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Biomedical subjects

I K Eide

Publications and source records attributed to I K Eide.

30 records · Page 2Linked to original sources
PubMed1990

Renal haemodynamic and sympathetic responses to head-up tilt in essential hypertension.

Nine mild-to-moderate hypertensive patients (HT), aged 41 +/- 0.6 years (mean +/- SEM) and nine age-matched normotensive control subjects (NT) were tilted to 60 degrees for 10 min. During tilt, both systolic (S) blood pressure (BP) (p less than 0.01) and diastolic (D) BP (p less than 0.05) increased in HT, but not in NT. At supine rest renal blood flow was higher in HT than in NT and increased by 17% in HT during tilt, while a decrease of 13% was observed in NT (p less than 0.05). Renal vascular resistance was unchanged in HT during tilt, while a significant increase (p less than 0.01) was observed in NT. Arterial plasma noradrenaline increased in both groups (p less than 0.05) during tilt, significantly more in HT than in NT (p less than 0.05). No statistically significant difference was observed between the groups in renal catecholamine uptake or release. Our data indicate enhanced general sympathetic and circulatory responses to tilt in subjects with mild-to-moderate essential hypertension. However, the enhanced haemodynamic and sympathetic responses were not shared by hypertensive kidneys and renovascular resistance remained unaffected by tilt.

Adult↗
PubMed1989

Arterial plasma norepinephrine correlates to blood pressure in middle-aged men with sustained essential hypertension.

Increased plasma catecholamine levels assessed from the venous blood have been found in a number of studies of younger patients with essential hypertension, but hypertensive-normotensive differences could not easily be demonstrated in subjects above 40 years of age. For several reasons, measurement of arterial plasma catecholamines may be a more sensitive tool for the detection of hypertensive-normotensive differences. The present study therefore aimed at examining both venous and arterial plasma catecholamines in a group of white men, all 50 years of age, with never-treated, established essential hypertension (n = 61, blood pressure 165 +/- 2/112 +/- 1 mm Hg, means +/- SE) and comparing them with a similar group of normotensive men (n = 51, blood pressure 128 +/- 1/85 +/- 1 mm Hg). Arterial and venous plasma epinephrine, heart rate, and body weight were significantly elevated in the hypertensive group. Plasma norepinephrine was similar between the groups in the venous blood, whereas in the arterial blood the values in hypertensive subjects were moderately, but significantly increased (p less than 0.03). However, stepwise multiple regression analysis suggested arterial plasma norepinephrine was the only significant independent explanatory variable of raised blood pressure in the hypertensive group (r = 0.51, t = 4.05, p = 0.0002). Such a relationship was not found in the normotensive group. Thus based on measurements in arterial blood, we conclude that plasma norepinephrine, representing sympathetic tone, may be an important pathogenetic factor for high blood pressure in middle-aged men with established hypertension.

Blood Pressure↗
PubMed1989

Increased erythrocyte magnesium in untreated essential hypertension.

In the present study we tested the hypothesis of magnesium deficiency and intracellular magnesium depletion in essential hypertension. Atomic absorption was used to determine the erythrocyte content of magnesium in 50-year-old otherwise healthy white men with never-treated, essential hypertension (n = 12, supine blood pressure 155 +/- 4/109 +/- 2 mmHg) and in a group of particularly well-matched normotensive control subjects. The erythrocyte magnesium content was higher in the hypertensive group (P less than 0.001). No significant difference between the groups was detected for serum concentration or the 24-h urinary excretion of the magnesium. In conclusion, magnesium deficiency is unlikely in white middle-aged hypertensive men.

Blood Pressure↗
PubMed1988

Decreased platelet-free dopamine and unchanged noradrenaline and adrenaline in essential hypertension.

The content of free-catecholamines in blood platelets is much higher than in plasma and platelet catecholamines must be taken up from plasma, since platelets lack the enzymes for catecholamine synthesis. There is some evidence that platelet catecholamine content under certain circumstances may be an integrated measure of plasma catecholamine concentrations over time. Platelet-free catecholamines were therefore assayed in 18 untreated patients with essential hypertension and in 16 normotensive control subjects. Mean platelet-free dopamine in the hypertensive group was 3.7 +/- 0.4 pg/mg platelet weight, i.e. significantly less than the 6.5 +/- 0.9 pg/mg found in the normotensive (p less than 0.005). Platelet contents of noradrenaline and adrenaline did not differ. Decreased platelet-free dopamine and unchanged platelet noradrenaline and adrenaline persisted after adjustment for increased body weight in the hypertensive group. Although the reasons for decreased platelet-free dopamine in the hypertensive group remain unknown, this finding may add to previous result showing facilitated release of granular contents from blood platelets in patients with essential hypertension. Our data do not support platelet levels of free-catecholamines to be a marker of increased sympathetic tone in essential hypertension.

