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

Five male subjects with essential hypertension received chlorthalidone at each of four dose levels (25, 50, 100, and 200 mg/day) for eight week periods each preceded by an eight week placebo period. Dosage order was randomized and double-blind. During the last week of each active and placebo period an upright bicycle exercise study was carried out at three loads (100, 200, 300 kpm/min) for 6 min each. Oxygen consumption at the maximal workload was 42% of predicted at a heart rate of 170. During placebo therapy, increasing workloads were associated with a progressive increase in blood pressure, heart rate, and pressure-rate index (systolic pressure times heart rate). With increasing doses of chlorthalidone up to 100 mg/day, there was a progressive reduction in blood pressure and pressure-rate index. At 200 mg/day there were paradoxical increases in diastolic pressures, heart rates and pressure-rate indices above values observed at 100 mg/day. With increasing doses of chlorthalidone, there was a progressive increase in arterial blood CO2 content and pH. Increasing workloads were associated with increased arterial blood lactate and decreased arterial blood lactate and decreased arterial blood pH. The changes in lactate and pH were not different at the different dose levels. The best antihypertensive effect in these exercising subjects was observed at a daily dose of 100 mg of chlorthalidone. The exercise response was useful in the determination of potentially adverse hemodynamic consequences of the larger dose of chlorthalidone.
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PMID:Cardiovascular response to exercise under increasing doses of chlorthalidone. 0 91

Venous distensibility in essential hypertension has been reported to be unchanged or decreased; its pathophysiologic role is uncertain. In 27 male hypertensive patients and 21 normotensive control subjects, forearm venous distensibility and capillary filtration rate at 30 cm of H2O distending pressure were measured by strain gauge plethysmography. Plasma renin activity (PRA), plasma volume (PV) by the Evans blue dye dilution technique, mean arterial pressure (MAP) by cuff, and cardiac output (CO) by the CO2 rebreathing method were also measured. Compared to values in normotensive control subjects, forearm venous distensibility in hypertensive subjects was decreased (P less than 0.05); the forearm venous pressure-volume curves (deflation phase) were shifted in the direction of the pressure axis (P less than 0.02); and the capillary filtration rate was increased (P less than 0.05). Venous distensibility changes in hypertensive subjects were unrelated to PRA, MAP, PV, CO, stroke volume, and total peripheral resistance. These findings confirm previous reports of decreased venous distensibility in hypertension and provide direct evidence for increased capillary filtration rate. In view of the lack of significant correlation between venous distensibility and the measured hemodynamic parameters, a patho-physiologic role for venous distensibility in hypertension could not be established.
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PMID:Decreased venous distensibility in essential hypertension: lack of systemic hemodynamic correlates. 37 15

Oxprenolol is a beta-adrenergic blocker with intrinsic sympathomimetic activity. Such drugs are not currently available in the United States, although they have the advantage of less negative inotropic effect than the available propranolol. In 18 patients with mild essential hypertension, oxprenolol (9 patients) or propranolol (9 patients) was added to thiazide in random double-blind fashion and continued for 7 wk during which supine heart rate, blood pressure, and noninvasively measured cardiac output (by CO2 rebreathing) were determined weekly. With thiazide dosage constant throughout, maximal dose titration to 386. +/- 52.1 (SEM) mg/day of oxprenolol and 360.0 +/- 45.4 mg/day of propranolol was achieved over the first 5 wk. Blood pressure fell with both (141.8 +/- 4.8/96.0 +/- 2.3 to 128.0 +/- 5.1/87.2 +/- 1 mm Hg on oxprenolol, p less than 0.01; 150.8 +/- 5.5/98.0 +/- 1.7 to 129.9 +/- 5.5/86.8 +/- 3.4 mm Hg on propranolol, p less than 0.01). Cardiac output fell from 6.85 +/- 0.63 to 5.77 +/- 0.45 1/min (p less than 0.01) on oxprenolol, and from 6.79 +/- 0.61 to 5.37 +/- 0.37 1/min (p less than 0.02) on propranolol. Oxpranolol. Oxprenolol reduced heart rate from 76.4 +/- 2.0 to 65.6 +/- 2.1 beats/min (p less than 0.001) and it fell from 82.0 +/- 3.8 to 65.3 +/- 3.7 beats/min (p less than 0.001) with propranolol; the fall in heart rate was less but not significantly so for oxprenolol (-14.2 +/- 1.8% and -19.8 +/- 2.8%, p less than 0.1). Thus oxprenolol is equivalent to propranolol in antihypertensive action; minor hemodynamic differences between the two drugs might reflect intrinsic sympathomimetic activity of oxprenolol. Oxprenolol should be considered as an alternative to propranolol.
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PMID:Hemodynamic effects of oxprenolol and propranolol in hypertension. 38 30

