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)

Despite effective antihypertensive therapy, essential hypertension is still associated with considerable residual risk of cardiovascular complications. The aim of the present study was to investigate the state of the endogenous fibrinolytic system in young subjects with borderline hypertension. Thirty-nine young (age, 24 to 34 years) male subjects with borderline hypertension (systolic BP [SBP] 140 to 160 mm Hg and/or diastolic BP [DBP] 85 to 95 mm Hg) and 17 normotensive control subjects (age, 22 to 31 years; SBP 110 to 130 and DBP 60 to 80 mm Hg) were recruited from a population screening. Plasma levels of tissue-type plasminogen activator (t-PA) antigen and activity and plasminogen activator inhibitor 1 (PAI-1) antigen were determined at rest and in response to a venous occlusion test. Borderline-hypertensive subjects had metabolic and anthropometric characteristics similar to normotensive individuals. In comparison with normotensive subjects, borderline-hypertensive subjects had higher plasma concentration of t-PA antigen both at rest and after venous occlusion but similar levels of t-PA activity or PAI-1 antigen. The increase in t-PA antigen and activity in response to venous occlusion was significantly greater in borderline-hypertensive subjects than in normotensive control subjects (P < .0001 and P = .003, respectively). In stepwise regression analyses, 24-hour mean arterial pressure emerged as the single most powerful predictor of t-PA antigen levels, but body mass index was the most important determinant of t-PA activity and PAI-1 antigen. However, PAI-1 was explained by both body mass index (partial r = .48, P < .001) and 24-hour mean arterial pressure (partial r = .29, P < .05). Thus, early hypertension may be associated with significant alterations in endogenous fibrinolysis.
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PMID:Enhanced levels of tissue-type plasminogen activator in borderline hypertension. 759 Oct 20

We compared the antihypertensive activity of DL- and D-nebivolol in patients with essential hypertension on clinic and 24-h ambulatory blood pressure (BP) and during dynamic exercise as well. After a 4-week placebo run-in period, 30 patients (mean age 48 years) were randomly allocated to double-blind treatment with either DL-nebivolol 5 mg or D-nebivolol 2.5 mg once daily for 4 weeks. After an interim single-blind placebo washout of 2-4 weeks, all patients crossed over double-blind to the alternative DL- or D-nebivolol treatment for 4 weeks. The results show that DL- and D-nebivolol produced similar reductions in clinic trough (delta systolic/delta diastolic BP (delta SBP/delta DBP): -10/-8 and -13/-9 mm Hg, respectively, all p < 0.0001 vs. placebo), 24-h ambulatory (-12/-11 and -13/-11 mm Hg, respectively, all p < 0.0001), and peak exercise BP (-13/-6, both p < 0.01; and -13/-7 mm Hg, both p < 0.0001, respectively) as compared with placebo (SBP/DBP clinic 147/99, ambulatory 147/94, exercise 211/103 mm Hg). Our results showing superimposable clinic and ambulatory BP profiles as well as exercise BP responses with DL- and D-nebivolol treatment do not confirm results of animal pharmacologic experiments in which the L-isomer potentiated the antihypertensive effect of the D-isomer.
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PMID:Comparative assessment of antihypertensive efficacy of DL-nebivolol and D-nebivolol in patients with confirmed mild to moderate hypertension. 759 31