Blood Platelets↗
PubMed1988

Decreased serum phosphate in essential hypertension. Related to increased sympathetic tone.

Forty-year old men with untreated mild essential hypertension (n = 35) had decreased serum phosphate (P less than 0.001) concomitant with elevated resting plasma epinephrine (P less than 0.05) and heart rate (P less than 0.001) compared with age-matched, normotensive control men (n = 44). Blood pressure correlated negatively with serum phosphate (P less than 0.001) and positively with plasma epinephrine (P less than 0.01) and heart rate (P less than 0.01). Serum phosphate was significantly lowered during infusion of epinephrine, increasing arterial plasma epinephrine within the lower pathophysiological range corresponding to arousal reactions. Serum concentrations of immunoreactive parathyroid hormone were unchanged. Thus, hypophosphatemia in patients with mild essential hypertension appears to be inversely related to sympathetic adrenal tone and may be caused by increased plasma epinephrine within pathophysiologic arterial concentrations.

Adult↗
PubMed1988

Sodium depletion increases platelet and plasma catecholamines in hypertensive men.

The catecholamine content in blood platelets is considerably higher than that in plasma, and platelet catecholamines must be taken up from plasma, since blood platelets lack enzymes for catecholamine synthesis. However, it is unknown whether platelets take up and store catecholamines during physiological in vivo increments in plasma catecholamines. Previously untreated 50-year-old men (n = 17) with mild to moderate essential hypertension were given a low sodium diet for 2 weeks. Urinary excretion of sodium decreased from 201 +/- 11 (SE) to 24 +/- 5 and 19 +/- 4 mmol/24 hr after 1 and 2 weeks, respectively. During the first week, the blood platelet concentration of norepinephrine increased from 27.2 +/- 2.9 to 39.6 +/- 4.7 pg/mg (p less than 0.005) and venous plasma norepinephrine increased from 3.7 +/- 0.4 to 5.6 +/- 0.5 pg/ml (p less than 0.005), and venous plasma dopamine increased from 26 +/- 4 to 41 +/- 5 pg/ml (p less than 0.05). During the second week, both plasma and platelet norepinephrine and dopamine remained elevated. Platelet epinephrine showed a small increase from baseline to the second week (p less than 0.05), but no concomitant increase in plasma epinephrine occurred. Thus, sodium depletion increases both platelet and plasma catecholamines and blood platelets may take up catecholamines in vivo. Platelet catecholamine content may be an integrated measure of plasma catecholamine concentrations during variations caused by sodium depletion.

Blood Platelets↗
PubMed1987

Increased platelet release reaction in 50-year-old men with essential hypertension: correlation with atherogenic cholesterol fractions.

Beta-thromboglobulin (BTG) is a platelet-specific release product. Plasma BTG was significantly increased (p less than 0.01) in 50-year-old, untreated essential hypertensive men (1.22 +/- 0.13 nmol/L, n = 39, mean +/- SE) compared to 50-year-old, healthy normotensive control men (0.82 +/- 0.07 nmol/L, n = 31). Plasma BTG in the hypertensive group correlated significantly with the total serum cholesterol concentration (r = 0.47, p less than 0.01) and with the atherogenic cholesterol fractions low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol (r = 0.50, p less than 0.01). In the normotensive group, no significant correlation was observed between plasma BTG and total serum cholesterol (r = 0.14) or between plasma BTG and LDL + VLDL cholesterol (r = 0.08). Neither was any significant correlation found between plasma BTG and serum high-density lipoprotein (HDL) cholesterol or total triglycerides in either group. Thus, middle-aged men with untreated essential hypertension have an increased blood platelet release reaction related to their concentrations of atherogenic blood lipids. This relationship may be of pathogenetic importance for atherogenesis in hypertension.

Blood Platelets↗
PubMed1987

Severe sodium restriction alone and with potassium supplementation does not alter blood lipoproteins in essential hypertension.

Seventeen 50-year-old men, previously untreated and all with mild to moderate essential hypertension, were given a low sodium diet for 2 weeks. During the second week, the diet was supplemented with potassium. Urinary excretion of Na+ decreased from 201 +/- 11 to 24 +/- 5 and 19 +/- 4 mmol 24 h-1, respectively, after 1 and 2 weeks (means +/- SE) while the urinary Na+: K+ ratio changed from 2:1 to 1:4 and 1:11. Despite significant changes in blood pressure, body weight, serum electrolytes, sympathetic noradrenergic tone, haemoglobin concentration and haematocrit, no significant change appeared in serum total cholesterol, HDL-cholesterol or triglycerides. Thus, low sodium diet alone and combined with potassium supplementation seems neutral to blood lipoproteins in the treatment of 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

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↗