M. F. Menadue

Activation of GABA receptors in the hypothalamus stimulates secretion of growth hormone and prolactin

Localized intracerebral microinjections of GABA, muscimol, picrotoxin and bicuculline were made in the anterior and basal hypothalamus to determine possible sites of action of GABA in the regulation of prolactin and growth hormone (GH) secretion. Studies were carried out in unanesthetized male rats with chronic indwelling atrial cannulae and intracerebral guide cannulae which permitted stress free blood sampling and intrahypothalamic injections, respectively. Preoptic/anterior hypothalamic area. (PO/AHA) injection of muscimol (0.16 nmol) stimulated both prolactin and GH secretion. GABA (1600 nmol) stimulated prolactin. Bicuculline (0.016 and 0.16 nmol) inhibited GH secretion. Medial basal hypothalamic (MBH) injection of muscimol (0.1 and 1.0 nmol) and GABA (1000 nmol) stimulated prolactin but had no effect on GH secretion. Picrotoxin and bicuculline did not stimulate GH. These findings indicate that activation of PO/AHA GABAergic receptors facilitates secretion of GH and prolactin and activation of MBH GABAergic receptors stimulates secretion of prolactin. It is proposed that GABA inhibits somatostatin neurons in the PO/AHA to facilitate GH and inhibits tuberoinfundibular dopamine or GABA neurons in the MBH to stimulate prolactin.

Evidence That the Regulation of Growth Hormone Secretion Is Mediated Predominantly by a Growth Hormone Releasing Factor

Spontaneous pulsatile growth hormone (GH) secretion and stress-induced suppression of GH was examined in chronically cannulated male rats with electrolytic lesions of the periventricular preoptic anterior hypothalamic area (PO/AHA) where somatostatin neurons innervating the median eminence are known to be located. Median eminence somatostatin was depleted in lesioned animals by 85%. Bursts of GH secretion occurred more frequently than in sham-lesioned animals (1.9 +/- 0.2 vs. 2.6 +/- 0.2 h, respectively, p less than 0.025), however, average concentrations of GH were reduced by lesions (118.4 +/- 11.6 vs 192.3 +/- 28.4 ng/ml, p less than 0.025). Suppression of GH by stress was unaffected by PO/AHA lesions. It is concluded that somatostatin plays only minor roles in the generation of GH troughs during rhythmic GH secretion, and in the suppression of GH during stress. Inhibition of GH releasing factor secretion, therefore, is presumed to be the likely method by which GH suppression is achieved in these physiological situations.

Atrial natriuretic factor release during rapid ventricular pacing: Interplay between autonomic and hemodynamic stimulants

Plasma levels of atrial natriuretic factor (ANF) and norepinephrine are markedly elevated during episodes of ventricular tachycardia. Although atrial distention appears to be the major stimulus for ANF release, reflex changes in autonomic tone might also contribute. Plasma ANF and norepinephrine levels, sinus node cycle length, systolic blood pressure, and mean right atrial pressure were therefore assessed during rapid right ventricular pacing at 150 beats/min for 10 minutes. In five patients (group 1) observations were made without autonomic blockade, and another five patients (group 2) had ventricular pacing after cardiac autonomic blockade. In group 1 systolic blood pressure fell during ventricular pacing from 122 +/- 4 to 105 +/- 5 mm Hg (p < 0.02), norepinephrine levels increased from 195 +/- 26 to 411 +/- 71 pg/ml (p < 0.02), and sinus node cycle length decreased from 936 +/- 99 to 688 +/- 58 msec (p < 0.02). Right atrial pressure was elevated from 2.6 +/- 0.6 to 7.4 +/- 0.6 mm Hg (p < 0.02), and ANF levels increased from 161 +/- 23 to 240 +/- 26 pg/ml (p < 0.05). Whereas systolic blood pressure, norepinephrine, sinus cycle length, and right atrial pressure returned promptly to baseline levels when ventricular pacing was stopped, ANF levels continued to rise (296 +/- 37 pg/ml; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)