Thomas O.F. Wagner

Acute psychological stress increases plasma levels of cortisol, prolactin and TSH

The effects of acute stress during a parachute jump on hormonal responses were studied in 12 experienced and 11 inexperienced military parachutists. Each subject performed two jumps. Prior to and immediately after each jump blood samples were drawn and analysed for plasma levels of cortisol, prolactin, thyrotropin (TSH), somatotropin (STH), and luteinizing hormone (LH). While there was a significant increase in cortisol, prolactin and TSH levels after both jumps, no alterations could be observed in STH and LH levels. Stress-induced hormonal responses were not affected by jump experience. There was also no association between the endocrine variables and anxiety scores.

Psychophysiological, Neuroendocrine and Cellular Immune Reactions under Psychological Stress

Emotional stress is often followed by increased susceptibility to infections. Natural killer (NK) cells play a major role in the immediate immune response controlling this susceptibility. In this study on 45 first-time parachutists, it is demonstrated that highly controlled psychological stress increased psychophysiological variables, enhanced the secretion of sympathetic-adrenal hormones and also led to a significant increase of NK cells and their cytotoxic activity followed by a decrease below starting values. This immunological alteration is correlated with the secretion of noradrenaline during the emotional strain. Quick mobilization of these cytotoxic effector cells is suggested as a major mechanism for the effective adaptation of the immune system to stress situations.

Urodilatin (Ularitide, INN): a potent bronchodilator in asthmatic subjects

Abstract. Atrial natriuretic peptide (CDD/ANP‐99–126) has been identified as a bronchodilator in various species including humans. We investigated the effect of urodilatin (CDD/ANP‐95–126) in 18 clinically stable asthmatics showing an increase of the FEV1 by ≥15% after salbutamol inhalation. Prior to the study inhaled β2‐agonists were withheld for 8 h. After baseline measurements of lung function parameters (FEV1, VC, PEF, MEF75, MEF50, MEF25), blood pressure, and heart rate in intravenous infusion of 20, 40 or 60 ng kg‐1 min‐1 urodilatin was administered for 40min in the morning. All measurements were repeated every 10 min during the infusion, for 30 min thereafter, and after the inhalation of l.25 mg salbutamol. Forty and 60 ng kg‐1min‐1 urodilatin showed a significant effect on the central (FEVl, PEF, MEF75) and peripheral airways (MEF50, MEF25) after 10 min infusion (P<0.05). A broncho‐dilation not significantly different from l.25 mg salbutamol was induced by 40 ng kg‐1 min‐1 in the central airways only, while 60 ng kg‐1 min‐1 led to a similar effect at all levels of the bronchial tree. Lung function parameters returned to baseline within 30 min after cessation of the urodilatin infusion. Heart rate showed a tendency to increase after 40min infusion (P<0.05), but blood pressure did not change significantly. In conclusion, the maximal bronchodilating effect of intravenous urodilatin in clinically stable asthmatics was comparable to l.25 mg salbutamol.

Bronchodilating effects of natriuretic and vasorelaxant peptides compared to salbutamol in asthmatics

In animal studies, the bronchial effects of urodilatin (URO, CDD/ANP-95-126, INN: ularitide) were superior to those of cardiodilatin/atrial natriuretic peptide (CDD, CDD/ANP-99-126). We compared the bronchodilating properties of intravenous URO and CDD in 36 clinically stable asthmatics showing a beta 2-agonist-induced increase of the FEV1 by > or = 15%. Any aerosol medication was discontinued for at least 8 h prior to the study. After baseline measurements of lung function parameters (FEV1, VC, PEF, MEF75, MEF50, MEF25) an intravenous infusion of 5.7, 11.4 or 17.1 pmol/kg/min URO or CDD was administered for 40 min in the morning. All measurements were repeated every 10 min during the infusion, for 30 min thereafter, and after the inhalation of 1.25 mg salbutamol (SALB). Both peptides had significant effects. While 11.4 pmol/kg/min URO dilated the central airways (FEV1, PEF, MEF75) slightly more potently than the peripheral bronchioles (MEF50, MEF25), 17.1 pmol/kg/min URO was as effective as SALB at all levels of the tracheobronchial tree. CDD reached only 50% of the SALB effect without a predominant localization of its action. The cardiovascular parameters revealed a significantly stronger vasorelaxant activity of CDD. In conclusion, the dose-dependent bronchodilating properties of intravenous URO were significantly superior to those of CDD.

Type A natriuretic peptides exhibit different bronchoprotective effects in rats

The protective effect of 11.4, 22.8 or 45.6 pmol/kg/min cardiodilatin/atrial natriuretic peptide (CDD/ANP-(99-126)), urodilatin (CDD/ANP-(95-126)) or vehicle intravenously against acetylcholine-induced bronchoconstriction was compared in spontaneously breathing, halothane-anesthetized Wistar rats. The inhalation of acetylcholine induced significant alterations of the spontaneous breathing parameters evaluated by whole-body plethysmography without significant differences between the treatment groups. Forced parameters detect airflow changes with a greater sensitivity and were measured in hyperventilation-induced temporary apnoea after the challenge. The forced expiratory volume in 0.1 s revealed a significant protective effect of 11.4 pmol/kg/min urodilatin compared to the controls whereas the parameters of the forced expiratory flow-volume curve were significantly preserved by 11.4 and 22.8 pmol/kg/min urodilatin (P < 0.05). Urodilatin showed protective effects against an acetylcholine challenge whereas CDD/ANP-(99-126) was without significant influence.

Regulation of NK Cells During Acute Psychological Stress by Noradrenaline

Stress has been suggested for a long time to be associated with a decrease in natural killer (NK) activity. There is also accumulating evidence from psychoneuroimmunological research1 that stress situations such as examination2,3 or bereavement4 may alter a wide range of immunological functions, especially NK cell function. Moreover, increased incidence of viral infections or cancer have been reported in stressed populations5,6.