Neuropeptide Y (NPY) is a vasoconstrictor sympathetic cotransmitter and a modulator of adrenergic function whose role in hypertension is yet unknown. We studied the co-release of NPY and noradrenaline (NA) in patients with essential hypertension (13 females, 11 males, age 42 +/- 13 years) by measuring plasma levels of NPY-immunoreactivity (-ir, radioimmunoassay) and NA (radioenzymatic method) following administration of clonidine (CL 300 micrograms, p.o.). At rest, only NPY-ir levels significantly correlated with diastolic blood pressure (DBP, r = 0.42, p < 0.05). Three hours after CL, there were a decrease in mean arterial pressure and plasma NA (by 31 +/- 14 mmHG, p < 0.05 and 92 +/- 10 pg/ml, p < 0.01) but no change in NPY-ir levels. Patients were subsequently subdivided into groups with high (> or = 90 mmHg) or normal DBP (< or = 89 mmHg) and with or without elevated plasma NA levels (above or below 414 pg/ml, a normotensive mean +1 standard deviation). In hypertensives, but not in those with normal DBP, plasma NPY-ir correlated not only with DBP but also with systolic and mean blood pressure (r = 0.53 and r = 0.60, respectively) at rest. Hypertensives with "high" NA had significantly lower resting plasma NPY-ir levels than those with "low" NA (7.1 +/- 3.6 vs 14.7 +/- 6.0 fmol/ml, p < 0.05). In the former group, CL evoked the greatest fall in plasma NA, and also decreased NPY-ir levels by 50% (p < 0.05). Thus, patients with essential hypertension were found to display differential patterns of changes in sympathetic cotransmitters to clonidine. NPY may contribute to the increased blood pressure in hypertensives and together with NA, mediate hypotensive action of clonidine but only in the hyperadrenergic subgroup of hypertensives.
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PMID:Neuropeptide Y and alpha-adrenoceptor interactions in patients with essential hypertension. 766 76

Twelve patients with essential hypertension were randomized in a double-blind cross-over study to investigate the blood pressure BP-lowering activity of isradipine regular formulation (RF) 2.5 mg twice daily (between 7 and 8 a.m. and at approximately 6 p.m.), and isradipine modified release (MR), 5 mg once daily (between 7 and 8 a.m.). The two randomized treatment periods were separated by a placebo period. Patient compliance was similar between placebo and isradipine RF and MR treatment. As compared with placebo, isradipine RF decreased daytime BP by 10 mm Hg systolic (SBP, p < 0.001) and by 6 mm Hg diastolic (DBP, p < 0.01), and night SBP and DBP by 7 (p < 0.05) and 3 mm Hg (P = NS), respectively. Isradipine MR reduced the daytime SBP 8 mm Hg (p < 0.05) and DBP by 3 mm Hg (p = NS), and the night SBP by 1 mm Hg (p = NS) and DBP by < 1 mm Hg (P = NS). Analysis of variance showed that the interaction terms between the effects of treatment and time of day were not significant for SBP (F = 1.56, p = 0.24) or DBP (F = 1.40, p = 0.26) with isradipine RF treatment, but they were significant for SBP (F = 6.33, p = 0.03) and DBP (F = 5.12, p = 0.04) with isradipine MR treatment. Therefore, the BP-lowering effect of isradipine MR 5 mg once daily appears to weaken as the day progresses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does isradipine modified release 5 mg once daily reduce blood pressure for 24 hours? 769 73

To evaluate the metabolic effects of two anti-hypertensive agents with different actions, nifedipine 20 mg twice daily and furosemide 60 mg twice daily, 23 patients with untreated essential hypertension performed a double-blind, cross-over study in treatment periods of 5 months. Metabolic effects were evaluated by serum lipoprotein determinations, the intravenous glucose tolerance test and the hyperinsulinaemic euglycaemic clamp technique. Nifedipine and furosemide reduced blood pressure to the same extent (-14 to -15 mm Hg for supine SBP and -9 to -10 mm Hg for supine DBP, both P < 0.0001). Whereas both drugs significantly increased the levels of glycolysated haemoglobin (HbA1c, +0.24%, P < 0.005 for nifedipine and +0.43%, P < 0.001 for furosemide), only furosemide increased fasting blood glucose (+0.3 mmol/L, P < 0.01) and fasting insulin (+2.2 mU/L, P < 0.05) but impaired the early insulin response to i.v. glucose (-15 mU/L, P < 0.05). Insulin sensitivity on the other hand was significantly impaired by nifedipine treatment only (-1.6 mg/kg/min, P < 0.01). Whereas treatment with nifedipine did not change serum lipids, furosemide caused an increase in serum cholesterol (+0.2 mmol/L, P < 0.05) because of a rise in the LDL fraction (+0.32 mmol/L, P < 0.001). The insignificant change in heart rate induced by nifedipine treatment correlated with the change in HbA1c (r = 0.50, P = 0.05) and was inversely related to the change in insulin sensitivity (r = -0.56, P < 0.05). In conclusion, both furosemide and nifedipine caused abnormalities in glucose metabolism. In the nifedipine group the effects on glucose metabolism were related to the occurrence of tachycardia suggesting that sympathetic nerve activation could be involved in the metabolic impairments.
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PMID:Metabolic effects of anti-hypertensive treatment with nifedipine or furosemide: a double-blind, cross-over study. 775 76

