-adrenoreceptor (beta-AR) blockers propranolol and ridazolol on melatonin synthesis and on sleep quality was examined in 42 patients suffering from essential hypertension. Before and after 6 and 10 weeks of beta-AR-blocker administration urinary sulfatoxymelatonin excretion rates were measured and sleep factors were evaluated by using a standardized sleep inventory consisting of self-rating sleepiness scales. After 6 and 10 weeks of treatment, a significant about 50 percent reduction of sulfatoxymelatonin was measured. No relationship between these reductions and changes in sleep factors was found. The results indicate that a reduced nightly amplitude of melatonin has minor significance for the organization of physiological sleep. Furthermore, it is suggested that pineal mechanisms beside the beta 1-adrenergic receptor transduction system serve to maintain the melatonin signal to a considerable extent during a chronic beta 1-AR blockade.
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PMID:Influence of chronic beta-adrenoreceptor blocker treatment on melatonin secretion and sleep quality in patients with essential hypertension. 785 85

Beta-adrenoceptors on lymphocytes are acutely increased after dynamic exercise in normotensive subjects, but not in hypertensives. It was thus of interest to evaluate the acute regulation of the lymphocyte beta-adrenoceptor-adenylate-cyclase-cAMP-system (BAAS) in patients with primary hypertension during dynamic stress after acute beta-blockade. Density and affinity of beta 2-adrenoceptors, and intracellular cAMP concentrations (baseline and isoprenaline stimulated values) were measured on the peripheral mononuclear cells in 8 male patients with primary hypertension before and immediately after dynamic exercise on a bicycle (50-200 W) at baseline and after acute beta-blockade (2 h following 100 mg atenolol). Dynamic exercise causes no significant changes in receptor density and affinity, nor in basal cAMP values. After acute beta-blockade the dynamic stress-induced rise in mean arterial blood pressure was significantly (p < 0.01) reduced from 33 to 24 mmHg, and beta-adrenoceptor density significantly (p < 0.05) increased from 1320 to 2102 molecules/cell, whereas affinity remained unchanged. Baseline and stimulated cAMP concentrations increased significantly (p < 0.05) from 5.3 to 7.0 and from 2.1 to 3.5 pmol/10(6) cells, respectively. These findings suggest that in primary hypertension the regulation of the beta 2-adrenoceptor-adenylate-cyclase-cAMP-system is impaired on exercise and can be normalised by acute beta-blockade. Since atenolol predominantly blocks beta 1-adrenoceptors, the observed normalisation of the lymphocyte BAAS may reflect only an unspecific effect of antihypertensive therapy per se.
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PMID:Regulation of the beta-adrenoceptor-cAMP-system during dynamic exercise in patients with primary hypertension after acute beta-blockade. 791 72


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