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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of metoprolol, a selective beta adrenergic receptor antagonist, on blood pressure, beta receptor blockade (antagoinst of isoproterenol and exercise tachycardia), and plasma renin activity (PRA) have been compared with those of placebo in 16 patients with essential hypertension. The dose of metroprolol was 25 mg three times daily for 1 wk and thereafter 100 mg three times daily for 5 wk. The mean decrease in blood pressure during treatment with metoprolol was 24 +/- 3.8 (SEM)/10 +/- 2.1 mm Hg in the lying position and 23 +/- 4.4/9 +/- 3.1 mm Hg after 1 min in the standing position. At a dose of 2.9 to 5.4 mg/kg, steady-state plasma concentrations of metoprolol varied 17-fold (from 20 to 341 ng/ml) between patients and correlated with the interindividual variability in isoproterenol antagonism (r = 0.58, p less than 0.05) and decrease in exercise tachycardia (r = 0.65, p less than 0.01). By contrast, neither of these variables correlated with the dose of metoprolol in mg/kg. Metoprolol decreased PRA by 67 +/- 1.9 and 71 +/- 1.2% in the lying and standing positions, respectively. The decrease in the mean arterial blood pressure in the lying position was significantly correlated to the PRA during the placebo period (r = 0.61, p less than 0.05) but not to the plasma steady-state levels of metoprolol, the degree of beta receptor blockade, and the decrease in PRA.
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PMID:Plasma levels and effects of metoprolol on blood pressure, adrenergic beta receptor blockade, and plasma renin activity in essential hypertension. 0 73

1. A Valsalva-like manoeuvre was used to elicit graded rises in total peripheral resistance (TPR) in conscious rabbits. The rises were reflex and mediated through sympathetic constrictors. Propranolol infused at different rates reaching plasma concentrations up to 240 (SEM 33) ng/ml had no effect on this reflex but reduced mean arterial pressure. However, the response was attenuated by clonidine in a dose-dependent manner. 2. Valsalva manoeuvres were used to elicit graded sympathetically mediated rises in TPR index in twenty-nine subjects with mean arterial pressure ranging from 75 to 165 mmHg. Absolute sensitivity of the constrictor response increased with rising resting TPR index, resulting in some enhancement of constrictor responses in the hypertensive subjects. It seems likely that non-autonomic factors (e.g. vessel structure) rather than hyperactive neural constrictor effects are involved in the enhanced constrictor responses in essential hypertension.
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PMID:Valsalva vasoconstrictor reflex in human hypertension in after beta-adrenoreceptor blockade in conscious rabbits. 1 55

We have established a simplified assay system for the measurement of urinary kallikrein activity by utilizing the sensitive and specific radioimmunoassay system of kinins previously reported from our laboratory. Kinins were generated by incubating urine samples (50 microliter) with kininogen (1500 ng) in the presence of kininase inhibitors, and the generated kinins were measured by radioimmunoassay. Since the cross reactivity of kininogen in the kinin radioimmunoassay system was not recognized at dose up to 1.0 microgram, the amount of untreated kininogen in the radioimmunoassay samples did not interfere with the measurement of kinins. This eliminated the necessity for a kininogen extraction procedure. A good linear correlation (r = 0.939, p less than 0.001) was observed between the urinary kallikrein activity determined by this assay system (kininogenase activity) and that by esterolytic acitvity. Urinary kallikrein activity was 3.3 +/- 0.9 microgram/min/24 hour urine (mean +/- SEM), 1.4 +/- 0.4 microgram/min/24 hour urine and 0.25 +/- 0.06 microgram/min/24 hour urine in 6 normal subjects, 7 patients with non-complicated essential hypertension and 4 patients with chronic renal failure, respectively. Thus, urinary kallikrein activity was significantly lower in the patients with essential hypertension (p less than 0.05) and the patients with chronic renal failure (p less than 0.01) than in the normal subjects.
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PMID:Measurement of urinary kallikrein acitvity by kinin radioimmunoassay. 10 45

