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Biomedical subjects

T L Garthwaite

Publications and source records attributed to T L Garthwaite.

At least 19 recordsLinked to original sources
PubMed1988

Cardiovascular fitness and selected adrenal hormone responses to cognitive stress.

Individuals manifesting high maximal oxygen consumption (VO2max) have augmented adrenal responsivity to physical stress. We subjected 17 males representing a wide range of VO2max to cognitive stress and measured their forearm venous plasma epinephrine, norepinephrine, and cortisol responses. Six repeated blood samples were collected at resting, stress, and recovery intervals. Significant increases were observed for epinephrine (X +/- SD; rest, 50 +/- 30; stress, 81 +/- 77 pg/ml; p less than or equal to 0.05) and norepinephrine (rest, 404 +/- 235; stress, 481 +/- 314 pg/ml; p less than or equal to 0.05). Cortisol changes were not significant. A positive association (r = 0.54; p less than or equal to 0.05) was observed between epinephrine and VO2max during the first collection of the stress period. An inverse association (r = 0.49; p less than or equal to 0.05) was present between VO2max and norepinephrine. No significant correlations occurred with cortisol. These results indicate that enhanced cardiovascular fitness is characterized by augmented epinephrine responsivity to cognitive stress. This association exists in the presence of an inverse relationship between plasma free norepinephrine response and VO2max.

Adult↗
PubMed1987

Central administration of motilin stimulates feeding in rats.

Peripheral administration of motilin has been found to stimulate feeding behavior in rats. Since motilin immunoreactivity has been found in discrete brain sites, we tested the effect of motilin administered intracerebroventricularly on feeding in rats. Injection of 1 microgram of motilin significantly increased food consumption at 2 hours, 22 hours, and at 24 hours in animals tested either at or 2 hr prior to lights out. Motilin also significantly increased food consumption in animals maintained under continuous lights-on at 2 hours (488% of control), 22 hours (128% of control), and at 24 hours (140% of control).

Animals↗
PubMed1986

Influence of endogenous opioids on the response of selected hormones to exercise in humans.

To examine the influence of endogenous opioids on the hormonal response to isotonic exercise, eight males were studied 2 h after oral administration of placebo or 50 mg naltrexone, a long-lasting opioid antagonist. Venous blood samples were obtained before, during, and after 30 min of bicycle exercise at 70% VO2max. Naltrexone had no effect on resting cardiovascular, endocrine, or serum variables. During exercise epinephrine was higher [mean 433 +/- 100 (SE) pg/ml] at 30 min with naltrexone than during placebo (207 +/- 26 pg/ml, P less than 0.05). Plasma norepinephrine showed the same trend but the difference (2,012 +/- 340 pg/ml with naltrexone and 1,562 +/- 241 pg/ml with placebo) was not significant. Plasma glucose was higher at all times with naltrexone. However, the difference was significant only 10 min into recovery from exercise (104.7 +/- 4.7 vs. 94.5 +/- 2.8 mg/dl). Plasma growth hormone and cortisol increased during recovery and these elevations were significantly (P less than 0.05) augmented by naltrexone. Plasma vasopressin and prolactin increased with exercise as did heart rate, blood pressure, lactic acid, and several serum components; these increases were not affected by naltrexone. Psychological tension or anxiety was lower after exercise compared with before and this improved psychological state was not influenced by the naltrexone treatment. These data suggest that exercise-induced activation of the endogenous opioid system may serve to regulate the secretion of several important hormones (i.e., epinephrine) during and after exercise.

Adult↗
PubMed1986

Antisera to vasoactive intestinal polypeptide inhibit basal prolactin release from dispersed anterior pituitary cells.

Vasoactive intestinal polypeptide (VIP) has been identified in hypothalamic tissue, is secreted into hypophysial portal blood, and stimulates prolactin (PRL) release in vivo and in vitro. It has been proposed, therefore, that VIP is a physiologic PRL-releasing factor. In this study, we confirm that VIP stimulates PRL release from rat pituitary cells in vitro, and demonstrate that an anti-VIP antiserum blocks VIP-induced PRL secretion. Surprisingly, the anti-VIP antiserum inhibited basal PRL secretion from rat pituitary cells in 3 separate experiments. Data from these experiments were pooled, as the responses were similar, revealing basal PRL release of 10.7 +/- 1.3 ng rPRL/10(5) cells (X +/- SE), while anti-VIP antisera significantly inhibited release to 4.4 +/- 0.6 ng rPRL/10(5) cells (p less than 0.001). PRL release in incubates containing control non-immune sera did not differ from basal release, 8.1 ng rPRL/10(5) cells. A further control experiment was conducted wherein cells were incubated with an anti-ACTH antiserum, representing another hyperimmune serum, which had no effect on PRL secretion. These data suggest that VIP, in addition to its possible role as a hypothalamic-derived PRL-releasing factor, may play a role within the pituitary as a regulator of basal PRL secretion.