The effect of both administration and withdrawal of doxazosin on patients with essential hypertension was evaluated by twenty-four-hour ambulatory blood pressure (BP) monitoring. Six hypertensive men were treated with doxazosin starting at 1 mg/day, and the dosage was titrated at weekly intervals up to a maximum of 8 mg/day. The twenty-four-hour BP profile was monitored noninvasively before treatment, in the fourth week of treatment, and on days 2 and 7 after the discontinuation of doxazosin. The average twenty-four-hour systolic and diastolic BPs (SBP and DBP) were lowered by doxazosin treatment and returned to the pretreatment levels within two days of doxazosin withdrawal. Doxazosin treatment produced a significant decrease in the daytime SBP and DBP but not in the nighttime BP values. The daytime BP decrease was no longer detected on days 2 and 7 after drug withdrawal. The twenty-four-hour pulse rate was not influenced by either doxazosin administration or discontinuation. The plasma norepinephrine concentration and plasma renin activity were increased by doxazosin treatment and were decreased by drug withdrawal. There was no rebound hypertension following doxazosin withdrawal. Thus, the present study using twenty-four-hour BP monitoring showed that doxazosin treatment reduced the daytime BP in patients with essential hypertension and that this reduction was abolished within two days after doxazosin discontinuation.
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PMID:Effect of administration and withdrawal of doxazosin on ambulatory blood pressure in patients with essential hypertension. 781 52

To investigate the effects of enalapril and hydrochlorothiazide on erythrocyte sodium and potassium in relation to their effects on BP, 28 men (mean age 46 years, range 22-64 years) with previously untreated essential hypertension (casual DBP > or = 95 mmHg) were randomised to enalapril (n = 14) or hydrochlorothiazide (n = 14) treatment. BP was also measured intraarterially (brachial artery) and the mean arterial pressure (MAP) recorded. Intraerythrocyte sodium and potassium were measured by flame photometry at baseline and after 26 weeks of active treatment in the hypertensive patients and also in 28 age- and sex-matched normotensive control subjects. There was a significant positive relationship between intra-arterial BP and intraerythrocyte sodium in untreated hypertensives, but there was no significant difference in mean intraerythrocyte sodium or potassium content between hypertensive and normotensive subjects at baseline. The distribution of values of intraerythrocyte sodium, however, differed between hypertensive and normotensive subjects. Supine MAP was lowered from 113 +/- 4 to 97 +/- 3 mmHg and from 110 +/- 3 to 102 +/- 2 mmHg on enalapril and hydrochlorothiazide treatment, respectively. BP reduction with enalapril was associated with a significant decrease in intraerythrocyte sodium (P = 0.02), while hydrochlorothiazide had no effect. There was no significant correlation between delta MAP and delta intraerythrocyte sodium after 26 weeks in any of the groups. Intraerythrocyte potassium did not change on treatment with either drug. In conclusion, there wa a significant relationship between intra-arterial BP and intraerythrocyte sodium in untreated hypertensives. Both enalapril and hydrochlorothiazide reduced BP effectively while enalapril only reduced intraerythrocyte sodium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship between change in erythrocyte sodium and antihypertensive response to enalapril. 785 27

