Effect of testosterone on the pressor response to common carotid occlusion in gonadectomized conscious male rats with lesion of the median eminence

The influence of testosterone on the development of the pressor response to common carotid occlusion was investigated in control and median eminence-lesioned male rats. In control rats (N-9), gonadectomy performed 21 days before the experiments reduced by 22% (from 51 ñ 2 to 40 ñ 2 mmHg) and treatment with testosterone (330 µg for 4 days before the measurements) increased the initial peak pressor response (from 51 ñ 2 to 57 ñ 2 mmHg) which depends on carotid innervation. The maintained response which is of central origin (propably ischemic was less affected. In non gonadectomized rats (N=6), lesions of the median eminence (6 days) decreased the initial peak by 19% (from 52 ñ 2 to 42 ñ 3 mmHg) and the maintained response by 56% (from 32 ñ 2 to 14 ñ 1 mmHg). Sham-operated rats served as controls. In gonadectomized animals (N=6) the lesion reduced only the maintained response (from 23 ñ 2 to 11 ñ 1 mmHg). Testosterone supplementation restored the maintained response but did not alter the initial peak. These results indicate that the pressor response to common carotid occlusion in male rats is modulated by testosterone and that the depresiin in the maintained response caused by median eminence lesion can be reversed by steroid supplentation

The effect of tubero-infundibular dopaminergic neurons on prolactin and alpha-melanocyte stimulating hormone release

The effect of tubero-infundibular dopaminergic neurons (TIDA) on the release of prolactin (PRL) and alpha-melanocyte stimulating hormone (alpha-MSH) was studied in median eminence-lesioned (MEL) male rats (N = 6-28). Plasma PRL and alpha-MSH levels were significantly elevated 2(86.1 ñ 19.8 and 505.1 ñ 19.1 ng/ml), 4(278.7 ñ 15.5 and 487.4 ñ 125.1 ng/ml), 7 (116.2 ñ 16.2 and 495.8 ñ 62.6 ng/ml) and 14 (247.3 ñ 26.1 and 448.4 ñ 63.8 ng/ml) days after MEL when compared to sham-operated control animals (55.5 ñ 13.4 and 56.2 ñ 6.1 ng/ml, repectively). MEL altered plasma PRL and alpha-MSH levels in a diffential manner, with 1.5-to5.0-fold increase in PRL and an 8.0- to 9.0-fold increase in alpha-MSH. The increase of alpha-MSH levels occured abruptly and remained constant from days 2 to 14. These observations indicate that TIDA plays an important role in the pituitary release of PRL and alpha-MSH and provide evidence that the release of the two hormones occurs in a differential manner

Blockde of volume expansion-induced release of atrial natriuretic peptide by median eminence lesions in the rat

Since stimulation of the anteroventral third ventricle region (AV3V) induced a rapid elevation of plasma atrial natriuretic peptide (ANP) associated with rapid changes in brain and pituitary content of ANP, whereas lesions of the AV3V were followed by marked by a merked decline in plasma, brain and pituitary content of the peptide, we hypothesized that release of ANP from the median eminence (ME) might be an important pathway to control plasma ANP. Consequently, electrolytic lesions were placed in the ME and the response to hypertonic-expansion was determined in conscieous rats. In sham-operated controls volume expansion produced a 3.5-fold increase in plasma ANP concentrations within 5 min. Values rapidly declined to enar initial levels at 15 and 30 min. Median eminence lesions almost completely blocked the response to volume expansion at 24 and 120 h post-lesion and initial anp concentrations were lower than those of the sham-operated controls. The results indicate that increased release of ANP from the neurohypophysis may play an important role in the increased plasma ANP concentrations whic follow volume expansion