Preeclampsia - a state of sympathetic overactivity.
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Epinephrine↗
Biomedical subjects
I K Eide
Publications and source records attributed to I K Eide.
Metabolic and adrenergic characteristics of young men with insulin resistance.
The primary site of insulin resistance, as measured by the euglycaemic glucose clamp technique, is skeletal muscle. We used the euglycaemic hyperinsulinaemic glucose clamp technique to assess insulin sensitivity (glucose disposal rate, GDR). We aimed at clarifying the demographic, metabolic, haemorrheological, haemodynamic, and by mental stress test the adrenergic characteristics of 21-year-old men grouped in tertiles according to their insulin (I) sensitivity index (GDR/I); insulin resistant group (GDR/I < 5.5 a.u., n = 17), intermediate group (5.5 < GDR/I < 9.5 a.u., n = 16) and insulin sensitive group (GDR/I > 9.5 a.u., n = 17). Insulin resistance was characterized by higher body mass index (p = 0.002, analysis of variance), triglycerides (p = 0.001), total cholesterol/high density lipoprotein cholesterol ratio (p = 0.002), haemoglobin (p = 0.013), haematocrit (p = 0.017) and resting heart rate (p = 0.041) but not resting blood pressure or catecholamines in arterialized blood. However, the mental stress caused by announcement of a forthcoming arithmetic stress test increased diastolic blood pressure and plasma epinephrine dependent on insulin resistance (p = 0.006 and p = 0.012, respectively) with a similar trend also for the maximal increases in heart rate and plasma norepinephrine during arithmetic. Thus, in healthy young men, insulin resistance is not associated with differences in baseline blood pressure but is characterized by higher body weight, disorders in blood lipids and haemorrheology and a hyperadrenergic response to mental stress that even involves blood pressure. We suggest that the sympathetic nervous system may be involved in the pathophysiology of the characteristic insulin resistance or metabolic cardiovascular syndrome in young men.
Adult↗
[How to combine antihypertensive drugs?].
Many hypertensive patients do not respond adequately to single-drug therapy and may therefore require two or more drugs to reach the treatment goal. The drugs used in combination therapy should have additive or synergistic effects on blood pressure. A potential benefit of combinations is to use lower doses of each drug, which may attenuate or abolish the occurrence of side effects. Different combinations are discussed, as well as the inhibition of compensatory mechanisms that may otherwise counteract the antihypertensive effect.
Antihypertensive Agents↗
[Refractory hypertension].
Resistant hypertension is a common disorder in general practice, and poses a challenge to clinicians. It is generally defined as failure to reduce blood pressure adequately despite the use of at least three different antihypertensive agents with different modes of action. The importance of recognizing expansion of plasma volume as a mediator of resistance to therapy is emphasized. Some patients may have white-coat hypertension. An even larger group of patients may fail to comply with the prescribed medication. A good physician-patient relationship is vital, and education of the patient is crucial for obtaining better adherence to the medication.
Antihypertensive Agents↗
Effect of dietary counselling on blood pressure and arterial plasma catecholamines in primary hypertension.
There is still a need of support for nonpharmacologic treatment of uncomplicated, mild-to-moderate essential hypertension. We investigated whether a low sodium-based diet implemented by a nutritionist could lower blood pressure and affect sympathetic activity. Middle-aged, otherwise healthy men with never-treated essential hypertension (n = 95) were randomized to an intervention group, a blood pressure control group, and a time control group. The intervention group was advised to use less sodium chloride in their diet, and if necessary, less saturated fat and decrease body weight. They attended regular clinic visits as did the blood pressure control group. After 1 year, the intervention group had achieved on average 72 mmol/24 h lower urinary sodium excretion (P < .001) and a decrease in body weight of 2.7 +/- 0.5 kg (P < .001). Both supine and standing mean blood pressure were on average 8 to 10 mm Hg lower after intervention compared with the two control groups (P < .001). Arterial plasma epinephrine, measured in all 40-year-old subjects (n = 30), decreased in parallel in all three groups (P < .05), indicating some habituation to the invasive procedure and clinic visits. However, the decrease in norepinephrine was significant (P < .001) only in the intervention group; it correlated with the weight loss (r = 0.76, P < .05) and was significantly higher (P < .05) than in both control groups. These results suggest that broad dietary advice (ie, low intake of sodium chloride, saturated fat and energy), implemented by a nutritionist, may have a significant blood pressure lowering effect and a favorable sympathicolytic effect in uncomplicated, mild-to-moderate essential hypertension.
