11Beta-hydroxysteroid dehydrogenase bioactivity is increased in the colon but not kidneys of rats given supplementary thyroxine.

The aim of this study was to investigate the effect of altered thyroid status on 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD type 1) and type 2 (11beta-HSD type 2) bioactivity in rat kidney and colon. Male Sprague-Dawley rats (250 g) were treated with either L-thyroxine (T4) or propylthiouracil (PTU) for 4 weeks. Blood were then analysed for serum thyroxine, sodium (Na+) and potassium (K+). The kidneys and colon were assayed for 11beta-HSD type 1 and 11beta-HSD type 2 bioactivity. In T4 treated rats the serum thyroxine was significantly elevated (p<0.05) whilst PTU decreased serum thyroxine significantly (p<0.001) compared to controls. Serum Na+ and K+ were within normal limits. There were no significant changes in 11beta-HSD type 1 bioactivity in both treatment groups compared to controls. However, the 11beta-HSD type 2 bioactivity in rats given thyroxine was significantly higher in the colon (p<0.003) compared to controls. We conclude that altered thyroid status had no effect on 11beta-HSD type 1 bioactivity but 11beta-HSD type 2 bioactivity was elevated in the colon of rats given supplementary thyroxine.

Effects of glycyrrhizic acid and steroid treatment on corticotropin releasing factor and beta-endorphin containing neurons of the hypothalamus of the rat.

Corticotrophin releasing factor (CRF) and beta-endorphin (beta EP) containing neurons are shown to be present in the hypothalamus and both neurons are found at the paraventricular nucleus (PVN). Steroid hormones have been found to alter the plasma level of these neurotransmitters. Glycyrrhizic acid (GCA) is the active component of liquorice. GCA inhibits the enzyme 11 beta-hydroxysteroid dehydrogenase (11HSD) which is needed for the inactivation of the steroid pathway, so therefore would cause changes to these neurons. The aim of this study was to investigate the effects of GCA as well as deoxycorticosterone (DOC) and dexamethasone (DM) on the modulation of CRF and beta EP containing neuron at the PVN of the hypothalamus. Rats were given either DM, DOC or GCA and adrenalectomized (ADX) and given either DM or DOC. At the end of treatment rats were transfused transcardially before sacrifice and the brain were dissected for immunohistochemical analysis. We found that immunostaining of the CRF containing neurons demonstrate a reduction in the number of positive neurons in DM treated rats. DOC and GCA treated rats showed the same result as in DM rats but the reduction is less. ADX, DM, DOC and GCA treated rats did not show any changes in the number of beta EP containing neurons but naloxone increased the number of beta EP containing neurons markedly. In conclusion, GCA and DOC have similar effects on CRF and beta EP containing neurons at the PVN.

Effects of glycyrrhizic acid on right atrial pressure and pulmonary vasculature in rats.

Glycyrrhizic acid (GCA) the active component of liquorice acts by inhibiting 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) which catalyses the reversible conversion of cortisol to cortisone. The aim of this study was to examine the effect of GCA on pulmonary arterial pressure. Male Sprague-Dawley rats (200g) received drinking water containing 0.1 mg/ml and 1.0 mg/ml GCA for 12 weeks. Tail blood pressure (BP) was recorded every three weeks and serum Na+ and K+ were measured at the beginning and the end of the experiment. Right atrial pressure (RAP) were measured at the end of 12 weeks just before the animals were sacrificed. Lung tissues were taken for histological examination using the elastic-van Gieson (EVG) staining method. There was a significant increase in tail BP in GCA treated rats compared to controls, for both dosages used. This was associated with an increase in serum Na+ and a decrease in K+ level. The mean RAP increased significantly from 2.69 +/- 0.23 mmHg to 4.47 +/- 0.32 mmHg (P < 0.001) in 0.1 mg/ml GCA treated rats and 6.86 +/- 0.54 mmHg (P < 0.0001) in rats receiving 1.0 mg/ml GCA in their drinking water. Histological examination showed increased thickness of pulmonary arterial wall (P < 0.0001). In conclusion GCA caused an increase in right atrial pressure as well as thickening of the pulmonary vessels suggesting pulmonary hypertension.

Mineralocorticoid and glycyrrhizic acid block stress induced hypotension in rats.

1. The aim of this study was to investigate the effect of repeated exposure to stress on tail blood pressure (TBP) of normal as well as GCA (glycyrrhizic acid) and steroid treated rats. Male Sprague-Dawley rats (250 g) were exposed to ether vapour to achieve light anaesthesia prior to TBP recording. Rats were injected with either normal saline or naloxone prior to exposure to stress. Tail blood pressure was recorded daily for 2 weeks. 2. We found that ether stress caused a transient drop in TBP in control as well as in dexamethasone (DEX) treated rats. The stress-induced fall in blood pressure was reduced by naloxone in control rats but not in DEX treated rats. However the transient drop in TBP following stress was not seen in either GCA or deoxycorticosterone (DOC) treated rats. 3. We conclude that first, the reduction in TBP was due to the release of endogenous opioids caused by stress. Second, DOC may block the release of such endogenous opioids, preventing the drop in TBP in response to stress, while DEX did not. Third, GCA caused a similar mineralocorticoid effect on reversing stress induced hypotension.