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Biomedical subjects

T Hedner

Publications and source records attributed to T Hedner.

At least 163 records · Page 9Linked to original sources
PubMed1994

Functional autoimmune epitope on alpha 1-adrenergic receptors in patients with malignant hypertension.

Because of the growing evidence that hypertensive disease is accompanied by immunological dysfunction, we have investigated autoimmunity in patients with malignant hypertension. Peptides corresponding to the sequence of the second extracellular loops of the human alpha 1-adrenergic receptor and the M2-muscarinic receptor were used as antigens in an ELISA. Serum from 4 (12%) of 33 healthy controls, 3 (20%) of 15 patients with malignant essential hypertension, and 7 (64%) of 11 with secondary hypertension showed positive responses in the ELISA for the alpha 1-adrenergic receptor peptide. Positive responses were significantly more common among the patients with secondary hypertension than in the other two groups (p < 0.01). By contrast, no autoantibodies against the M2-muscarinic receptor peptide were detected in either hypertensive group. Autoantibodies against the alpha 1-adrenergic receptor, affinity-purified from patients with positive responses, specifically recognised bands with molecular masses of 68, 40, and 37 kDa on immunoblotted membrane proteins of rat ventricles. The patients' autoantibodies caused a decrease in tritiated prazosin binding sites and an increase in heart beating frequency of neonatal cultured rat cardiomyocytes; antibodies purified from the controls had no effect. Circulating autoantibodies against the alpha 1-adrenergic receptor are present in a subgroup of patients with malignant hypertension. These autoantibodies have pharmacological activity in vitro, which suggests that they may be involved in the pathogenesis of malignant hypertension.

Adult↗
PubMed1994

Atrial natriuretic peptide and its relation to cardiac dimensions and function in patients with systemic sclerosis.

OBJECTIVES: Were to determine whether plasma atrial natriuretic peptide (ANP) is increased in patients with systemic sclerosis (SScl) and to evaluate its relation to cardiac dimensions and function. METHODS: Using radio-immunoassay, plasma ANP was determined in 30 patients with SScl and 48 age and sex matched controls. The plasma ANP level was related to cardiac structure and function as determined by two-dimensional echocardiography (2-D echo). RESULTS: Plasma ANP was markedly elevated among patients as compared to controls (239,4 +/- 59 vs 178.2 +/- 36 pmpl/l, p < 0.0005). The left atrial long-axis and area were increased, and ANP was directly related to both measurements (r = 0.27, p < 0.05 and r = 0.40, p < 0.005, respectively). Plasma ANP was also related to the increased right atrial long-axis (r = 0.27, p < 0.05). The ANP level was not related to LV systolic function as estimated by ejection fraction, fractional area change and end-systolic wall stress, neither did these measures differ between patients and controls. However, there was an inverse correlation between ANP level and stroke volume (r = -0.35, p < 0.05), which was lower among the patients (p < 0.005). ANP displayed also an inverse relation to LV long axis diameter (r = -0.37, p < 0.005) and area (r = -0.42, p < 0.005) as well as to LV end-diastolic volume (r = -0.42, p < 0.005). Various measurements indicated LV hypertrophy among the SScl patients in spite of a small LV cavity. ANP was directly related to measures of LV hypertrophy, as interventricular septum thickness (r = 0.44, p < 0.005), LV posterior wall thickness (r = 0.34, p < 0.05), the wall thickness to cavity dimension ratio (r = 0.36, p < 0.05), and LV myocardial area (r = 0.36, p < 0.05). There was no relationship between ANP concentration and heart rate, blood pressure or total peripheral resistance. CONCLUSION: These results suggest that the ANP production is not reduced in SScl. Rather, circulating ANP is elevated in relation to the degree of LV hypertrophy. This implies that ANP may be useful for the identification of cardiac involvement in patients with SScl.

Adult↗
PubMed1994

Dyspnoea, asthma, and bronchospasm in relation to treatment with angiotensin converting enzyme inhibitors.

