Stressful social interactions have been shown to elicit increases in heart rate as well as in plasma levels of epinephrine, norepinephrine, and cortisol in humans. We sought to determine whether a competitive oral examination would affect plasma levels of the pituitary hormones ACTH, beta-endorphin, beta-lipotrophic hormone, and prolactin in a group of healthy young males. Seven min after beginning the examination, heart rate increased 27% and plasma levels of ACTH, beta-endorphin, beta-lipotropic hormone and prolactin rose 59%, 79%, 42%, and 46%, respectively, compared to values shortly before the examination. These hormone values returned to initial levels after the subjects returned to the waiting room. Plasma cortisol changes were similar in direction to those of ACTH but occurred about 15 min later. The present study demonstrates that a stressful social interaction can elicit rapid increases in plasma levels of the proopiomelanocortin derived peptide hormones and prolactin in man.

Serotonin reuptake inhibitor (SRI) antidepressants have been associated with sexual dysfunction, though there have been few prospective reports specifically examining this problem. The purpose of this study was to determine if three SRIs affected sexual function in patients with an anxiety disorder or major depressive disorder over a 3-month period. Sixty-one patients were evaluated for at least 2 months in a prospective study of the effects of fluoxetine, sertraline, and paroxetine on five aspects of sexual function: libido, erection/lubrication, orgasm quality, orgasm delay, and sexual frequency. Measurements were made at baseline and at each month on visual analog scales. For men and women, orgasm quality was lower and orgasm delay longer at Months 1, 2, and 3 compared with baseline (p < .001). Erection scores were lower over time (p < .02) but this change was less dramatic. Lubrication, libido, and sexual frequency were not appreciably changed over 3 months. Anorgasmia was significantly more common in women than men at Months 1 and 2. Orgasm appears to be a primary sexual function affected by SRIs.

Apomorphine, a direct-acting dopamine agonist, stimulates release of growth hormone (hGH) and suppresses release of prolactin (PRL) from the anterior pituitary. Previous studies comparing the magnitude of these responses in schizophrenics and controls suggest that many acute (and some chronic) schizophrenics have exaggerated hGH responses; many chronic schizophrenics (and patients with tardive dyskinesia) have blunted hGH responses to apomorphine, and possibly blunted PRL responses. The present studies extend and confirm these findings in chronic schizophrenics; in addition, several studies were undertaken to further characterize these apomorphine-induced endocrine responses. Studies in which apomorphine was given on 2 or 3 separate occasions to each of five subjects indicate that the hGH response is a highly reproducible individual index, but PRL suppression is a less satisfactory measure. hGH responses to apomorphine were consistently antagonized by pretreatment with haloperidol, supporting the concept that the hGH-releasing effect of apomorphine is mediated by its action on dopamine receptors. Cyproheptadine pretreatment was associated with erratic increases or decreases in the hGH response to apomorphine, but did not alter PRL levels or apomorphine-induced PRL suppression. The relationship of these findings to biological hypotheses of schizophrenia and to neuroleptic-induced receptor changes is discussed.

The differences between the mechanisms of muscarinic and nicotinic receptor‐mediated catecholamine secretion with respect to their dependence on voltage changes and extracellular Ca were examined using perfused adrenal glands of the guinea‐pig. Acetylcholine (ACh, 10−6 to 10−3 m) caused a dose‐dependent increase in catecholamine secretion. The ED50 value for ACh was 7 × 10−5 m. In the presence of atropine (10−5 m), the dose‐response curve for ACh was shifted to the right. Hexamethonium (5 × 10−4 m) preferentially reduced the responses to higher concentrations of ACh (> 10−5 m). Pilocarpine (5 × 10−4 m) and nicotine (3 × 10−5 m) also stimulated catecholamine release. During perfusion with isotonic KCl solution, ACh and pilocarpine, but not nicotine, evoked catecholamine secretion. These responses were abolished by atropine (10−6 m). Pilocarpine‐stimulated catecholamine secretion was enhanced during perfusion with isotonic KCl solution. Under these conditions, hexamethonium (10−3 m) significantly augmented ACh‐evoked catecholamine release. During perfusion with either Ca‐free isotonic KCl or Ca‐free Locke solution, ACh and pilocarpine caused a partial increase in catecholamine secretion whereas nicotine and high K solution (56 mm) did not. The responses to ACh and pilocarpine were completely inhibited by atropine but not by hexamethonium. When guinea‐pig adrenal glands were perfused with isotonic KCl solution containing 2.2 mm Ca which was subsequently removed and replaced with EGTA, ACh‐induced catecholamine secretion was similar in magnitude to that observed during perfusion with Locke solution. We conclude that both nicotinic and muscarinic receptors are involved in ACh‐induced catecholamine secretion from guinea‐pig adrenal chromaffin cells. Activation of muscarinic or nicotinic receptors appears to stimulate catecholamine release through different mechanisms with respect to both voltage‐dependence and Ca requirements.

