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Biomedical subjects

A Westheim

Publications and source records attributed to A Westheim.

At least 73 records · Page 4Linked to original sources
PubMed1986

Hormonal responses to treatment of high blood pressure with low-salt diet alone and combined with added potassium.

One week strict sodium depletion in essential hypertensive men (n = 17) decreased blood pressure and body weight. Plasma renin concentration increased four-fold (p less than 0.001), plasma noradrenaline with 38% (p less than 0.001), plasma dopamine with 58% while plasma adrenaline remained unchanged. The urinary excretion of vasopressin was reduced with 50% (p less than 0.001). Extra potassium induced only small changes when already sodium depleted. Thus, vasopressin was the only pressor hormone which varied directly with sodium intake, blood pressure and body weight during sodium depletion.

Arginine Vasopressin↗
PubMed1986

Effect of exercise training in patients with essential hypertension.

After 12 weeks of regular exercise training in 34 patients with moderate essential hypertension, supine systolic blood pressure at rest decrease from 152 +/- 2 (means +/- SEM) to 149 +/- 2 mmHg (p less than 0.05), and diastolic blood pressure from 106 +/- 1 to 102 +/- 1 mmHg (p less than 0.001). At corresponding submaximal exercise levels, diastolic blood pressure also decreased significantly from 110 +/- 2 to 98 +/- 3 mmHg (p less than 0.001), but no significant reduction in systolic blood pressure was observed. Heart rate at the same submaximal work load was significantly reduced (p less than 0.01). This data shows that exercise training might have blood pressure lowering effect in patients with moderate essential hypertension, and might in some patients be an alternative to pharmacological treatment.

Adult↗
PubMed1986

Central dopaminergic control of prolactin in essential hypertension.

An exaggerated, early prolactin response (p less than 0.01) was observed in ten patients with untreated essential hypertension (148 +/- 4/97 +/- 1 mmHg, means +/- SE) compared with ten healthy normotensive men of the same age (124 +/- 3/78 +/- 2 mmHg) after administration of metoclopramide, a competitive dopamine antagonist. The normotensive peak value of prolactin never exceeded that of the hypertensive (p less than 0.05). Since prolactin is considered an indicator of central dopaminergic activity, these findings suggest an altered central dopaminergic activity in mild essential hypertension.

Adult↗
PubMed1986

Serum phosphate and sympathetic tone in mild essential hypertension.

Forty-year old, normocalcaemic men with mild essential hypertension (n = 35) had decreased serum phosphate (p less than 0.001) concomitant with elevated plasma adrenaline (p less than 0.03) and heart rate (p less than 0.001). All had unchanged serum immunoreactive parathyroid hormone concentrations compared to age-matched normotensive control men (n = 44). Serum phosphate levels correlated negatively with plasma adrenaline (p less than 0.05), plasma noradrenaline (p less than 0.05), mean blood pressure (p less than 0.001) and heart rate (p less than 0.05). Serum phosphate was significantly lowered by infusion of small amounts of adrenaline at all four infusion rates in a hypertensive group (n = 12) while a similar effect was obtained only at the two highest infusion rates in a normotensive group (n = 10). No change in serum calcium was observed in either group. Thus, hypophosphataemia appears to be inversely related to sympathetic tone in essential hypertension.

Adult↗
PubMed1986

Blood platelet release correlates with serum lipids in 50 year old men with essential hypertension.

50 year old men with moderate, essential hypertension (n = 39) were compared to normotensive males of similar age (n = 31). The hypertensive men were heavier (10 kg in average, p less than 0.01), and had a higher pulse rate (5 beats per minute (p less than 0.05). Plasma beta-thromboglobulin, a marker of platelet release reaction, was 49% higher in the hypertensive group (p less than 0.01). Total cholesterol, LDL + VLDL cholesterol and serum triglycerides were not significantly different between the groups. In the hypertensive group, plasma beta-thromboglobulin concentration correlated significantly with total cholesterol (r = 0.47, p less than 0.01) as well as with LDL + VLDL cholesterol (r = 0.50, p less than 0.01). In the normotensive group no such correlation was found. The results suggest activation of platelets in hypertension, and suggest that in hypertension, even a normal cholesterol concentration may influence platelet function.

Blood Platelets↗
PubMed1986

Platelet volume, platelet release reaction and platelet response to infused adrenaline are increased in essential hypertension.