OBJECTIVE: To evaluate the occurrence of asthma and dyspnoea precipitated or worsened by angiotensin converting enzyme inhibitors. DESIGN: Summary of reports of adverse respiratory reaction in relation to treatment with angiotensin converting enzyme inhibitors that were submitted to Swedish Adverse Drug Reactions Advisory Committee and to World Health Organisation's international drug information system until 1992. Sales of angiotensin converting enzyme inhibitors in Sweden were also summarised. SUBJECTS: Patients receiving angiotensin converting enzyme inhibitors who reported adverse respiratory reactions. MAIN OUTCOME MEASURES: Clinical characteristics of adverse reactions of asthma, bronchospasm, and dyspnoea. RESULTS: In Sweden 424 adverse respiratory reactions were reported, of which most (374) were coughing. However, 36 patients had adverse drug reactions diagnosed as asthma, bronchospasm, or dyspnoea. In 33 of these cases the indication for treatment with angiotensin converting enzyme inhibitors was hypertension, in only three heart failure. The respiratory symptoms occurred in about half of the patients within the first two weeks of treatment, and about one third needed hospitalisation or drug treatment. Dyspnoea symptoms occurred in conjunction with other symptoms from the airways or skin in 23 out of the 36 cases. In the WHO database there were 318 reports of asthma or bronchospasm, 516 reports of dyspnoea, and 7260 reports of cough in relation to 11 different angiotensin converting enzyme inhibitors. CONCLUSION: Symptoms of airway obstruction in relation to treatment with angiotensin converting enzyme inhibitors seem to be a rare but potentially serious reaction generally occurring within the first few weeks of treatment.

Adult↗
PubMed1994

Autoantibodies against cardiac G-protein-coupled receptors define different populations with cardiomyopathies but not with hypertension.

It was previously shown that the second extracellular loop of cardiovascular G-protein-coupled receptors is an antigenic target for pharmacologically active autoantibodies in patients with idiopathic dilated cardiomyopathy. To extend these observations to cover patients with the same disease from different geographical origins or to patients with other cardiac diseases, peptides corresponding to the sequences of the second extracellular loops of the human M2 muscarinic receptors and beta adrenoceptors were used as antigens in an enzyme immunoassay. Sera from patients from Sweden and Japan with idiopathic dilated cardiomyopathy (DCM, n = 32), hypertrophic cardiomyopathy (HCM, n = 23), malignant essential hypertension (MEH, n = 11), malignant secondary hypertension (MSH, n = 10), and sera from healthy blood donors (HBD, n = 49) were tested. Sera from patients with DCM recognized the muscarinic receptor peptide in 38% of cases and the beta 1 adrenoceptor peptide in 31% of cases. In 50% of the positive patients, autoantibodies against both peptides coexisted as shown by competition experiments using both peptides as inhibitors. In HCM patients, there was a lower frequency of autoantibodies but with a higher but not significant predominance against the M2 peptide. No autoantibodies were detected in sera from patients with MEH or MSH. Autoantibodies against the M2 muscarinic receptors, affinity-purified from positive patients, displayed pharmacological activity as demonstrated by changes in the affinity and number of radioligand binding sites. In contrast, antibodies purified from positive HBD had no effect. These results confirm that autoantibodies displaying pharmacological activity against G-protein-coupled cardiovascular receptors are mainly restricted to patients with idiopathic dilated cardiomyopathy and that different autoantibody populations are responsible for the recognition of the different receptors.

Adult↗
PubMed1994

Atrial natriuretic peptide: relation to left ventricular filling properties in patients with systemic sclerosis.

To determine the relation between left ventricular filling properties and plasma atrial natriuretic peptide in systemic sclerosis, we evaluated 30 consecutive patients and 48 age- and sex-matched controls. The venous plasma atrial natriuretic peptide was measured by radio-immunoassay. Left ventricular involvement was evaluated by echocardiography and mitral regurgitation was evaluated by Doppler. The patient group had markedly elevated plasma atrial natriuretic peptide as compared to the matched controls, (239.4 +/- 59 vs. 178.2 +/- 36 pmol/l, P < 0.0005). We found signs of impaired left ventricular filling properties among the patients with an increase of the Doppler A-wave velocity and A/E ratio. A relative reduction of early filling was found in spite of some degree of mitral regurgitation in two-thirds of the patients. The plasma atrial natriuretic peptide concentration was related to the A-wave velocity (r = 0.44, P < 0.0005), the A/E ratio (r = 0.40, P < 0.005), and also to the degree of mitral regurgitation (r = 0.43, P < 0.005). The relationship to the A-wave velocity remained when considering possible confounding factors. We conclude that the previously observed fibrotic process in systemic sclerosis does not prevent production and liberation of plasma atrial natriuretic peptide in relation to factors distending the left atrium, such as altered left ventricular filling properties and the presence of mitral regurgitation. However, the moderate relationships between atrial natriuretic peptide and haemodynamic variables indicate that the peptide might also be an independent indicator of cardiac involvement in systemic sclerosis.