A new device (called a hemodynamometer) employing the principle of the CO2 rebreathing method has been developed for the noninvasive automatic measurement of pulmonary blood flow (cardiac output = CO). The device can also measure oxygen consumption (VO2) and indirect blood pressure and record electrocardiographs (heart rate) at the same time and can automatically calculate total peripheral vascular resistance (TPR) by means of a computer. In this study, the hemodynamometer was used in 28 normotensive subjects and 42 patients with essential hypertension (27 with WHO stage I and 15 with WHO stage II) to evaluate hemodynamics during rest or ergometer exercise. To evaluate accuracy, the dye-dilution (cuvette) method was simultaneously employed in some subjects. The correlation coefficient (r) between CO measured by means of the hemodynamometer and CO measured by the cuvette method was 0.96 (n = 39) with a differential of 0.08 +/- 0.53 l/min and reproducibility was good (r = 0.88, n = 70). The average CO index for normotensive subjects at rest was 3.22 +/- 0.37 l/min/m2 (VO2 = 210 +/- 30 ml/min/m2) and agreed with previously reported values. A significant difference was observed between the hemodynamics (CO and TPR indices) of the WHO-I group and those of the WHO-II group during rest or mild exercise (25-watt load). Because it can measure CO and TPR easily and noninvasively, the hemodynamometer is considered useful for evaluating hemodynamic changes in hypertensive patients.
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PMID:Fully automatic, noninvasive measurement of cardiac output by means of the CO2 rebreathing method and its clinical application to hypertensive patients. 212 43

Twenty-seven patients with mild to moderate essential hypertension were randomized to receive therapy with either hydrochlorothiazide or diltiazem. After a placebo run-in period of 2 weeks, patients received increasing doses of either drug for 14 weeks. Those in whom hypertension was effectively controlled continued for 26 weeks of total treatment. Those not controlled, i.e. blood pressure greater than 140/90 mm Hg or less than 10 mm Hg reduction of pressure, were unblinded and crossed over to therapy with both drugs. Eleven of 14 patients (79%) were effectively treated with diltiazem alone, and 8 of 13 patients (62%) were effectively treated with hydrochlorothiazide alone. Supine blood pressures fell from 152 +/- 5/97 +/- 1 to 142 +/- 4/87 +/- 3 mm Hg in the 11 patients treated with diltiazem, from 152 +/- 2/99 +/- 1 to 134 +/- 3/88 +/- 2 mm Hg in the 8 patients treated with hydrochlorothiazide, and from 151 +/- 4/104 +/- 3 to 140 +/- 5/92 +/- 1 mm Hg in the 8 patients who received both drugs (p less than 0.01 for each group). Diltiazem patients had significant increases in alkaline phosphatase and urinary magnesium. Hydrochlorothiazide patients had increases in serum uric acid, serum globulin, CO2 content, and plasma renin activity. Serum potassium, serum chloride, urinary osmolality, and urinary calcium decreased after treatment with hydrochlorothiazide. Patients receiving both drugs had increases in serum glucose, serum BUN, serum uric acid, serum globulin, and CO2 content. These patients had decreased serum chloride and urinary calcium. Diltiazem monotherapy was comparable to hydrochlorothiazide in efficacy of lowering blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal-metabolic consequences of antihypertensive therapy with diltiazem versus hydrochlorothiazide. 332 Jul 20