Hypertensive men aged 42 (n = 35) were compared to normotensive men of similar age (n = 44). Platelet numbers were similar in the two groups, but hypertensive men had larger venous platelets than the normotensive (7.46 versus 7.12 femtoliter, p = 0.01). Plasma concentration of beta-thromboglobulin (BTG), a marker of platelet release reaction, was increased in arterial blood in hypertension (40 versus 21 micrograms/l, p = 0.02). The normotensive subjects had markedly higher BTG concentration in venous compared to arterial blood (p less than 0.01), but this arterio-venous difference was not present in the hypertensive group. Twelve normotensive subjects received infused saline, which did not induce changes in platelet variables. Adrenaline was infused to 13 hypertensive and 12 normotensive subjects, with dose gradually increasing to 0.04 microgram/kg/min. Platelet count increased in both groups, but significantly more in the hypertensive group. Platelet volume and BTG both increased markedly in the hypertensive group, but not in the normotensive men. Thus, young men with hypertension have increased platelet activity and increased sensitivity to exogenous adrenaline.

Adult↗
PubMed1986

Increased plasma vasopressin in low renin essential hypertension.

Baseline plasma vasopressin concentrations were measured in 48 men (all 50 years old) with decreased plasma renin concentration and untreated, sustained essential hypertension and in 29 healthy normotensive men. Mean hypertensive plasma vasopressin concentration was more than twice as high as the corresponding normotensive level (15.7 +/- 2.2 [SE] vs 7.5 +/- 1.0 pg/ml; p less than 0.001). Plasma renin concentration in the hypertensive group was reduced compared with that in the normotensive group (0.28 +/- 0.04 vs 0.46 +/- 0.06 Goldblatt units X 10(-4)/ml). These differences appeared despite virtually identical serum osmolality, creatinine clearance, and urinary sodium excretion in the two groups. In the first 38 hypertensive subjects, arterial plasma epinephrine concentrations were significantly increased over those of the first 28 control subjects (99 +/- 12 vs 68 +/- 6 pg/ml; p less than 0.025). In contrast to those with low renin essential hypertension, 35 men with normal renin essential hypertension (all 40 years old) had normal plasma vasopressin levels that were not significantly different from those in a comparable normotensive control group (3.7 +/- 0.8 vs 3.5 +/- 0.4 pg/ml). Arterial epinephrine concentrations were not significantly different between normal renin subjects and the control group. After 6 weeks of treatment with the nonselective beta-adrenergic receptor blocker oxprenolol in 11 subjects with low renin hypertension, blood pressure was reduced and the plasma vasopressin concentration fell from 27.6 +/- 6.4 to 13.5 +/- 4.2 pg/ml (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1986

Plasma adrenaline and noradrenaline during orthostasis in man: the importance of arterial sampling.

Plasma adrenaline and noradrenaline were measured in arterial blood and in forearm venous blood during supine rest and after 30 min standing in normotensive, healthy 50-year-old men (n = 16). After 30 min standing, venous noradrenaline had increased from 1.61 +/- 0.11 to 4.22 +/- 0.30 nmol/l and arterial from 1.43 +/- 0.06 to 2.93 +/- 0.15 nmol/l. Orthostasis induced a seven-fold increment in the forearm arterial-venous difference of noradrenaline from -0.18 +/- 0.08 to -1.29 +/- 0.25 nmol/l (p less than 0.001). Orthostasis more than doubled the forearm arterial-venous difference of adrenaline from 0.15 +/- 0.03 to 0.31 +/- 0.05 nmol/l (p less than 0.001) since arterial adrenaline increased from 0.31 +/- 0.03 to 0.53 +/- 0.05 nmol/l and venous from 0.16 +/- 0.02 to 0.22 +/- 0.02 nmol/l. Arterial adrenaline correlated significantly with venous in the supine (r = 0.64, p less than 0.01) but not in the standing position (r = 0.34, NS). The results indicate that arterial concentrations of adrenaline are a much better indicator of sympatho-adrenal activity during orthostasis than peripheral venous concentrations. For noradrenaline, measurements of arterial concentrations during the orthostatic manoeuvre seem to provide information about the total noradrenergic sympathetic reactivity, while the corresponding measurements in peripheral venous blood represent the forearm locally.

Arm↗
PubMed1985

Acute hemodynamic effects of propranolol, glycerylnitrate, and exercise in coronary patients with left ventricular dysfunction.

