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Biomedical subjects

R L Hauger

Publications and source records attributed to R L Hauger.

85 records · Page 5Linked to original sources
PubMed1978

Control of aldosterone secretion during sodium restriction: adrenal receptor regulation and increased adrenal sensitivity to angiotensin II.

The mechanism of increased adrenal sensitivity to angiotensin II during the aldosterone response to sodium restriction was investigated in the rat. Sodium restriction for 36 hr markedly increased the aldosterone-stimulating effect of low-dose (1 ng/min) infusion of angiotensin II and caused enhanced binding of (125)I-labeled angiotensin II to the zona glomerulosa in vivo. Conversely, in vivo binding of (125)I-labeled angiotensin II was significantly decreased after 36 hr of high-sodium intake. In isolated glomerulosa cells, the increased binding of angiotensin II after sodium restriction was shown to result from a significant increase in receptor affinity (+80%) and a smaller increase in receptor concentration (+25%). The corresponding aldosterone responses in dispersed cells showed an increase in sensitivity to angiotensin II, commensurate with the increased receptor affinity. More prolonged sodium restriction (4 days) caused a further increase in angiotensin receptor concentration (+70%) and maximal aldosterone response (+50%), whereas the binding affinity of adrenal receptors and the sensitivity of the in vitro aldosterone response had returned to normal. During sodium loading for 36 hr and 4 days, the converse effects on adrenal angiotensin II receptors and aldosterone production were observed. Also, in contrast to the consistent increase in angiotensin II receptors in the adrenal glands of sodium-restricted animals, the angiotensin II binding capacity of uterine smooth muscle was decreased by 40% after 7 days of sodium restriction.The rapid regulation of receptor affinity and concentration during changes in sodium intake provides a basis for the dynamic modulation of aldosterone responses by dietary sodium content. During sodium restriction, the sequential changes in receptor affinity and concentration account for the enhanced binding and steroidogenic actions of angiotensin II in vivo and in vitro. These receptor changes, and the converse effects of sodium loading, serve as a local regulatory mechanism in the physiological control of adrenal sensitivity and aldosterone secretion. The opposite finding in smooth muscle-that sodium restriction decreases the concentration of angiotensin II receptors-is consistent with the divergent effects of changing sodium balance upon vascular and adrenal responses to angiotensin II.

Adrenal Glands↗
PubMed1977

A new concept for control of the estrous cycle of the ewe based on the temporal relationships between luteinizing hormone, estradiol and progesterone in peripheral serum and evidence that progesterone inhibits tonic LH secretion.

The temporal relationships between LH, estradiol and progesterone in peripheral serum of the ewe were characterized throughout the estrous cycle. Between successive preovulatory LH sruges, serum concentrations of LH fluctuated markedly in a manner indicative of pulsatile discharges. Mean serum LH and progesterone concentrations were inversely related, LH being highest during the early and late luteal phases of the estrous cycle and lowest in the mid-luteal phase. A progressive, 5-fold increase in serum LH concentrations occurred between the onset of the precipitous fall in circulating progesterone attendant to luteolysis and the initiation of the preovulatory LH surge. Two major increments in circulating estradiol were observed in each cycle, both occurring when serum LH concentrations were relatively high. One estradiol increment occurred during the early luteal phase, the other during the 2-3 days prior to onset of the preovulatory LH surge. The latter estradiol increment thus accompanied the progressive, 5-fold increase in circulating LH which precedes the LH surge. The observations are inconsistent with the view that tonic LH secretion in the ewe is solely a function of a negative feedback action of estradiol. Rather, the temporal relationships between circulating hormones, in conjunction with recent findings that progesterone can inhibit tonic LH secretion in the ewe, lead to the conclusion that progesterone plays a major role in the regulation of tonic LH secretion during the estrous cycle of sheep.

Animals↗
PubMed1977

Pituitary regulation of Leydig cell function in the adult male rat.

The effects of hypophysectomy on serum testosterone, 125I-labelled hCG binding to testicular membranes and on testicular responsiveness were studied in adult rats. Serum testosterone decreased rapidly over the first 6 h after hypophysectomy. LH receptors were determined (pmol/testis) by measuring the specific binding of 125I-labelled hCG in membrane preparations of testes of rats hypophysectomized 1, 2, 3, 6, 9, or 15 days earlier. Hypophysectomy did not result in a decrease in 125I-labelled hCG binding on day 1 but this had decreased to 40% of that in intact controls by day 2. A gradual decline was found between days 2 and 6 at which time hCG binding had decreased to 15%. No further decrease occurred between days 6 and 15. Scatchard analysis indicated that the decline in hCG binding was due to a decreaffinity. FSH, testosterone, dihydrotestosterone, and oestradiol were unable to prevent the decline in hCG binding. Although serum testosterone, testicular testosterone content, and 125I-labelled hCG binding decreased rapidly after hypophysectomy, testicular responsiveness to LH was biphasic. The intraperitoneal administration of 25 microgram LH 2 h before decapitation increased testosterone in the circulation to a greater extent extent in animals hypophysectomized for 1 day than in intact controls while hCG binding affinities and capacities had not changed. Two or three days after hypophysectomy testicular responsiveness to LH was similar to that of intact controls even though hCG binding in hypophysectomized animals had decreased to 40 and 28% of intact controls respectively. It is concluded that (1) the testis is dependent on anterior pituitary hormones for maintenance of testicular LH receptors and testosterone secretion, (2) FSH, testosterone, dihydrotestosterone, or oestradiol cannot prevent the decline in testicular LH receptors resulting from hypophysectomy, and (3) steroidogenic capacity of the testis persists significantly longer than the hCG binding capacity of the testis.