Early systemic hemodynamic adjustments to antihypertensive therapy with the cardioselective beta inhibitor, atenolol, were investigated in 12 hospitalized men, mean age 52 years, with uncomplicated mild-to-moderate essential hypertension. Twice daily measurements of cardiac output (CO) by CO2 rebreathing, blood pressure by cuff, and heart rate were performed in all subjects for 3 days before and 5 days after initiation of oral atenolol therapy (50 or 100 mg daily). Cardiac output by CO2 rebreathing was checked with dye dilution just before, and 4 hours and 4 days after the start of therapy. Plasma volume (radioiodinated albumin) was measured before therapy and on Day 5 of therapy. The CO results obtained with the two methods were not significantly different (r = 0.88, p less than 0.01, n = 12). A reduction in heart rate, 18 +/- 2 beats/min (mean +/- SE), occurred in all patients while taking atenolol. By 4 hours after the first dose of atenolol, CO fell from 5.49 +/- 0./30 to 4.24 +/- 0.21 liters/min (p less than 0.01), while the control mean arterial pressure (MAP) of 108 +/- 4 mm Hg was not significantly changed, 110 +/- 4 mm Hg. At 24 hours, CO returned near baseline (5.10 +/- 0.21 liters/min) but MAP was reduced (95 +/- 3 mm Hg, p less than 0.001) and remained so thereafter. CO remained at baseline at 48 hours (5.50 +/- 0.29 liters/min) but fell again (p less than 0.01) to 4.81 +/- 0.11 on Day 4 and to 4.68 +/- 0.25 liters/min on Day 5 of atenolol therapy. Plasma volume, 3110 +/- 100 ml before therapy, was reduced to 2850 +/- 100 by Day 5 of atenolol therapy (p less than 0.01). The findings indicate a delayed onset of the antihypertensive action of atenolol. The transient return to baseline of CO on Day 2 and 3 of atenolol therapy suggests a reverse autoregulatory adjustment to the initial fall in CO.
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PMID:Short-term systemic hemodynamic adaptation to beta-adrenergic inhibition with atenolol in hypertensive patients. 611 32

We report on four patients with hemodynamic brain infarction and pathological circadian blood pressure patterns with nocturnal hypotension which gave rise to a prolonged disturbance of the blood-brain barrier. Besides at least one severe stenosis of the internal carotid artery, there was an untreated chronic arterial hypertension and a pathologically reduced vasomotor reactivity after CO2 stimulation in all patients. The 24-h blood pressure monitoring then carried out showed a distinctly pathological circadian profile with hypertensive day values and nocturnal hypotension with minimum values of 95/50 mm Hg. The range of variation between day and night values was significantly raised (systolic: 20% +/- 2.15%; diastolic: 22.9% +/- 2.58%) compared to patients with essential hypertension as well as normotensive subjects (P < 0.01), and was in excess of 40% in the individual case. There was a slow recovery of the blood-brain barrier after drug-induced normalization of the pathological circadian blood pressure profile. We conclude that the registration of circadian blood pressure patterns may be of prognostic and therapeutic relevance. It may also contribute to further clarification of the pathophysiological significance of blood pressure variability for the development of brain infarction.
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PMID:Circadian blood pressure patterns in four cases with hemodynamic brain infarction and prolonged blood-brain barrier disturbance. 824 65

Hemodynamic consequences of the withdrawal of arterial chemoreceptor drive (ACD) by brief systemic hyperoxia were studied in 16 mild hypertensive subjects (HT) and in 16 healthy subjects (NT) in horizontal position at resting metabolic rate. In another 9 mild HT and match NT measurements were made in resting sitting position and during steady-state mild physical exercise on cycloergometer, (30% of VO2 max.) Tidal volume, minute ventilation, end tidal CO2 and O2 concentration, K+, Na+, pO2, pCO2 values in blood were recorded. Impedance reography was used for recording stroke volume (SV) and arm blood flow (ABF). Cardiac output (CO), ABF and arterial blood pressure (ABF) values were used for calculation of the total peripheral resistance (TPR) and vascular resistance in the arm (AVR). To assess the neurogenic circulatory response to withdrawal of ACD in HT attenuated by opposite peripheral effects of high oxygen, the values of AVR, ABP, TPR and AVR changes during brief hyperoxia in NT, assumed to be of peripheral origin, were subtracted from respective values in HT, assumed to be of mixed neurogenic and peripheral origin. In HT hyperoxia applied in sitting position produced a brief decrease in systolic and diastolic ABP by 5.4 +/- 0.8% and 3.4 +/- 1.1% respectively, of TPR by 12.4 +/- 3% and of AVR by 4.7 +/- 4.6%. Decrease in AVR during hyperoxia was significantly greater in sitting than in horizontal position. In NT hyperoxia produced opposite effects in ABP, TPR and AVR, as compared to those in HT. In HT subjects during steady-state exercise the TPR decreased by 21 +/- 3.7% reaching a value no different from that in NT. We suggest, that in primary hypertension neurogenic sympathoexcitatory ACD is augmented and interacts with the peripheral mechanisms related to tissue oxygen supply.
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PMID:Hemodynamic responses to brief hyperoxia in healthy and in mild hypertensive human subjects in rest and during dynamic exercise. 880 52

