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Biomedical subjects

P Bouloux

Publications and source records attributed to P Bouloux.

5 recordsLinked to original sources
PubMed1992

X chromosome-linked Kallmann syndrome: stop mutations validate the candidate gene.

Kallmann syndrome represents the association of hypogonadotropic hypogonadism with anosmia. This syndrome is from a defect in the embryonic migratory pathway of gonadotropin-releasing hormone synthesizing neurons and olfactory axons. A candidate gene for the X chromosome-linked form of the syndrome was recently isolated by using a positional cloning strategy based on deletion mapping in the Xp22.3 region. With the PCR, two exons of this candidate gene were amplified on the genomic DNAs from 18 unrelated patients affected with the X chromosome-linked Kallmann syndrome. Three different base transitions--all leading to a stop codon--and one single-base deletion responsible for a frameshift were identified. We thus conclude that the candidate gene is the actual KAL gene responsible for the X chromosome-linked Kallmann syndrome. Furthermore, unilateral renal aplasia in two unrelated patients carrying a stop mutation indicates that the KAL gene is itself responsible for this Kallmann syndrome-associated anomaly. The gene is, therefore, also involved in kidney organogenesis. Additional neurologic symptoms in Kallmann patients are also discussed.

Base Sequence↗
PubMed1991

High-dose naloxone modifies cardiovascular and neuroendocrine function in ambulant subjects.

To determine the role of the opioids in the control of the cardiovascular system in awake ambulatory subjects, eight healthy men were infused with a high dose of naloxone (10 mg bolus plus 7 mg/hr), or saline placebo, for 12 hr. Ambulatory monitoring of blood pressure and heart rate every 10 min indicated no differences between trials for blood pressure (p greater than 0.80), but a significant difference for the maximal heart rate response during stair climbing or 1 km walks (p less than 0.02). Plasma cortisol concentration were increased during the naloxone trials (p less than 0.05), as was total urinary epinephrine and dopamine output (p = 0.005 and less than 0.03, respectively). Plasma FSH and LH concentrations were elevated during naloxone infusion (FSH: p less than 0.02, LH: p less than 0.01), but neither exercise or mental tasks significantly altered their levels (p greater than 0.20). The cardiovascular responses during moderate mental tasks were not affected by naloxone (p greater than 0.05). These results indicate that in the normal ambulatory state the opioid system has a minor role in cardiovascular regulation, as demonstrated by the urinary catecholamines. Its role becomes more evident when considerable stress is imposed.

Adult↗
PubMed1990

The role of alpha-2-adrenoceptors in the control of ACTH secretion; interaction with the opioid system.

This study examined the effects of an alpha-2-adrenoceptor antagonist on the secretion of ACTH basally and in response to the opioid antagonist naloxone, which is known to stimulate ACTH secretion by an adrenergic mechanism. Eight normal men were given, in double-blind, random order, intravenous infusions of normal saline (placebo), idazoxan (alpha-2-adrenoceptor antagonist), naloxone and the combination of idazoxan and naloxone. Naloxone increased plasma ACTH and cortisol concentrations in comparison to placebo. Idazoxan significantly enhanced the ACTH and cortisol responses to naloxone but had no effect on plasma ACTH or cortisol concentrations when given alone. These findings suggest that during some conditions of increased ACTH secretion, inhibitory alpha-2-adrenoceptors are activated and that these receptors limit the ACTH response. This provides an explanation for some of the apparent contradictions in interpreting the data from previous studies on the effects of catecholamines on the secretion of ACTH.

Adrenergic alpha-Antagonists↗
PubMed1978

Effect of the dopamine agonist, lergotrile mesylate, on circulating anterior pituitary hormones in man.

The effects of the ergoline derivative, lergotrile mesylate, on the serum levels of PRL, GH, TSH, LH, FSH, cortisol, and blood sugar were studied in six normal males. The effects of lergotrile mesylate on the serum levels of GH and PRL were also studied in eight patients with acromegaly and in two with idiopathic hyperprolactinemia. In the normal subjects, 2 mg oral lergotrile lowered basal PRL levels after 90 min and markedly impaired the PRL response to TRH (200 micrograms iv); the mean peak value +/- SE was 8.3 +/- 1.1 micrograms/liter, compared to the control value of 66.6 /+- 11.3 micrograms/liter. Lergotrile raised serum GH levels in five of the six subjects to peaks of 8-49 micrograms/liter, compared to 2-8 micrograms/liter after placebo. In three subjects, the GH response to lergotrile was attenuated by the prior administration of the dopamine antagonist, metoclopramide (10 mg orally). Lergotrile had no effect on FSH and LH levels under basal conditions or after the gonadotrophin-releasing hormone (GnRH; 100 micrograms iv). Circulating TSH levels were unaltered basally but impaired after TRH. Blood sugar levels were unaltered; serum cortisol was elevated in five of six subjects; there was a brief depression of diastolic blood pressure, but no change in pulse rate. The side effects after lergotrile were variable, with drowsiness as a consistent feature. These actions are similar to those of bromocriptine (an ergot derivative treatment of hyperprolactinemia and acromegaly, to suppress PRL and GH secretion, and in parkinsonism. Therefore, it may be expected that lergotrile could fulfill these clinical uses; however, in the studies comparing the effects of single oral doses of lergotrile (2 mg) and bromocriptine (2.5 mg) on GH and PRL secretion in patients with acromegaly and hyperprolactinemia, lergotrile in the dose used has been found to have an earlier onset and shorter duration of action.

Acromegaly↗