Adult↗
PubMed1994

Acetaminophen blocks spinal hyperalgesia induced by NMDA and substance P.

The hypothesis tested was that inhibition of the L-arginine-nitric oxide (NO) pathway may represent a potential central mechanism of action for acetaminophen (paracetamol). Spinal administration of N-methyl-D-aspartate (NMDA, 0.5 nmol), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA, 0.1 nmol) or substance P (SP, 0.5 nmol) to the rat provoked a specific behaviour characterized by biting, scratching and licking (BSL). This behaviour was antagonized by pretreatment with acetaminophen for NMDA and SP but not for AMPA. Further, the antinociceptive effect of acetaminophen was readily reversed by administration of the natural substrate for nitric oxide synthase (NOS), L-arginine, but not by D-arginine. This suggests that the analgesic effect of acetaminophen is related to inhibition of NO generation. Potential mechanisms for this may involve NMDA and SP. Our data suggest that a significant portion of the analgesic effect of acetaminophen, when used clinically, may be related to an interaction with the central nervous system L-arginine-NO pathway.

Acetaminophen↗
PubMed1994

Inhibition of 17 beta-estradiol metabolism by grapefruit juice in ovariectomized women.

In an open, randomized, cross-over study the concentrations of 17 beta-estradiol and estrone in serum were measured over 192 hours in 8 ovariectomized women after a single oral dose intake of 2 mg micronized 17 beta-estradiol. The subjects were studied with and without grapefruit juice intake containing the three natural flavonoids, naringenin, quercetin and kaempherol, which are found as glycosides in citrus fruit. These flavonoids interact with the metabolism of drugs such as 17 beta-estradiol and other steroids that are extensively metabolised through the P-450NF (P-450 IIIA4) enzyme or closely related P-450 systems. After administration of grapefruit juice, peak estrone (between 2-6 hours after tablet intake) concentrations increased significantly. The AUC0-48 and AUC0-192 for estrone but not 17 beta-estradiol, resulting from a single administration of micronized 17 beta-estradiol, were significantly altered. Combined measured estrogens (i.e. 17 beta-estradiol and estrone) also increased significantly. The relationship between the AUCs for 17 beta-estradiol and estrone was not altered by juice intake indicating that a metabolic step after estrone, i.e. further A and/or D ring conversion was inhibited. This study demonstrates that grapefruit juice may alter the metabolic degradation of estrogens, and increase the bioavailable amounts of 17 beta-estradiol and its metabolite estrone, presumably by affecting the oxidative degradation of estrogens. This food interaction may be one factor behind the interindividual variability in 17 beta-estradiol, estrone and estriol serum concentrations after exogenous administration of 17 beta-estradiol to patients.

Beverages↗
PubMed1994

Airway effects of direct left-sided cervical vagal stimulation in patients with complex partial seizures.

Airway nerves have been implied in obstructive lung diseases for many years. In experimental animals, vagal stimulation produces several features of asthma, including airflow obstruction and airway plasma exudation. Vagal stimulation is a novel and effective therapy in patients with refractory epilepsy. We evaluated the airway response to left-sided cervical electrical stimulation using 1 Hz (low stimulation: 30 s, once every 90 min) and 30 Hz (high stimulation: 30 s, every 5 min) in a randomized double-blinded fashion for 3 months in epileptic patients participating in a phase two efficacy study. In eight patients with high stimulation and six with low stimulation, no effect on FEV1 (forced expiratory volume in 1 s) was seen over 3 months chronic stimulation. In a follow-up, up to 9 months, no further deterioration of lung function was observed. Of five patients without concomitant lung disease who consented to more extended experiments, one patient produced a reduction of FEV1 with variable frequency and current stimulation (10-87 Hz and 0.5-2.5 mA respectively). In one patient with obstructive lung disease, however, increased frequency and current stimulation led to a stimulation-dependent decrease in FEV1. After the addition of inhaled ipratropium bromide (160 micrograms, dry powder) to this patient, there was a clear improvement of baseline FEV1, but only a slight improvement of the stimulation-induced deterioration of FEV1. We conclude that long-term vagal stimulation in patients without concomitant lung disease does not induce any significant changes in FEV1. However, in patients with obstructive lung disease, intense vagal stimulation can cause a deterioration of lung function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Effects of atrial natriuretic peptide on renal function after cardiac surgery and in cyclosporine-treated heart transplant recipients.