As it has been suggested that parathyroid hormone (PTH) is implicated in the pathophysiology of essential hypertension, the effects of PTH(1-34) were assessed during infusion over 120 min in ten men with essential hypertension and in ten healthy men. Ionized calcium was kept constant by a clamping technique. Mean arterial blood pressure fell slightly in the patients (116 mm Hg, median, before, and 108 mm Hg during the infusion, P < .01), but remained unchanged in the controls (median 87 mm Hg). The pulse rate rose to a similar extent in the two groups, but cardiac output, measured by the CO2 rebreathing technique, was unchanged. The glomerular filtration rate (GFR) was slightly lower in the hypertensives than in the controls at baseline (92 v 109 mL/min, P < .02), but it increased similarly during PTH infusion in both groups (+13% v +9%, medians), as did the effective renal plasma flow (+50% v +38%). The urinary rate of sodium excretion, which was similar at baseline, increased more in the patients than in the controls (+191% v +46%, P < .05); this was mainly attributable to a reduction in the tubular reabsorption of sodium. Calculations based on lithium clearance indicated that mainly the proximal tubular reabsorption of sodium decreased during PTH infusion. Baseline plasma PTH(1-84) was higher in the patients than in the controls (20.5 ng/L v 16.5 ng/L, P < .05). The baseline plasma values of renin, aldosterone, atrial natriuretic peptide, endothelin, and noradrenaline were similar in the two groups. During infusion of PTH, renin increased less in the patients than in the controls (P < .02), and aldosterone increased only in the controls (P < .01). The other hormonal values remained unchanged. In conclusion, the patients with essential hypertension had increased baseline PTH values, but nevertheless PTH had more marked vasodilative and natriuretic effects than in the controls. PTH thus seems to counteract rather than aggravate elevation of blood pressure in these patients.
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PMID:Effects of PTH(1-34) on blood pressure, renal function, and hormones in essential hypertension: the altered pattern of reactivity may counteract raised blood pressure. 944 71

A role for vitamin D in the pathophysiology of essential hypertension has frequently been suggested, but acute direct effects on blood pressure, cardiac output, renal hemodynamics, or hormones have not previously been demonstrated. The rapid effects of 1,25-dihydroxycholecalciferol (1,25-D) were assessed over 120 min after a bolus injection (0.02 microg/kg body weight) in eight men with essential hypertension and in nine healthy men. A placebo group of 10 healthy men was also included. Ionized calcium was monitored closely during the study, and was kept constant with a clamping technique. In the hypertensive patients, a transient increase in blood pressure and a reciprocal fall in cardiac output measured by a CO2 rebreathing technique (-15%, P < .05) were observed after 1,25-D injection. In the control group, both blood pressure and cardiac output remained unchanged. The glomerular filtration rate, effective renal plasma flow, and urinary sodium and water excretions were unchanged in both groups. Plasma levels of atrial natriuretic peptide at baseline were higher in the hypertensive patients than in the control subjects (P < .02); plasma levels of renin, aldosterone, norepinephrine, endothelin, and parathyroid hormone(1-84) were similar in the two groups. None of these hormones was affected during the observation time after the injection of 1,25-D. In conclusion, acute administration of 1,25-D caused a fast and likely nongenomic-mediated decrease in cardiac output in patients with essential hypertension, which together with a transient BP increase implies a 1,25-D-induced increase in total peripheral resistance. These data suggest an enhanced cardiovascular responsiveness to 1,25-D in hypertensive compared to healthy normotensive subjects.
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PMID:Acute cardiovascular effect of 1,25-dihydroxycholecalciferol in essential hypertension. 1019 37


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