KISS1 and KISS1R expression in the human and rat carotid body and superior cervical ganglion

KISS1 and its receptor, KISS1R, have both been found to be expressed in central nervous system, but few data are present in the literature about their distribution in peripheral nervous structures. Thus, the aim of the present study was to investigate, through immunohistochemistry, the expression and distribution of KISS1 and KISS1R in the rat and human carotid bodies and superior cervical ganglia, also with particular reference to the different cellular populations. Materials consisted of carotid bodies and superior cervical ganglia were obtained at autopsy from 10 adult subjects and sampled from 10 adult Sprague-Dawley rats. Immunohistochemistry revealed diffuse expression of KISS1 and KISS1R in type I cells of both human and rat carotid bodies, whereas type II cells were negative. In both human and rat superior cervical ganglia positive anti-KISS1 and -KISS1R immunostainings were also selectively found in ganglion cells, satellite cells being negative. Endothelial cells also showed moderate immunostaining for both KISS1 and KISS1R. The expression of both kisspeptins and kisspeptin receptors in glomic type I cells and sympathetic ganglion cells supports a modulatory role of KISS1 on peripheral chemoreception and sympathetic function. Moreover, local changes in blood flow have been considered to be involved in carotid body chemoreceptor discharge and kisspeptins and kisspeptin receptors have also been found in the endothelial cells. As a consequence, a possible role of kisspeptins in the regulation of carotid body blood flow and, indirectly, in chemoreceptor discharge may also be hypothesized

Involvement of neuropeptides in the regulation of growth, structure and function of the adrenal cortex

Current data on the influence of neuropeptides on the growth, structure and function of cells comprising the hypothalamo-pituitaq-adrenal axis were presented and discussed. The action of vasopressin, oxytocin, neurotensin, bombesin, neuropeptide Y, substance P and VTP have been evaluated. The hypothesis has been introduced that in vivo effect of some neuropeptides on the structure and function of the adrenal cortex is mediated by vasopressin

Neuromedins and their involvement in the regulation of growth, structure and function of the adrenal cortex

Current data on the synthesis and the mechanism of action of neuromedins on adrenal cortex are presented. The localization of these biologicallyactive peptides in all components of the hypothalamopituitary- adrenal axis as well as their action on the adrenal cortex both in vivo and in vitro suggest their involvement in the regulation of growth, structure and function of the adrenal cortex. Neuromedins may exert both direct and indirect effect on the adrenal cortex. Direct effect is proven by the stimulation of glucocorticoid synthesis by adrenocortical cells in culture (NMK, NML) while indirect effects may be mediated by ACTH, vasopressin (aldosterone secretagogue effect) and angiotensin (prompt proliferative response) or by substances of medullary origin. The last mechanism of action is well documented for NMU

Compensatory adrenal growth in aldosterone-treated male and female hamsters

The aim of the study was to investigate the compensatory adrenal growth in aldosterone-treated male and female hamsters. Hemiadrenalectomised and sham-operated animals were treated for 5 days with a daily d-aldosterone dose of 25 pglanimal. In both male and female aldosterone-treated hamsters monoadrenalectomy did not change the relative adrenal weight if compared with sham-operated groups. The fasciculata zonae of monoadrenalectomised aldosterone- treated males was larger and contained more parenchyma1 cells than in appropriate control group. There was no difference in the volume of adrenocortical zones, average cell volume and in cell number between sham-operated and unilaterally adrenalectomised females. In vitro 3H-thymidine incorporation per adrenal was markedly higher in monoadrenalectomised than in sham-operated aldosterone-treated males while the opposite was true for female hamsters. Thus, the action of aldosterone on CAG in the hamster seems to depend on sex, with no effect in males and inhibitory action in females

Effects of bombesin and neuromedin-B on the proliferative activity of the rat adrenal cortex

