The plasma concentration of arginine vasopressin (AVP) is closely regulated by plasma osmolality. In this study, we used intronic in-situ hybridization to investigate the transcriptional activity of the AVP gene in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) after intraperitoneal (i.p.) injection of hypertonic saline inducing small changes in plasma osmolality in rats. After ip injection of 900 mOsm/kg saline (2% BW), plasma [Na] reached the highest level at 10 min (900 mOsm/kg, 146+/-1 mEq/l; 290 mOsm/kg, 139+/-1 mEq/l, P<0.01) and maintained that level until 30 min. The expression of AVP heteronuclear (hn) RNA in the SON and PVN increased significantly as early as 10 min and peaked 30 min after ip injection of the hypertonic saline. AVP hnRNA expression showed a significant increase even after a 2 mEq/L elevation in plasma [Na] concentration, and increased dose-dependently in response to the concentration of saline injection (290-900 mOsm/kg). These results demonstrate that, similar to AVP secretion, AVP gene transcriptional activity in the SON and PVN is closely regulated by plasma osmolality.

Probucol administered beginning 4 weeks before PTCA appears to reduce restenosis rates.

We investigated the baroregulation of arginine vasopressin (AVP) gene transcription in the supraoptic (SON) and paraventricular nuclei (PVN) in conscious rats by use of intronic in situ hybridization. Hemorrhage of 16 ml/kg body wt decreased mean arterial pressure (MAP) by 57% and increased both plasma AVP (control, 1.2 +/- 0.3 pg/ml; 16 ml/kg body wt, 38.9 +/- 3.2 pg/ml) at 10 min and AVP heteronuclear (hn)RNA levels (SON, 150%; PVN, 140% of control values) at 20 min. On the other hand, hemorrhage of 7 ml/kg body wt had no significant effect on MAP, plasma AVP, or the AVP hnRNA levels. To better understand the baroregulation, we also examined the effects of sodium nitroprusside (SNP), which induces hypotension without a change in blood volume. The subcutaneous injection of 2 mg/kg body wt SNP, which decreased the MAP by 60%, increased both plasma AVP (control, 1.6 +/- 0.4 pg/ml; 2 mg/kg body wt, 8.1 +/- 0.4 pg/ml) at 10 min and AVP hnRNA levels (SON, 150%; PVN, 140% of control values) at 30 min. The injection of 0.1 mg/kg body wt SNP, which reduced the MAP by 10%, failed to increase either the plasma AVP or AVP hnRNA levels. These results indicate that AVP gene transcription increases rapidly after both hypotensive hemorrhage and normovolemic hypotension. In addition, it is suggested that the set point for AVP synthesis in the baroregulation is similar to that for AVP release.

No abstract

GH secretagogue (GHS) is a small, synthetic compound that has the potential to stimulate GH release via its specific receptors (GHS-R). Ghrelin is a novel 28-amino acid peptide recently isolated from human and rat stomach, and it is thought to be the endogenous ligand for GHS-R. Ghrelin has a variety of physiological functions such as the stimulation of GH release or the increase of food intake by activating NPY neurons. In the present study, we investigated the effects of ghrelin on AVP release in conscious rats. Intracerebroventricular (icv) administration of ghrelin increased the plasma AVP concentration in a dose-dependent manner (1-1000 pmol/rat), and its effect was observed as late as 60 min after the administration. Icv injection of ghrelin caused no significant change in plasma osmolality, plasma volume, or arterial blood pressure. Iv administration of ghrelin (10 nmol/rat) also increased the plasma AVP concentration, which was accompanied by a significant decrease in arterial blood pressure. Pretreatment with antiserum against NPY significantly reduced the plasma AVP increase induced by icv administration of ghrelin. These results suggest that ghrelin plays a stimulatory role in AVP release, which is possibly mediated by NPY neurons.