Adult↗
Insulin resistance and sympathetic nervous system activity in hypertensive and normotensive premenopausal women.
The aim of the present study was to compare insulin sensitivity and catecholamine responses to insulin in lean, hypertensive (HT) and normotensive (NT) premenopausal women. HT (BP 149 5/99 +/- 2 mmHg, n = 14) and NT (BP 128 +/- 4/81 +/- 2 mmHg, n = 12) were matched for age (46 +/- 1 vs. 47 +/- 1 years) and body mass index. Insulin sensitivity was determined by fasting serum insulin, glucose disposal rate (GDR) and insulin sensitivity index (GDR/I) using euglycemic hyperinsulinemic glucose clamp technique. Sympathetic nervous system activity was assessed by plasma adrenaline and noradrenaline in arterialized venous blood at baseline and during euglycemic hyperinsulinemic glucose clamp. Insulin sensitivity index correlated negatively with total cholesterol in HT (r = -0.57, p < 0.05) and with body mass index (r = -0.42, p < 0.05, n = 26). The response in catecholamines to euglycemic hyperinsulinemia in HT differed from NT with an increase both in noradrenaline and adrenaline. Blood pressure and heart rate responses, however, did not differ between HT and NT. Fasting serum glucose did not differ between the two groups (4.7 +/- 0.1 mmol/l in HT vs. 4.9 +/- 0.1 mmol/l in NT), nor did fasting serum insulin (16 2 mU/l vs. 13 mU/l). Glucose disposal rate (8.8 +/- 0.5 vs. 8.7 +/- 0.7 mg kg-1 body weight min-1) and insulin sensitivity index were similar (7.3 +/- 0.8 vs. 7.6 +/- 0.8 arbitrary units). We conclude that in lean, premenopausal hypertensive women insulin sensitivity is not reduced compared with age- and weight-matched normotensive women, but the hypertensives respond to hyperinsulinemia with increased plasma catecholamines, i.e. sympathetic nervous systemic activity. Also, insulin sensitivity correlates negatively with serum cholesterol. Thus, an insulin-hyperadrenergic interaction may possibly be involved as a pathogenetic factor in lean hypertensive women.
Analysis of Variance↗
Effects of losartan on insulin sensitivity in severe hypertension: connections through sympathetic nervous system activity?
Angiotensin II (Ang II) is one of the most potent vasoconstrictors, and the first specific and orally available Ang II-receptor antagonist, losartan (MK-954, DuP-753), has now come into clinical use. The primary site of insulin resistance, as measured by the glucose clamp technique, is skeletal muscle. Losartan specifically blocks Ang II-induced vasoconstriction, namely causes vasodilation, and may thus increase glucose delivery to skeletal muscle. We used the euglycaemic hyper-insulinaemic glucose clamp technique to assess insulin sensitivity (glucose disposal rate, GDR) or insulin (I) sensitivity index (GDR/I). In 21-year-old men we found negative correlations between GDR/I and blood viscosity (r = -0.69), haematocrit (r = -0.65), fibrinogen (r = -0.50), cholesterol/HDL ratio (r = -0.45), triglycerides (r = -0.46), body mass index (r = -0.64), waist/hip ratio (r = -0.57), resting heart rate (r = -0.46) and diastolic blood pressure (DBP) (r = -0.43), and with DBP (r = -0.62) and plasma adrenaline (r = -0.36) during mental arithmetic stress. In the Losartan Severe Hypertension Study five patients with a record of DBP > or = 115 mm Hg were examined before and on losartan monotherapy for an average of 6 weeks. GDR increased 27% and plasma noradrenaline decreased 40% (P < 0.05 for both) during treatment with losartan. Calculated whole blood viscosity decreased on losartan (P = 0.04) and the changes in GDR correlated with the changes in viscosity (r = 0.89). These results suggest that losartan, possibly by a sympathicolytic effect, lowers blood viscosity, causes vasodilation, and improves insulin sensitivity in essential hypertension.