Splanchnic blood flow (SBF) was measured simultaneously with cardiac output (dye dilution) and intrarterial blood pressure by constant infusion of indocyanine green in 11 control subjects, 13 patients with essential hypertension (EH) and seven hypertensive patients with renal artery stenosis (RAS). The cardiac index (CI) was lower (P less than 0.05) in patients with EH (3.17 plus or minus 0.07 L/min/m-2) (mean plus or minus SEM) than in control subjects (3.43 plus or minus 0.09). Associated with the lower CI was a significantly (P less than 0.01) lower SBF (0.797 plus or minus 0.02 L/min/m-2 vs 0.889 plus or minus 0.04). Patients with RAS presented with higher (P less than 0.01 vs EH, nonsignificant vs control subjects) cardiac index (3.66 plus or minus 0.17) and even lower SBF (0.749 PLUS OR MINUS 0.02). Furthermore, there was a negative correlation (r = - 0.652) between the mean arterial pressure and the SBF when results for all patients were considered. The correlation remained (r = - 0.568) in the EH group and the slope of regression line was not different from that for all subjects. The CI and SBF were weakly correlated (r = 0.423) in control subjects and patients with EH, whereas in patients with RAS, a negative correlation was found (r = - 0.778). This study indicates that the SBF, although significantly decreased in patients with EH, remains proportional to the CI in control subjects and in essential hypertensive patients. No redistribution of CI in regard to the splanchnic circulation occurs in EH. In contrast, in patients with RAS a dissociation of CI and SBF occurs and the fraction of the CI which passes through the splanchnic vascular bed is markedly reduced. The close correlation between mean arterial pressure and SBF suggests that both parameters are influenced by a common pathophysiological factor.
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PMID:Splanchnic blood flow in essential hypertension and in hypertensive patients with renal artery stenosis. 12 33

Aldosterone receptors from rat kidney slices were utilized in a competitive binding technique to analyze the contribution of various steroids to plasma "mineralocorticoid" activity and to assess their possible role in hypertension. To consider simultaneously the plasma binding, steroids were incubated with slices in undiluted plasma; competitor activities for [3H]aldosterone binding were aldosterone, 100%; deoxycorticosterone, 16.2%; cortisol, 0.4%; and 18-hydroxy-deoxy-corticosterone and d18-hydroxy-corticosterone, 0.1%. These steroids were more active in buffer than plasma, suggesting that they bind to plasma and that this reduces their receptor binding. Analysis of the competition data suggests that at normal plasma concentrations, aldosterone occupies the receptors to a major extent, cortisol occupies some of the receptors, and deoxycorticosterone and 8-hydroxydeoxycorticosterone contribute little to receptor occupancy. Two steroids implicated in low-renin essential hypertension, 16beta-hydroxy-dehydro-epiandrosterone and 16-oxoandrostenediol, did not have significant competitor activity. Competitor activity in plasmas from normal subjects taken at 12 noon (upright) was greater than that in those taken at 8 a.m. (supine). Since the 12 noon samples had higher aldosterone and lower cortisol levels than the 8 a.m. samples, the competitor activity under these physiological circumstances reflects aldosterone more than cortisol. The competitor activities of plasmas from patients relative to normal subjects (100+/-12.1%; mean+/-SEM) were: normal renin "essential" hypertension, 117+/-14%; low-renin essential hypertension, 101+/-6.6%; and primary aldosteronism, 176+/-14.3%. Thus a significant increase in activity of steroids that interact with mineralocorticoid receptors was detected in primary aldosteronism (P LESS THAN 0.01) BUT WAS NOT DETECTED IN LOW-RENIN OR NORMAL-RENIN ESSENTIAL HYPERTENSION.
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PMID:Aldosterone receptors and the evaluation of plasma mineralocorticoid activity in normal and hypertensive states. 18 23

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

Under basal conditions prostaglandin (PG) E2-excretion was significantly lower in 35 patients with essential hypertension studied than in 22 age- and sex-matched controls (p less than 0.02). PGF 2 alpha--excretion was similar in both groups. Within the first 15 minutes after furosemide i.v., PGE2-excretion rose substantially less in the patients than in the controls (p less than 0.001), while the increase in PGF 2 alpha-excretion was not different for both groups. The coincident rise of plasma renin activity was significantly lower in the hypertensive (167% +/- 11, SEM) than in the normotensive (386% +/- 46) group (p less than 0.001). Our results support the assumption that a decrease in renal cortical (vascular?) synthesis of vasodilatating PG's may be the cause for both, the diminished secretion of renin and the increase of vascular resistance in the kidney, which are often associated in essential hypertension.
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PMID:[Reduced urinary prostaglandin E2-excretion and diminished responsiveness of plasma renin activity in patients with essential hypertension (author's transl)]. 45 71

