The effects of pineal gland on kidney-adrenal axis have been studied in male rats. Rats were pinealectomized and exposed to a photoperiod of 12 h light: 12 h dark. Plasma renin activity (PRA), corticosterone and corticotropin (ACTH) levels were measured at 10, 20 and 35 days postpinealectomy. Pinealectomy increased corticosterone and ACTH levels and decreased PRA in all age groups. A significant negative correlation was found between corticosterone and PRA, which suggest that changes in PRA were due to changes in circulating corticosterone, via feedback mechanism on renin secretion. On the other hand, melatonin administration prevents these effects of pinealectomy. It is suggested that the lack of this pineal indol is responsible for the pinealectomy-induced alterations in male rats.
In the isolated and perfused kidney of the rat, the stimulant effect of dopamine on renin release is blocked by propranolol and not by haloperidol. This suggests that the release of renin induced by dopamine is due to the activation of beta-receptors.
The endocrine (plasma renin activity, insulin and ADH) and hemodynamic responses (heart rate and mean arterial pressure) to isoprenaline infusion were examined in conscious deoxycorticosterone-salt hypertensive rats (DS) and compared with uninephrectomized-salt control rats (US). A dose-related rise in plasma renin activity and plasma insulin values was found in US rats, while no change in either parameter was observed in DS rats after 30 min of isoprenaline infusion. ADH was not increased in US rats at any dose of isoprenaline infusion. However, in DS rats the largest dose (450 ng/kg/min) produced a significant rise. Isoprenaline infusion increased the heart rate in both groups, but the increases in the DS group were significantly lower than in the US group for the 200-ng/kg/ min dose (p < 0.01). The drop in mean arterial pressure was found to be more pronounced in DS rats than in US rats at 50, 100 and 200-ng/kg/min isoprenaline doses. Recovery of the mean arterial pressure to basal levels was also found in US rats with the various doses of isoprenaline administered. However, in DS rats the different doses of isoprenaline produced a progressive drop in mean arterial pressure with no recovery at the end of 30 min of isoprenaline infusion. The present results provide no evidence of subsensitivity to isoprenaline in the resistance vessels of conscious DS rats and suggest that the greater hypotensive response observed in these rats may be due to the inability of the renin-angiotensin system to adequately compensate the vasodilation produced by isoprenaline.
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