Animals↗
PubMed1986

Vasoactive intestinal polypeptide is synthesized in anterior pituitary tissue.

Previous studies have suggested that vasoactive intestinal polypeptide (VIP) is involved in regulation of PRL secretion within the pituitary gland. In order to determine whether VIP is synthesized in anterior pituitary tissue, we performed three experiments. In all experiments, anterior pituitaries were obtained from male rats. The tissue was then labeled by incubation in leucine-free minimum essential medium containing [3H]leucine, 14 microCi/ml. In Exp I, the labeled tissue was homogenized, centrifuged, and the supernatant was chromatographed on Sephadex G-50F. The fractions indicated a large peak of counts near the void volume and another peak coeluting with VIP. These latter fractions were pooled and subjected to reverse phase HPLC. Fractions from the HPLC indicated: a protein peak, VIP immunoreactivity, and maximum counts immunoprecipitated by anti-VIP serum at the retention time of synthetic porcine VIP. Exp II consisted of perifusion of labeled pituitary quarters over a 120-min period followed by an additional 60 min in the presence of 56 mM KCl. During this latter period of KCl depolarization, a large amount of 3H-labeled material was secreted. These fractions were then chromatographed on Sephadex G-50F, and the fractions coeluting with [125I]porcine VIP were subjected to immunoprecipitation with anti-VIP serum. In addition, all fractions from the Sephadex column were assayed for VIP, and the only activity was at the elution volume of [125I]porcine VIP. In Exp III, the pituitary labeling procedure included 3.6 X 10(-5) M cycloheximide. Subsequently, the tissue was perifused and the perifusate collected during the 60-min 56 mM KCl perifusion phase was pooled and immunoprecipitated with anti-VIP serum. No immunoprecipitable counts were obtained. These experiments indicate that anterior pituitary tissue synthesizes VIP on the basis of the HPLC profile and immunoprecipitation with specific anti-VIP antiserum. These results, in addition to other studies by our laboratory and others, suggest that intrapituitary VIP may be an important regulator of anterior pituitary hormone secretion, particularly PRL.

Animals↗
PubMed1985

Activation of renal 1,25-dihydroxyvitamin D3 synthesis by phosphate deprivation: evidence for a role for growth hormone.

In vitro 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] production in kidney slices from normal intact rats averaged 16 +/- 4 pmol/g . h and was increased about 8-fold by phosphate deprivation and 5-fold by calcium deprivation to levels averaging 128 +/- 12 and 84 +/- 19 pmol/g x h, respectively. Hypophysectomy in phosphate-deprived rats completely abolished any increase in 1 alpha-hydroxylase activity, while calcium deprivation in hypophysectomized (hypox) rats resulted in a 4-fold increase in 1 alpha-hydroxylase activity. Replacement of hypox rats fed a low phosphorus diet with pituitary extracts resulted in a 4-fold stimulation of 1 alpha-hydroxylase activity in response to the hypophosphatemic stimulus. However, replacement of hypox rats fed a normal phosphorus diet with pituitary extract stimulated 1 alpha-hydroxylase activity only 2-fold. Replacement of hypox rats fed a low phosphorus diet with GH resulted in a 3.5-fold elevation in plasma 1,25-(OH)2D3 levels, while no such elevation in plasma 1,25-(OH)2D3 levels was observed in similarly treated animals replaced with PRL, ACTH, TSH, or T3. Replacement of hypox rats eating a normal diet with GH resulted in no significant change in plasma 1,25-(OH)2D3 levels. These results suggest that GH is required for maintenance of elevated plasma 1,25-(OH)2D3 levels during dietary phosphate deprivation and that this effect is mediated by increased renal 1,25-(OH)2D3 synthesis.

Animals↗
PubMed1984

Hormonal, metabolic and morphologic studies of aged C57BL/6J obese mice.