The feasibility of differentiating patients with pheochromocytoma from other hypertensive patients by measuring urinary excretion rates of norepinephrine during sleep, a period of physiologic suppression of norepinephrine release, was investigated. The mean excretion rates of norepinephrine in 248 normal subjects and in 109 patients with essential hypertension were 1.03 +/- 0.03 and 1.12 +/- 0.06 (SEM) micrograms/hour, respectively, whereas the lowest excretion rate among the six patients with pheochromocytoma was about seven times higher. Plasma norepinephrine concentration in patients with pheochromocytoma was also consistently above the range observed in both normotensive and hypertensive subjects. CT scan correctly identified the same tumors visualized by selective arteriography. It is suggested that the usefulness of these approaches will provide simpler means of screening and detecting pheochromocytoma.
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PMID:Diagnosis and localization of pheochromocytoma. Detection by measurement of urinary norepinephrine excretion during sleep, plasma norepinephrine concentration and computerized axial tomography (CT-scan). 46 12

Plasma renin activity (PRA) was measured during the administration of clonidine (0.1 mg twice daily) to 11 patients with essential hypertension. After eigth weeks a trend toward an increase in PRA was noted. This increase was significant in "low renin" subjects (less than 1 ng Al/ml/hr, n = 7) in whom PRA (ng/ml/hr +/- SEM) rose from a control value of 0.7 +/- 0.1 to 2.0 +/- 1.1 at one week, 5.6 +/- 2.1 at four weeks, and 4.4 +/- 1.0 at eight weeks (p less than 0.05). In contrast, in a small group of "normal renin" patients (n = 4), PRA did not change significantly but tended to decrease on clonidine therapy from 9.2 +/- 3.4 at control to 3.3 +/- 2.0 at one week, 3.4 +/- 0.6 at four weeks, and 4.7 +/- 1.7 ng Al/ml/hr at eight weeks. Plasma renin substrate and serum and urinary electrolytes did not change significantly in either group and blood pressure reduction was comparable in the two groups. A strong negative correlation (r = -0.84, p less than 0.001) was found between changes in creatinine clearance and changes in PRA. Previous studies have implicated alpha-adrenergic receptors as the site of clonidine actions on blood pressure and renin release. The observed renin stimulation during chronic administration of clonidine to "low renin" patients with essential hypertension may imply an altered intrarenal alpha-receptor function in "low renin" essential hypertension.
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PMID:Renin stimulation during clonidine therapy in "low renin" essential hypertension. 72 16

The effect of atenolol, a beta adrenoceptor autogonist, on arterial pressure in patients with benign essential hypertension has been investigated. Eighteen patients were started on atenolol, 75 mg/day; the dose was increased at 2-wk intervals to a maximum of 900 mg if tolerated. When the maximum effective dose was determined, each patient was randomly allocated into a double-blind crossover study comparing atenolol and placebo treatments. The mean supine and erect arterial pressures of the 16 patients completing the run-in period were markedly reduced by atenolol therapy. The pretreatment mean (+/-SEM) supine and erect arterial pressures of the 16 patients completing the run-in period (187 +/-4.7/114 +/-2.6 and 182 +/-4.5/115 +/-3.0 mm Hg, respectively) were reduced (150 +/-5.3/97 +/-2.9 and 151 +/-5.9/100 +/-2.7 mm Hg) with atenolol therapy (p less than 0.01). In the crossover study, the mean (+/-SEM) supine arterial pressure after 8 wk of atenolol therapy in 14 patients (144 +/-5.2/89 +/-1.7 mm Hg) was lower (p less than 0.01) than at the end of placebo therapy (163 +/-4.4/105 +/-2.8 mm Hg). Similar reductions in pressure were recorded in the erect position and after exercise. No severe side effects were observed.
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PMID:Atenolol in essential hypertension. 77 87


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