The study investigated the effects of intravenous infusion of atrial natriuretic peptide (human ANP 99-126) on renal function and central hemodynamics after coronary artery bypass grafting (CABG), and the ability of ANP to reverse the acute nephrotoxic effects of cyclosporine after heart transplantation. Ten patients with an EF > 0.5 and normal renal function were studied 2 to 4 hours after CABG surgery. Furthermore, six heart transplant recipients receiving cyclosporine for immunosuppression who developed renal dysfunction 2 to 4 days after transplantation were studied. Standard urinary clearance of 51Cr-EDTA and PAH was used to study the effects of ANP on glomerular filtration rate (GFR) and renal blood flow (RBF). Baseline measurements were first performed during two 30-minute periods. Incremental infusion rates of ANP were then administered for three consecutive 30-minute periods (25, 50, and 100 ng/kg/min), followed by two 30-minute post-ANP control periods. Marked increases in urinary flow (UF), GFR, filtration fraction (FF), and fractional urinary excretion of Na+ were observed in the CABG patients with increasing doses of ANP, while RBF was unchanged. Mean arterial pressure decreased by around 15% at the highest ANP dose. In the heart transplant recipients, baseline GFR was markedly reduced compared to pretransplantation values (-65%). UF, GFR, and RBF increased 240%, 69%, and 53%, respectively, while renal vascular resistance decreased 45% during the highest dose of ANP infused. At this ANP dose level, circulating ANP concentrations were sixfold to eightfold higher than the preinfusion control level.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

The role of diabetes mellitus and hypertriglyceridaemia as coronary risk factors in treated hypertension: 15 years of follow-up of antihypertensive treatment in middle-aged men in the Primary Prevention Trial in Göteborg, Sweden.

OBJECTIVE: To analyse the importance of diabetes mellitus and hypertriglyceridaemia as potential risk factors for coronary heart disease (CHD) in middle-aged, treated hypertensive men. DESIGN: A prospective, long-term observational study. SUBJECTS: Derived from a random population sample--686 hypertensive men aged 47-54 years at entry--followed for 15 years at a special out-patient hypertension clinic. INTERVENTION AND OUTCOME MEASURES: The patients were mainly treated with beta-adrenoceptor blockers and/or thiazide diuretics. Cardiovascular morbidity was closely monitored during follow-up. RESULTS: In all, 133 subjects suffered a CHD event during follow-up. The presence of diabetes mellitus at entry more than doubled the CHD risk and a 1 mmol l-1 increment of the serum triglyceride level at entry increased the CHD risk by 21%. In multivariate analyses, smoking, the presence of diabetes mellitus at entry, serum cholesterol and signs or symptoms of hypertensive end organ damage were found to be independent risk factors for CHD. In absolute terms the existence of cardiovascular damage was of much greater prognostic importance than were the presence of various metabolic abnormalities. Of the mean in-study variables, both the average serum cholesterol level and the achieved diastolic blood pressure were significantly associated with CHD. However, new diabetes mellitus which developed during follow-up as well as mean serum triglyceride levels were not associated with CHD. CONCLUSIONS: Diabetes mellitus and hypertriglyceridaemia present at the start of treatment have a prognostic impact in treated hypertensive men, whereas when such metabolic disorders develop during drug treatment they seem to be of much less importance. Smoking and already existing evidence of hypertensive end organ damage are of utmost importance for the prognosis in this type of patient.

Adrenergic beta-Antagonists↗
PubMed1994

Magnesium sulphate infusion decreases circulating calcitonin gene-related peptide (CGRP) in women with primary Raynaud's phenomenon.