Genetically obese mice (C57BL/6J-ob/ob), fed ad libitum, demonstrated a precipitous increase in the spontaneous death rate after 50 weeks. The first signs of morbidity were a ruffled hair coat and a progressive motor ataxia. Necropsy revealed that obese mice had pale and fatty livers, urolithiasis and grossly distended bladders. Microscopically, the hepatocellular changes observed in all aged obese mice included: a loss of orientation of hepatocytes, an enormous variability in the size of both hepatocytes and their nuclei, and an extensive deposition of both large and small lipid droplets, confirmed by an increase content of triacylglycerols. A subacute-to-chronic, multifocal, necrotizing hepatitis was also present. Kidneys from aged obese mice contained hypertrophied glomeruli and increased PAS-stained material. Tubular dilation with compaction of the tubular cells was also seen. There were no significant alterations in the microanatomy or mineralization of femurs from obese mice, yet there was a significant increase in plasma alkaline phosphatase activity. In obese mice at 62-63 weeks of age, hyperglycemia was present even in spite of hyperinsulinemia. Pituitary immunoreactive ACTH and its molar ratio to pituitary immunoreactive beta-endorphin were also increased in obese mice at this age. Even though the etiology of the decreased lifespan of genetically obese mice remains uncertain, the possibility is discussed that an overall defect in the central nervous system may be involved.

Adrenocortical Hyperfunction↗
PubMed1983

Plasma adrenocorticotropin and cortisol responses to submaximal and exhaustive exercise.

Adrenocorticotropic hormone (ACTH) levels were compared before and after submaximal and exhaustive isotonic exercise in six normally active college students (3 men and 3 women). Each subject participated in three experiments conducted at the same morning hour. Venous plasma was obtained before and immediately after 20-min runs at 65 and 80% of maximal O2 consumption (VO2 max) and after a run of gradually increasing work intensity which resulted in exhaustion (100% VO2 max) in 12.6 +/- 1.3 min. ACTH (mean +/- SE) was 48 +/- 15, 57 +/- 12, and 61 +/- 11 pg/ml before the 65, 80, and 100% VO2 max runs, and increased to 61 +/- 15 (NS), 128 +/- 18 (P less than 0.05), and 292 +/- 72 (P less than 0.05) pg/ml, respectively. Plasma glucose, growth hormone, cortisol, and lactic acid concentrations increased in a similar fashion. Cortisol and ACTH levels were significantly correlated at the higher levels of exertion: r = 0.18 (NS) for the 65% VO2 max run, r = 0.65 (P less than 0.05) for the 80% VO2 max run, and r = 0.64 (P less than 0.05) for the run to exhaustion. Both the change in ACTH with exercise and its postrun concentration were significantly related to the change in plasma lactic acid (r = 0.65, P less than 0.05) and the postrun plasma lactic acid (r = 0.64, P less than 0.05). We conclude that exercise-induced increases in plasma ACTH and their correlation with circulating cortisol depend on the intensity of isotonic exercise. Our observations also suggest that plasma lactic acid may influence ACTH release during exercise.

Adrenocorticotropic Hormone↗
PubMed1981

Running elevates plasma beta-endorphin immunoreactivity and ACTH in untrained human subjects.

Twenty minutes of submaximal treadmill running was associated with an elevation in plasma levels of beta-endorphin immunoreactivity (P less than 0.02). This increase was greater in men (14.9 +/- 3.4 fmole/ml) than women (2.6 +/- 1.2 fmole/ml)(P less than 0.05). Plasma levels of ACTH and growth hormone also increased after running. ACTH increased more in men (7.8 +/- 1.1 fmole/ml) than in women (1.1 +/-0.44 fmole/ml)(P less than 0.02). There was a similar growth hormone response in both sexes. No correlation can at this time be made with levels in the central nervous system. Changes in plasma levels of beta-endorphin immunoreactivity may be responsible for some of the euphoria and analgesia anecdotally associated with running.

Adrenocorticotropic Hormone↗
PubMed1980

Fasting associated with decrease in hypothalamic beta-endorphin.

In rats that were fasted for 2 to 3 days there was a decline in hypothalamic, but not pituitary, beta-endorphin. There was no change in pituitary or hypothalamic adrenocorticotropin content as a result of fasting. Endogenous opiates may be involved in physiological adaptation to fasting.

Adrenocorticotropic Hormone↗