Animals↗
PubMed1977

Testicular receptors for luteinizing hormone after immunoneutralization of gonadotrophin releasing hormone in the male rat.

The effects of immunoneutralization of endogenous gonadotrophin releasing hormone (GnRH) on the serum concentrations of testosterone and gonadotrophins and the binding of 125I-labelled human chorionic gonadotrophin (HCG) to testicular membrane fractions were studied in adult male rats. Four days after the administration of 1 ml anti-GnRH serum, the level of testosterone in the serum decreased to 44% of the concentration before the injection, whereas administration of normal rabbit serum had no effect. Multiple injections of anti-GnRH serum for 4 days dramatically suppressed the secretion of gonadotrophins in rats orchidectomized 2 months earlier. In intact male rats treated identically, immunoneutralization of GnRH decreased the level of serum testosterone to 32% of the concentration present in saline-treated controls, but did not decrease the number of testicular binding sites for HCG (LH). Administration of testosterone or oestradiol for 3 or 6 days caused a marked reduction in the concentration of serum gonadotrophins but did not decrease the number of LH receptors. This study provides further support for the concept that one releasing hormone governs secretion of both FSH and LH. In addition, these studies indicate that selective reduction of gonadotrophins for 3-6 days has no effect on the number of testicular LH receptors. This suggests that pituitary hormones other than gonadotrophins may be important in the maintenance of testicular receptors for LH.

Animals↗
PubMedDate not supplied

Brain and pituitary receptors for corticotropin releasing factor: localization and differential regulation after adrenalectomy.

Specific receptors for corticotropin releasing factor (CRF) were identified in two functionally distinct systems within the brain, the cortex and the limbic system. Autoradiographic mapping of the CRF receptors in the brain revealed high binding density throughout the neocortex and cerebellar cortex, subiculum, lateral septum, olfactory tract, bed nucleus of the stria terminalis, interpeduncular nucleus and superior colliculus. Moderate to low binding was found in the hippocampus, nucleus accumbens, claustrum, nucleus periventricularis thalamus, mammillary bodies, subthalamic nucleus, periaqueductal grey, locus coeruleus and nucleus of the spinal trigeminal tract. As in the anterior pituitary gland, CRF receptors in the brain were shown to be coupled to adenylate cyclase. However, in contrast to the marked decrease in CRF receptors observed after adrenalectomy in the anterior pituitary gland, CRF receptor concentration in the brain and pars intermedia of the pituitary was unchanged. The presence of CRF receptors in areas involved in the control of hypothalamic and autonomic nervous system functions is consistent with the major role of CRF in the integrated response to stress.

Adenylyl Cyclases↗
PubMedDate not supplied

Endogenous corticotropin-releasing factor modulates feeding induced by neuropeptide Y or a tail-pinch stressor.

Previous work has characterized an anorexic action for endogenous, central nervous system corticotropin-releasing factor (CRF). Central injection of CRF decreases food intake induced pharmacologically by various appetite stimulants and a CRF antagonist attenuates restraint stress anorexia. Also, stressful physiological stimuli that are relevant to ingestive regulation, such as glucoprivation and protein nutrient deficiency, activate CRF systems. The present experiments examined the effects of exogenously administered CRF and a CRF antagonist, alpha-helical CRF(9-41), on spontaneous feeding induced by neuropeptide Y (NPY) and by a tail-pinch stressor. Pretreatment with a low dose of the CRF antagonist (1 microgram ICV) enhanced the hyperphagia induced by NPY while reducing the latency to begin feeding and increasing the duration of eating during tail pinch. Higher doses of alpha-hel CRF (5 and 25 micrograms ICV) exhibited diminishing or opposite effects. In contrast, CRF pretreatment (0.02, 0.1, and 0.5 microgram ICV) blocked the acquisition of tail-pinch feeding. Hence, while CRF administration impairs intake in these and other feeding paradigms, alpha-hel CRF actually facilitated dose dependently the intensity of the feeding response to NPY and tail pinch. These results suggest that endogenous CRF systems may play a role in modulating excessive feeding under conditions of evoked appetite and that brain CRF systems regulate feeding when excessive intake threatens to compromise the performance of other noningestive behaviors.

Animals↗
PubMedDate not supplied

Longitudinal study of basal cortisol levels in healthy elderly subjects: evidence for subgroups.