An exaggerated pressor reaction to the isometric exercise and cold pressor test (CPT) is found to be a predictor or future hypertension. In the two groups of young males: 51 men with positive family history of essential hypertension (EH) (mean age: 24.3 +/- 3.3 years, group S) and 11 men with negative history of EH (mean age: 23.5 +/- 3.7 years, group K) the blood pressure responsiveness to the handgrip test (HG) and CPT were evaluated. Ambulatory systolic (SBP) and diastolic (DBP) blood pressure were higher in S then K (respectively: 136 +/- 11/81 +/- 10 mm Hg vs 126 +/- 4/76 +/- 6 mm Hg, p < 0.05). The elevation of blood pressure after HG (30% of maximal voluntary contraction for 3 min.) was higher in K than S (respectively: delta SBP = 37 +/- 20 vs 21 +/- 17 mm Hg i delta DBP = 27 +/- 20 vs 7 +/- 12 mm Hg, p < 0.05). Similarly, after CPT (by immersing the left hand and forearm in ice-cold water for 2 min.) the elevation of blood pressure was higher in K than S (respectively: delta SBP = 22 +/- 11 vs 12 +/- 12 mm Hg i delta DBP = 17 +/- 12 vs 9 +/- 9 mm Hg, p < 0.05). These results do not confirm an exaggerated blood pressure responsiveness to the HG test or CPT in young males with positive family history of EH, irrespectively to the diagnosis of normotension or borderline hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Isometric exercise and cold pressor test in young men with a family history of essential hypertension]. 786 83

This is the first report of long-term use (one year) of isradipine, a new dihydropyridine calcium channel blocker, in the treatment of elderly patients with essential hypertension. Patients completing a three month, double-blind, multicentre study comparing isradipine to hydrochlorothiazide (HCTZ) were eligible to enroll in this open-label, continuation study. At initial baseline, patients were at least 60 years of age and had DBP from 95 mmHg to 120 mmHg. Patients were titrated when necessary every two weeks with isradipine, 5 mg to 15 mg once daily or 2.5 mg to 10 mg twice daily, to maintain sitting DBP < or = 90 mmHg. HCTZ, 12.5 mg to 50 mg once daily, could be added for better BP control. A total of 136 patients completed the one year, open-label phase. One hundred and fourteen patients (84%) received isradipine as monotherapy (mean dose, 9.7 mg/day); 22 received concomitant HCTZ therapy at one year. Reduction in DBP was significant and similar among all age groups and races (mean change of -19 mmHg). Reduction in SBP was similar among all age groups. Ninety-four per cent of those receiving isradipine monotherapy achieved BP control during the last four months of treatment. Twenty-six patients (16%) withdrew from the study: 11 (7%) had adverse reactions (one with headache, two with pedal oedema, eight with other problems); 11 (7%) had nondrug-related problems; and in four (2%), the drugs were ineffective. Based on these observations, isradipine is a well-tolerated, safe and effective agent for long-term BP control in elderly patients with essential hypertension.
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PMID:One year experience of elderly hypertensive patients with isradipine therapy. 788 90

In a randomised, placebo-controlled design 40 patients with moderately severe essential hypertension were treated with bunazosin (CAS 52712-76-2) retard in increasing doses ranging between 6 and 18 mg/day. In intervals of 14 days titration steps were made, the minimal period of treatment was 4 weeks. In 34 patients (80.6%) a blood pressure response could be achieved with Bunazosin retard alone, the rest of the patients needed the additional administration of 25 mg hydrochlorothiazide daily. In all actively treated patients diastolic blood pressure could be normalised (DBP < or = 90 mmHg). After 4 weeks the mean blood pressure was lowered in the Bunazosin group by 16.2 mmHg (diastolic) and 25 mmHg (systolic). The mean heart rate at rest remained almost constant. Bunazosin was generally well tolerated; only very few adverse events occurred, and no patient collapsed. Compared to placebo the orthostatic tolerance was not influenced by bunazosin retard. Only when changing from resting to standing position the rise in heart rate was slightly more pronounced under bunazosin. Also the physiological blood pressure profile under bunazosin remained unchanged during the orthostatic tests.
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PMID:[Treatment of essential hypertension with the alpha-1 antagonist bunazosin retard. A multicenter, double-blind, placebo-controlled study]. 790 71


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