Plasma Noradrenaline Concentrations In Patients Research Articles

A polymorphism in the noradrenaline transporter gene is associated with increased blood pressure in patients with resistant hypertension.

Noradrenaline released from sympathetic nerves is rapidly inactivated via the action of the noradrenaline transporter (NET). We aimed to determine whether a single nucleotide polymorphism (SNP) in the NET gene, rs7194256, was associated with blood pressure and plasma noradrenaline concentration in patients with resistant hypertension. Ninety-two consecutive patients with resistant hypertension participated in this study (age 62 ± 1.3 years, BMI 32 ± 0.6 kg/m, mean ± SEM). Blood pressure was assessed using 24-h ambulatory blood pressure monitoring. Genotyping of rs7194256 (C/T) was performed using a predeveloped TaqMan SNP Genotyping Assay. Plasma catecholamines were analyzed using high-performance liquid chromatography. There were no differences in anthropometric measures between those carrying a T allele or the CC genotype. Patients carrying a T allele had significantly higher SBP: 24-h mean 148 ± 2.6 vs. 140 ± 2.4; 24-h max 189 ± 3.2 vs. 179 ± 2.6; 24-h min 114 ± 3.0 vs. 105 ± 2.3; night mean 141 ± 3.0 vs. 131 ± 2.5; night max 170 ± 3.6 vs. 159 ± 3.1; night min 118 ± 3.4 vs. 109 ± 2.4 (all P < 0.05). T-allele carriers had a significantly higher arterial noradrenaline concentration: 573 ± 53 vs. 377 ± 35 pg/ml (P = 0.002) and lower ratio of the intraneuronal noradrenaline metabolite, 3,4-dihydroxyphenylglycol, to noradrenaline (3.01 ± 0.4 vs. 4.08 ± 0.3 pg/ml; P = 0.024). A SNP in the NET gene in patients with resistant hypertension is associated with higher plasma noradrenaline concentration and elevated SBP. Impaired NET function may be a contributor to the pronounced activation of the sympathetic nervous system characteristic of patients with resistant hypertension.

Elevated Plasma Noradrenaline Concentrations in Patients with Low-Output Cardiac Failure: Dependence on Increased Noradrenaline Secretion Rates

1. Plasma noradrenaline concentrations are elevated in patients with congestive heart failure; however, the pathogenesis of these elevated noradrenaline levels is controversial. 2. Possible mechanisms for elevated noradrenaline concentrations in patients with congestive heart failure include increased noradrenaline secretion, decreased clearance of noradrenaline, and a combination of increased secretion and decreased clearance. 3. In the present study, plasma noradrenaline clearance and apparent secretion rates were determined using a whole-body steady-state radionuclide tracer method in six otherwise healthy patients with moderate degrees of low-output cardiac failure and in six normal control subjects. 4. The venous plasma noradrenaline level was elevated in the patients with congestive heart failure as compared with the control subjects (4.18 +/- 1.34 versus 1.54 +/- 0.16 nmol/l, P less than 0.05). There was no stimulation of the adrenal medulla as evident by normal plasma adrenaline levels in both groups (0.19 +/- 0.04 versus 0.18 +/- 0.02 nmol/l, not significant). The apparent secretion rate of noradrenaline was elevated in the patients with congestive heart failure (4.75 +/- 1.95 versus 1.78 +/- 0.18 nmol min-1 m-2, P less than 0.05), whereas the clearance rate of noradrenaline was similar in the two groups (1.26 +/- 0.27 versus 1.16 +/- 0.02 l min-1 m-2, not significant). 5. We conclude that the high peripheral venous plasma noradrenaline concentrations in patients with mildly decompensated low-output cardiac failure are initially due to increased secretion, rather than to decreased metabolic clearance, perhaps in response to diminished effective arterial blood volume.

Elevated plasma noradrenaline concentrations in duodenal ulcer patients are not normalized by vagotomy.

Plasma noradrenaline, heart rate, and serum gastrin were significantly greater in 12 patients with duodenal ulcer compared to 12 normal subjects. Arterial blood pressure was the same in patients and controls. Intravenous infusion of adrenaline resulted in a greater rise in serum gastrin in duodenal ulcer patients, while the rise in plasma adrenaline was very similar in both groups of subjects. This suggests that the clearance of catecholamines from plasma is not retarded in duodenal ulcer patients. The abnormally high plasma noradrenaline concentrations were unchanged after vagotomy, indicating that the elevated plasma noradrenaline in duodenal ulcer patients is not related to epigastric pain. The elevated plasma noradrenaline levels in patients with duodenal ulcer are not explained by a general difference in plasma noradrenaline and sympathetic nervous activity between patients and controls because plasma noradrenaline is not elevated in other groups of patients, viz. patients with essential arterial hypertension and diabetics without ketosis and neuropathy. It may be that patients with duodenal ulcers are subject to more stress than normal subjects, provided that chronic stress does not result in arterial hypertension. It is also possible that the elevated plasma noradrenaline concentrations in these patients are compensatory to other cardiovascular changes or derived from outside the cardiovascular system, e.g. from the gastrointestinal tract. {J Clin Endocrinol Metab49: 331, 1979)

Clinical significance of plasma adrenaline and noradrenaline concentrations in patients with subarachnoid haemorrhage.

Plasma adrenaline and noradrenaline concentrations were measured in 21 patients after subarachnoid haemorrhage and in 13 control patients. Plasma noradrenaline concentrations were significantly raised in patients recovering from subarachnoid haemorrhage, confirming clinical evidence of overactivity of the sympathetic nervous system. Plasma noradrenaline concentrations in patients with a poor result were significantly higher at the time of admission than in patients with a good result, and the differences became more significant two to three days later. Therefore, the measurement of plasma noradrenaline concentrations may be a valuable test to assist clinical assessment in distinguishing between the two groups preoperatively.