Adult↗
Haemodynamic and neurohumoral effects of cold pressor test in severe heart failure.
The effect of a cold pressor test (CPT) on haemodynamics in relation to general and regional sympathetic activity and arginin vasopressin (AVP), was studied in eleven patients with severe congestive heart failure (CHF). Compared to an age-matched control group (C), resting arterial plasma noradrenaline (NA) (419 +/- 77 vs. 182 +/- 15 pg ml-1), and adrenaline (A) (142 +/- 28 vs 54 +/- 10 pg ml-1) were higher (P less than 0.05) in CHF. AVP showed no significant difference (14 +/- 4 vs. 9 +/- 4 pg ml-1). During CPT systolic and diastolic blood pressure and systemic vascular resistance increased (P less than 0.01), as did NA (delta 114 +/- 39 pg ml-1, P less than 0.01), A (delta 33 +/- 10 pg ml-1, P less than 0.01) and heart rate (delta 10 beats min-1, P less than 0.01). The myocardial v-a difference of NA decreased (P less than 0.05), but was unchanged across the renal vascular bed during CPT. The a-v difference of NA in the hepatic vascular bed, and fractional extraction of A in the coronary sinus, renal and hepatic vascular beds remained unchanged during CPT. AVP did not change significantly and no change in cardiac index or left ventricular filling pressure was observed during CPT. These data suggest that despite an increased activation of the sympathetic nervous system at rest, a further increase in blood pressure and catecholamines took place during CPT. Thus, the effect of a CPT which activates the central sympathetic system seems not to be altered in patients with severe CHF.
Aged↗
The sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension.
The association between blood pressure and coronary artery disease may be caused by a concurrence of atherogenic biochemical abnormalities in hypertensive patients, i.e., the metabolic cardiovascular syndrome (increased total cholesterol, triglycerides, and insulin; decreased high-density lipoprotein (HDL) cholesterol; and insulin resistance, glucose intolerance, and blood platelet dysfunction). There are numerous reports of sympathetic nervous system overactivity in hypertensive subjects that could be of importance for the pathophysiology of the high blood pressure. Plasma catecholamines have metabolic hormonal effects at concentrations slightly above low normal resting levels. Even transiently and certainly chronically raised plasma catecholamine levels may cause biochemical abnormalities. Catecholamines may raise total cholesterol, triglycerides, and insulin, decrease HDL cholesterol, and cause insulin resistance and glucose intolerance, and recent evidence supports an in vivo influence of epinephrine on blood platelets, causing dysfunction in hypertensive subjects. Thus, the sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension. Hypertensive subjects may respond to environmental stimuli with larger sympathoadrenal responses than normal subjects. Furthermore, emotional stress has been associated with coronary artery disease. Thus, the metabolic hormonal effects of catecholamines, by causing the metabolic cardiovascular syndrome, may be the crucial link between "stress" and cardiovascular disease.
Blood Platelets↗
Effects of beta 1- and beta 2-blockade on blood pressure and sympathetic responses to flight phobia stress.