A group of 51 healthy elderly volunteer subjects participated in a 3- to 6-year longitudinal study of basal cortisol levels. Once per year basal cortisol levels were examined using hourly sampling over a 24-h period. Analyses of three cortisol measures (last measure obtained, mean cortisol levels across years, and the cortisol slope) revealed that the slope of the regression line measuring cortisol levels at each year was the most predictive measure of cortisol secretion over the years in this elderly population. Cortisol levels were shown to increase with years in one subgroup, to decrease in another, and to remain stable in a third. The age of the subjects was not related to either cortisol levels or to the pattern of change in cortisol secretion over years. Free and total cortisol levels were highly correlated and the groups did not differ with regard to plasma corticosteroid binding globulin. No group differences were observed for weight, height, body mass index, pulse, blood pressure and glucose. However, significant group differences were reported for plasma triglycerides levels as well as high density lipoproteins levels. Positive correlations were reported between the obsession/compulsion subscale of the SCL-90 questionnaire and the cortisol slope of subjects. Finally, previously reported group differences in neuropsychological performance are summarized. Thus, there exists considerable variation in hypothalamo-pituitary-adrenal function amongst aged humans. These results are consistent with recent animal studies showing the existence of subpopulations of aged rats which differ in hypothalamo-pituitary-adrenal activity and cognitive efficiency.

Adrenal Glands↗
PubMedDate not supplied

Aging effects on the startle response and startle plasticity in Fischer F344 rats.

The effects of aging on acoustic and airpuff startle reactivity, acoustic and airpuff startle habituation, acoustic and cross-modal (light-acoustic) prepulse inhibition (PPI), and fear-potentiated startle (FPS) were examined using 3- (Y: young), 11- (AD: adult), 17- (MA: middle-aged), and 22- (O: old) month-old Fischer F344 rats. AD rats had the highest acoustic startle reactivity with the Y and MA rats showing smaller and comparable startle levels. The O rats had diminished startle reactivity, with over a 65% reduction in responding. Airpuff startle reactivity was comparable in the Y and AD groups, while the MA and O groups had 40% and 80% reductions in airpuff startle respectively. There was an age-related increase in airpuff startle habituation. Acoustic and cross-modal PPI were reduced significantly in O rats when compared to other age groups. Finally, there were no effects of age on FPS. In summary, these studies suggest that in Fischer F344 rats, there are age-associated differences in startle reactivity, startle habituation, and PPI, but no aging effect on FPS.

Acoustic Stimulation↗
PubMedDate not supplied

Chronic life stress alters sympathetic, neuroendocrine, and immune responsivity to an acute psychological stressor in humans.

OBJECTIVE: Life stress is hypothesized to alter the dynamic regulation of the autonomic, neuroendocrine, and immune systems. This study examined the effects of antecedent chronic life stress on psychological and physiological responsivity after acute challenge with a psychological stressor. METHOD: Using a within-subject mixed design, male volunteers with (N = 12) and without chronic life stress (N = 11) were administered a 12-minute laboratory stressor (mental arithmetic) vs a video control. RESULTS: Acute psychological stress induced subjective distress, increases of circulating concentrations of epinephrine, norepinephrine, beta-endorphin, adrenocorticotropic hormone (ACTH), and cortisol, and a selective redistribution of natural killer (NK) cells into the peripheral blood as compared with the video control condition. Although the two groups were almost identical at baseline in psychological, sympathetic, neuroendocrine, and immune domains, the chronic stress group showed greater subjective distress, higher peak levels of epinephrine, lower peak levels of beta-endorphin and of NK cell lysis, and a more pronounced redistribution of NK cells in response to the acute psychological challenge than the controls. Furthermore, the acute stressor induced a protracted decline in NK lysis per NK cell in the chronic stress group but had no effect in the controls. CONCLUSIONS: In summary, when persons who are undergoing chronic life stress are confronted with an acute psychological challenge, an exaggerated psychologic and peak sympathomedullary reactivity occurs that is associated with decrements in individual NK cell function and is protracted beyond termination of the stressor and sympathomedullary recovery.

Adrenal Medulla↗
PubMedDate not supplied

Stress: an overview of the literature with emphasis on job-related strain and intervention.

Maintained stress produces a constellation of neurochemical and hormonal changes that involve both the hypothalamic-pituitary-adrenal axis and a variety of brain regions. Long-term stress can produce psychological and physiologic consequences including anxiety, depression, hypertension, impaired immune system function, and an increased risk of cancer and coronary heart disease. Negative responses to perceived job-related stress usually occur when an individual has relatively little control over the means to meet high job demands. Among the approaches to reduce workplace stress, changing the coping strategies of challenged employees, particularly by increasing decision latitude, can significantly relieve both the psychological and physiologic consequences. Nevertheless, behavioral intervention is not invariably successful, and benzodiazepines are often prescribed to manage inadequately alleviated anxiety. Evidence that excessive serotonergic neurotransmission may underlie anxiety has prompted the use of compounds such as buspirone. This partial agonist of the 5-HT1A receptor has been demonstrated to be as effective as benzodiazepines in controlling generalized anxiety symptoms and to have a more favorable side-effect profile.

Anxiety↗