Neuroendocrine and sympathoadrenal responses to exhaustive graded treadmill exercise were examined in 17 male subjects of varying degrees of fitness. The mean duration of exercise to exhaustion was 15.2 +/- 0.7 (+/- SE) min. Exercise duration was inversely correlated with baseline heart rate (P less than 0.05). Compared to standing baseline values, mean plasma norepinephrine and epinephrine levels increased 339% and 301%, respectively, in an integrated 2-min blood sample collected immediately after completion of exercise. Mean adrenocorticotrophic hormone (ACTH), beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and prolactin levels increased 282%, 720%, 372%, and 211%, respectively, in an integrated 4-min blood sample beginning 2 min after completion of exercise. Cortisol levels increased 183% in the sample collected 17-21 min after exercise. The magnitude of these neuroendocrine responses to exercise was similar among individuals at the same relative intensity of exhaustive exercise, regardless of the duration of exercise. The exercise-induced increases of the pro-opiomelanocortin (POMC)-derived peptides, ACTH, beta-EP, and beta-LPH, were highly correlated with each other (P values less than 0.001), and were correlated with prolactin increases, (P values less than 0.05). During a 20-min recovery period after exercise, changes in heart rate, ACTH, and beta-LPH levels were correlated with duration of exercise, (P less than 0.01, P less than 0.03, and P less than 0.03, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

A 4-stage model of evaluation anxiety incorporating ability, affective, cognitive, and performance variables was tested in the context of a career-related oral examination among enlisted personnel in the U.S. Army. A path analysis supported the stage model for the most part, showing the influence of dispositional anxiety, preexamination anxiety, self-efficacy, and negative thoughts before and during the examination on participants' oral examination performance. The nature of the examination-stage cognitive variable appears to be important, because in the path analysis negative thoughts were predictive of performance, but state of mind (the ratio of positive to positive-plus-negative thoughts) was not. Results have implications for career counseling and suggest that cognitive-behavioral interventions may be effective for individuals with anxiety related to job evaluations.

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The measurement of plasma norepinephrine (NE) and epinephrine (EPI) levels has provided a means to assess sympathetic and adrenal medullary responses to stressors. To address the issue of specificity of these responses to mental or physical stress, we measured plasma norepinephrine (NE) and epinephrine (EPI) levels in male volunteers who underwent either exhaustive graded treadmill exercise or a 30 min stressful interview. We found that graded treadmill exercise to exhaustion (mean duration of exercise 15.2 ± 0.7 min) was associated with similar increases in both NE (239 per cent) and EPI (201 per cent) immediately after completing exercise. Elevated values rapidly returned to baseline levels after exercise. In response to the 30min stressful interview where subjects remained seated throughout the stressor, there were smaller but highly significant increases in plasma levels of both NE (67 per cent) and EPI (82 per cent) within the first 10min of the interview. By the last 10min of the interview, EPI levels were already returning to baseline values while NE levels remained elevated throughout and for at least 5min after the exam. These findings demonstrate that a stressful interview is associated with increases in both NE and EPI levels which are qualitatively similar to the responses to a physical stressor.