The effects of two different vasodilating agents (MgSO4 infusion and the calcium antagonist nifedipine) on circulating levels of calcitonin gene-related peptide (CGRP) were studied in 12 women with pronounced primary Raynaud's phenomenon (PRP) and in 12 healthy females. There were no significant differences with regard to basal levels of circulating CGRP between women with PRP and the control group; median 15.5 (range 10-48) vs. 14 (range 10-69) pmol l-1, respectively. However, treatment with MgSO4 infusion significantly decreased circulating CGRP in women with PRP only from median 15.5 (range 10-48) to 10 (range 10-110) pmol l-1) (P < 0.05). On the other hand 14 days of treatment with nifedipine did not affect circulating CGRP in either of the investigated groups. Erythrocyte magnesium (ery-Mg) levels increased significantly after MgSO4 infusion in women with PRP (2.43 +/- 0.13 vs. 2.52 +/- 0.15 mmol l-1, P < 0.05) but not in the controls (2.51 +/- 0.24 vs. 2.57 +/- 0.28 mmol l-1, ns). In conclusion, the decrease of circulating CGRP after MgSO4 infusion in women with PRP provides further evidence that magnesium plays a significant role in the pathophysiology of PRP.

Adult↗
PubMed1994

Histamine-independent modulation of the neuropeptide Y-induced pressor response by alpha-trinositol in the pithed rat.

The modulatory effects of alpha-trinositol (D-myo-inositol-1.2.6- trisphosphate; PP 56) on the systemic arterial blood pressor responses induced by neuropeptide Y, preganglionic nerve stimulation, phenylephrine and vasopressin were studied in pithed rats. Intravenous administration (within 2 min.) of alpha-trinositol reduced the neuropeptide Y-induced increase in mean arterial pressure within a defined dose range without altering the heart rate. The influence of alpha-trinositol on the neuropeptide Y-induced pressor response in the presence of non-selective as well as H1- and H2-selective histamine antagonists (diphenhydramine, mepyramine and cimetidine respectively) were investigated. The maximal increase in mean arterial pressure induced by neuropeptide Y as well as the duration of the pressor response was enhanced after nonselective (diphenhydramine) or H1-selective (mepyramine) histamine blockade. The enhancement of the neuropeptide Y-induced pressor response by the H1 specific antagonist mepyramine was significantly more pronounced compared to the H2-selective agent. The exaggerated increase in mean arterial pressure in response to neuropeptide Y after histamine blockade was inhibited by alpha-trinositol to a similar extent as without such pretreatment. We conclude that neuropeptide Y interacts with histamine in the pithed rat and that this action may partially offset the pressor actions of the peptide. The neuropeptide Y-induced pressor responses may be inhibited by alpha-trinositol within a defined dose range indicating that this non-peptide agent may act as a functional inhibitor to neuropeptide Y in vascular tissue.

Animals↗
PubMed1994

Characteristics of renal sympathetic nerve activity in experimental congestive heart failure in the rat.

Recently emerging evidence has indicated that efferent renal sympathetic nerve activity (RSNA) is increased in congestive heart failure (CHF). In the present study the cyclic activity of the renal nerve in the normal and CHF rat was studied. An ischaemic myocardial lesion resulting in CHF was induced by left coronary artery ligation. Sham-operated rats subjected to thoracotomy served as normal controls. Renal sympathetic nerve activity was recorded under chloralose anaesthesia. The neural cycle activity was significantly higher in CHF (47 +/- 3%) compared with sham-operated rats (34 +/- 3%, P < 0.005). Baroreceptor control of RSNA was significantly attenuated in CHF compared with normal control rats (P < 0.005). In response to noxious thermal stimulation by 48 degrees C water immersion of the tail tip, the increase of RSNA was significantly higher in CHF compared with sham-operated rats. A stepwise 15% blood volume expansion over 5 min which induced no alterations of blood pressure or heart rate (HR) resulted in a gradual decrease of RSNA in control rats by approximately 25% at the end of the volume expansion procedure. In CHF rats however, there was no significant change in RSNA during volume expansion. It is concluded that in CHF rats: (1) efferent RSNA is increased; (2) baroreceptor control of RSNA is decreased; (3) RSNA in response to cutaneous thermal noxious stimulation is exaggerated; and (4) RSNA inhibition by cardiopulmonary receptors is blunted.