Bombesin (BM) and neuromedin-B (NMB) exert similar biological effects, acting via two functionally distinct BM-receptor subtypes. The present study aimed to investigate whether BM and NMB stimulate the proliferation of rat adrenocortical cells and to compare their mode of action. Adult female rats were treated with a single subcutaneous dose of 3 pg BM or NMB. Adrenocortical proliferative activity was assessed by the metaphase-arrest technique. BM administration resulted in a marked increase in the number of metaphases in zona glomerulosa (ZG) and zona fasciculata (ZF), and in the entire cortex. This increase appeared 24 h after injection in the ZG, and after 48 h in the ZF. NMB adrninistration, on the other hand, caused a prompt increase in the number of metaphases in the ZG and entire cortex at 12 h, followed by a subsequent drop below the control leve1 at 24 and 48 h of experiment. These findings indicate that BM and NMB enhance the proliferative activity of rat adrenocortical cells acting via different receptors or different mediators

Ovariectomy-induced changes in the adrenal cortex of spontaneously hypertensive rats

Many lines of evidence indicate that adrenocortical steroid hormones are involved in the development and maintenance of hypertension in spontaneously hypertensive rats (SHR). Twenty-eight days after ovariectomy a notable decrease in the sistolic blood pressure (BP) was found in SHR, along with a marked atrophy of their adrenal cortices. The hypothesis is advanced that the ovariectomy-induced lowering in BP in SHR may be, at least partly, mediated by the suppression of the adrenal secretory activity, due to the lack of circulating estrogens, which are well known to stimulate hypophyseal ACTH release

Different effects of neurotensin and neuromedin-N on the proliferative activity of rat adrenal cortex

Evidence indicates that neurotensin (NT) and neuromedin-N (NMN) exerts an adrenocorticotropic effect in the rat. The present study aimed to investigate whether these neuropeptides are able to stimulate the proliferation of rat adrenocortical cells in vivo and to compare their mode of action. Adrenocortical proliferative activity was assessed by the metaphasearrest technique and metaphases were counted per medulla-containing adrenal section. A bolus administration of NT (3 pglrat) resulted in a significant increase in the number of metaphases in both zona fasciculata and the entire cortex, an effect observed 48 h after the in.jection. The administration of NMN (3 yglrat) induced a notable rise in the number of metaphases in the zona fasciculata and the entire cortex within 12 h, followed by a subsequent drop after 24 h and a return to normal values at 48 h. These findings indicate that NT and NMN enhance rat adrenal growth in vivo acting via different mediators

Neuropeptide Y-related peptides and hypothalamo-pituitary-adrenal axis function

Current data on the localization of neuropeptide Y-related peptides in the hypothalamo-pituitaryadrenal gland (HPA) axis as well as the effects of these peptides on the function of cells comprising HPA axis are presented and discussed. The action of neuropeptide Y. peptide YY, and pancreatic polypeptide on HPA axis are evaluated. Moreover, we report the presence of pancreatic polypeptide immunoreactivity in subset of chromaffin cells in the medulla of rat adrenal gland

Proliferation and distribution of adrenocortical cells in the gland of ACTH- or dexamethasone-treated rats

The effects of prolonged (7-day) ACTH and dexamethasone administrations on rat adrenocorticalcell turnover have been investigated by combined stereological and metaphase-arrest techniques. ACTH was found to increase the number of parenchymal cells in each adrenal zone; however, ACTH altered the cell distribution in the cortex, lowering their percentage in the zona glomerulosa (ZG) and zona fasciculata (ZF) and enhancing it in the zona reticularis (ZR). The cell birth-rate was markedly raised by ACTH exclusively in ZG and ZF. Dexamethasone notably decreased the number of ZF and ZR cells, without altering that of ZG cells. Moreover. dexamethasone increased the percentage of parenchymal cells in ZG and ZF, and lowered it in ZR. In the adrenal cortices of dexamethasoneadministered animals, metaphases were virtually absent. These data indicate that ACTH increases the cell birthrate in ZG and possibly ZF, and enhances the centripetal migration of newly-formed cells and their accumulation in ZR. Dexamethasone inhibits both proliferation of adrenocortical cells in the outer cortical layers and their centripetal migration into ZR. Moreover, it appears to cause parenchymal-cell loss in the inner adrenocortical layers