Some adverse effects of beta-blockers in heart failure are counteracted by glycerylnitrate. However, the hemodynamics in this condition after giving both drugs are not well known. We examined the drug combination in exercising coronary patients with left ventricular dysfunction. Elevated left ventricular end-diastolic pressure was a measure of dysfunction. A right-heart catheterization with three successive exercise stress tests was done in 40 patients. At repeated exercise without drugs a "warming up" phenomenon was observed, consisting of small but statistically significant reductions in pulmonary capillary wedge pressure, and heart rate. At exercise propranolol reduced heart rate, cardiac output, systemic blood pressure, left ventricular work, and increased arteriovenous oxygen difference. Glycerylnitrate reduced pulmonary capillary wedge pressure at exercise, but, contrary to the findings at rest, it did not increase heart rate or reduce cardiac output. The drug combination resulted in hemodynamics that were similar to those after propranolol alone, except for a lower pulmonary capillary wedge pressure. The drug combination allowed the patients to exercise with the benefits of the beta-blocker, but at a lower ventricular filling pressure. Thus, the potential hazard of giving beta-blockers to patients with left ventricular dysfunction may be reduced by adding glycerylnitrate.

Angina Pectoris↗
PubMed1985

Effect of exercise training in patients with essential hypertension.

The aim of the present study was to examine the effect of regular exercise training in moderate essential hypertension. Twenty subjects (one woman and 19 men) trained for 45 minutes three times a week for 12 weeks, to 60% of their maximal heart rate. Blood pressure was measured at rest and during a maximal exercise test on bicycle ergometer. All subjects achieved training effect measured as a significant reduction in heart rate at comparable submaximal work level and a significant increase in duration of exercise. Diastolic blood pressure at rest decreased from 107 +/- 7 to 101 +/- 5 mmHg (P < 0.01), and at corresponding submaximal exercise level 116 +/- 11 to 106 +/- 11 mmHg (P < 0.01). No significant reduction in systolic blood pressure was found. Exercise training might in some patients with moderate essential hypertension be an alternative to pharmacological treatment.

Adult↗
PubMed1984

Venous thrombosis following diagnostic transvenous catheterization by percutaneous catheter insertion: an evaluation of desmopressin as a thromboprophylactic agent.

The preventive effect of desmopressin with respect to catheter induced thrombosis was studied in a randomized double-blind trial, consisting of 30 patients undergoing percutaneous transcubital right heart catheterization. Phlebography of the catheterized arm was performed after five days. The frequency of post-catheterization thrombosis was reduced by 33 per cent, from 86 per cent in the treatment group to 53 per cent in the control group (0.1 less than p less than 0.2). This effect was restricted to minor thrombi, whereas major thrombosis could not be prevented. Patient materials such as that of the present study, may become useful in preliminary investigations of thromboprophylactic agents.

Arginine Vasopressin↗
PubMed1984

Arteriovenous difference of plasma vasopressin in normal man and effect of posture.

In 13 normotensive 50-year-old men arterial plasma vasopressin (11.3 +/- 2.1 ng/l, mean +/- SE) was significantly increased over venous (7.8 +/- 1.4 ng/l) in the supine position with an arteriovenous difference of 3.5 +/- 1.2 ng/l (p less than 0.05). After 30 min in the upright position, an average increment of 45% to 11.3 +/- 1.8 ng/l was observed for venous vasopressin. Since a similar increase was not found for arterial vasopressin, the arteriovenous difference decreased with 29% to 2.5 +/- 2.1 ng/l and was no longer statistically significant. The correlation between supine and standing vasopressin was statistically significant both for arterial (p less than 0.001) and venous plasma (p less than 0.05). These data indicate a substantial removal of plasma vasopressin by receptors even in the peripheral vascular beds (forearm) and not only in the liver and the kidneys as previous literature claims. The arteriovenous difference decreases in the upright position, most likely because of reduced plasma vasopressin clearance.

Arginine Vasopressin↗
PubMed1982

Renal contribution to plasma catecholamines--effect of age.

In 18 subjects undergoing diagnostic cardiac catheterization renal venous noradrenaline during rest (296 +/- 26 ng/l, mean +/- SE) was significantly increased over arterial noradrenaline concentrations (250 +/- 20 ng/l, P less than 0.01) while, in contrast, the arterial adrenaline level (79 +/- 9 ng/l) was higher than the renal venous (41 +/- 4 ng/l, P less than 0.001). Age correlated positively with both renal venous noradrenaline (r = 0.56) and the renal venous-arterial difference of noradrenaline (r = 0.56), and negatively with arterial (r = -0.52) and renal venous adrenaline (r = -0.48). According to our data, a net renal venous secretion of noradrenaline and at the same time an uptake of adrenaline from the renal circulation take place at an extent that may influence plasma concentrations of both. With increasing age renal uptake of plasma adrenaline seems to decrease and net release of noradrenaline to increase. The fall in plasma adrenaline may be due to age-dependent involution of the adrenal medulla. In studies of plasma adrenaline concentrations and of the renal handling of plasma catecholamines the influence of age must be taken into account.

Adolescent↗