Cardiovascular and sympathoadrenal effects of short-term oral treatment with beta 1-blockade (atenolol, 50 mg, administered two times) and beta 2-blockade (ICI 118,551, 50 mg, administered three times) were compared with placebo during actual flying in subjects with flight phobia (n = 34). beta 1-Blockade lowered resting blood pressure and heart rate and prevented a heart rate response but not a blood pressure response to this psychologic stress. beta 2-Blockade minimally lowered resting heart rate and prevented a heart rate response, but it failed to lower resting blood pressure or blood pressure response to the stress. Plasma epinephrine increased with all three treatments and more with beta 1-blockade than with placebo. Plasma norepinephrine decreased with administration of beta 2-blockade. Thus neither beta 1- nor beta 2-blockade prevents an increase in blood pressure during acute flight phobia stress. Increased plasma epinephrine seems to be the sympathetic variable that is closest related to this increase in blood pressure. Norepinephrine may be less consistently related to the blood pressure rise during flight phobia stress as shown by the decrease in plasma norepinephrine with administration of beta 2-blockade.
Administration, Oral↗
Awareness of hypertension increases blood pressure and sympathetic responses to cold pressor test.
The present study was aimed at examining the effects of awareness of hypertension on blood pressure and sympathetic responses to the cold pressor test. Nineteen-year-old men with similarly elevated mean blood pressure at a medical screening, but without knowledge of this, were randomized into two groups. The first group (n = 16) was sent a letter saying that their pressure was too high, and the second (n = 13) was sent a neutral letter. Information increased mean blood pressure both after 15 min sitting, by an average of 11.5 mm Hg (P less than .01), and after 30 min supine rest, by an average of 4.5 mm Hg (P less than .05). Changes in heart rate (8.4 +/- 2.4 v 1.9 +/- 1.7 beats/min) and plasma epinephrine (0.11 +/- 0.04 v 0.01 +/- 0.03 nmol/L) during execution of a cold pressor test were significantly greater in the informed group (P less than .05). Plasma dopamine was lower in the informed group (P less than .05). Thus, psychological stress caused by the awareness of hypertension may increase blood pressure and sympathetic responses to a provocative maneuver. Ideally, studies on sympathetic function in essential hypertension should be undertaken on subjects unaware of their blood pressure status.
Adult↗
Increased erythrocyte magnesium in never treated essential hypertension.
In the present study we aimed at evaluating the intracellular concentrations of magnesium, potassium and sodium in 50-year-old, otherwise healthy white men with never treated, essential hypertension (n = 12) and in normotensive control subjects (n = 12) matched for age, sex, race, height, weight and smoking habits. Intraerythrocyte magnesium was significantly increased in the hypertensive group (P less than .001) and correlated positively and significantly to blood pressure in the total group (P less than .01). The intracellular potassium to sodium ratio tended to be lower in the hypertensive group (P less than .05). Thus, the present study supports increased intracellular magnesium probably unrelated to intracellular potassium-sodium imbalance in never treated, essential hypertension.
Blood Pressure↗
Increased erythrocyte magnesium content in essential hypertension.
The present study aimed at testing the hypothesis of decreased erythrocyte magnesium content and magnesium deficiency in essential hypertension. Atomic absorption was used to measure the erythrocyte content of total magnesium in 50-year-old otherwise healthy white males with essential hypertension (n = 12, blood pressure (mean +/- SE) 155 +/- 4/109 +/- 2 mmHg) that had never been treated and in normotensive control subjects (n = 12, blood pressure 128 +/- 2/88 +/- 1 mmHg) matched for age, sex, race, height, weight and smoking habits. The erythrocyte magnesium content was significantly increased in the hypertensive group (2.266 +/- 0.063 vs 1.903 +/- 0.069 mmol/l erythrocytes, p less than 0.001). No significant difference between the groups was detected for serum concentration or the 24-h urinary excretion of magnesium. In conclusion, the present study indicates increased rather than decreased erythrocyte content of magnesium in 50-year-old white males with 'never-treated', essential hypertension. Magnesium deficiency is, therefore, unlikely in this subset of critically selected and matched hypertensive patients.
Erythrocytes↗
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↗
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↗
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↗
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↗
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↗