Animals↗
PubMed1994

Cardiac neuropeptide Y and noradrenaline balance in patients with congestive heart failure.

OBJECTIVE: To measure plasma concentrations of noradrenaline and neuropeptide Y-like immunoreactivity in relation to cardiac function in patients with congestive heart failure. DESIGN: Retrospective analysis of plasma noradrenaline concentrations and neuropeptide Y-like immunoreactivity in the arterial and coronary circulations, in patients with a high or low ejection fraction (31.3% (1.3%) or 17.7% (1.1%) respectively) and in healthy volunteers. SETTING: Cardiology department of a university hospital. PATIENTS: 41 patients with congestive heart failure with various aetiologies. Ten healthy volunteers served as a reference group. MAIN OUTCOME MEASURES: Concentrations of noradrenaline measured by high performance liquid chromatography and of neuropeptide Y-like immunoreactivity measured by radioimmunoassay. Cardiac index, pulmonary capillary wedge pressure, pulmonary vascular resistance, and systemic vascular resistance were derived by catheterisation of the right heart. Ejection fraction was measured by radionuclide angiography, cineangiography, or M mode echocardiography. RESULTS: There were pronounced and significant increases in circulating arterial concentrations of neuropeptide Y-like immunoreactivity and noradrenaline in both the high and low ejection fraction groups compared with the healthy subjects. In the patients myocardial release of neuropeptide Y-like immunoreactivity tended to be greater compared with normal subjects, but not significantly so. While normal subjects showed myocardial noradrenaline uptake, patients with congestive heart failure showed significant and progressive myocardial noradrenaline release. Arterial as well as coronary sinus concentrations of neuropeptide Y-like immunoreactivity correlated significantly with plasma noradrenaline concentrations from the respective sites. Plasma noradrenaline concentrations in the artery and coronary sinus were negatively correlated with ejection fraction and cardiac index; no such relations were found for concentrations of neuropeptide Y-like immunoreactivity. CONCLUSIONS: Both circulating concentrations of neuropeptide Y-like immunoreactivity and noradrenaline are significantly increased in moderate to severe forms of congestive heart failure. Plasma concentrations of neuropeptide Y-like immunoreactivity correlated with plasma noradrenaline concentrations, but plasma noradrenaline concentrations alone correlated with ejection fraction and cardiac index. Thus plasma noradrenaline concentration seems to be a more sensitive index of cardiac dysfunction than the concentration of neuropeptide Y-like immunoreactivity in congestive heart failure.

Adolescent↗
PubMed1994

Effect of magnesium sulfate infusion on circulating levels of noradrenaline and neuropeptide-Y-like immunoreactivity in patients with primary Raynaud's phenomenon.

The effect of a short-term magnesium sulfate (MgSO4) infusion on venous plasma concentration of noradrenaline (NA) and neuropeptide-Y-like immunoreactivity (NPY-LI) was investigated in 12 women with primary Raynaud's phenomenon (PRP) and in 12 healthy matched controls. The Raynaud's patients did not demonstrate any significant changes in mean basal plasma NA concentration (0.29 +/- 0.15 vs 0.37 +/- 0.09 ng/mL, ns) after MgSO4 infusion. However, in the controls there was more than twice the amount of circulating noradrenaline (cNA) (0.21 +/- 0.14 vs 0.54 +/- 0.22 ng/mL, P < 0.001) after MgSO4 infusion, compared with the preinfusion value. Measurements during the cold pressor test prior to the MgSO4 infusion showed a significant increase of cNA in both the PRP group and the control group (from 0.29 +/- 0.15 to 0.33 +/- 0.16 ng/mL, P < 0.05, and from 0.21 +/- 0.14 to 0.29 +/- 0.16 ng/mL, P < 0.005, respectively). After MgSO4 infusion the levels of cNA during the cold pressor test increased significantly only in the PRP group (from 0.37 +/- 0.09 to 0.41 +/- 0.11 ng/mL, P < 0.05). Circulating NPY-LI concentrations increased significantly during MgSO4 infusion in the Raynaud's patients as well as in the controls from 105 +/- 21 to 127 +/- 23 pmol/L, P < 0.05, and from 107 +/- 17 to 132 +/- 27 pmol/L, P < 0.01, respectively. There were no detectable changes during the cold pressor tests in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