In urethane-anesthetized rats, intrathecal administration of endothelin-1 (ET-1), endothelin-3 (ET-3) (3-100 pmol/rat) or the C-terminal hexapeptide ET(16-21) (10-100 nmol/rat) dose-dependently increased mean blood pressure (MBP) and suppressed the supraspinal micturition reflex (SMR). ET(16-21), at 100 nmo-, produced a pressor response comparable to that induced by ET-1 at 100 pmol. Guanethidine and hexamethonium pretreatment significantly reduced the increase of MBP induced by ET-1 but was inactive in antagonizing inhibition of SMR. Neither naloxone nor adrenalectomy were effective in preventing the responses to ET-1. The high degree of lethality (60-100%), observed with ET-1 (10-100 pmol), was not reduced by guanethidine, naloxone, adrenalectomy or by hexamethonium. ET-3, at 100 pmol or 1 nmol, induced death in about 50% of cases. The symptoms before death were reduction of the respiratory rate followed by respiratory arrest. These findings indicate that the pressor response to intrathecally-administered endothelins involves activation of sympathetic preganglionic elements; induction of secretion of catecholamines from adrenal glands was excluded. Lethality and inhibition of SMR does not involve opioids, sympathetic activation or release of catecholamines from the adrenal glands.
Effect of intrathecal administration of ET-1, ET-3 and ET(16-21) on blood pressure and micturition reflex in anesthetized rats / Sandro Giuliani; Alessandro Lecci; Carlon A. Maggi; Paolo Rovero; Antonio Giachetti. - In: NEUROCHEMISTRY INTERNATIONAL. - ISSN 0197-0186. - STAMPA. - 18 (4):(1991), pp. 565-569. [10.1016/0197-0186(91)90157-9]
Effect of intrathecal administration of ET-1, ET-3 and ET(16-21) on blood pressure and micturition reflex in anesthetized rats
ROVERO, PAOLO;
1991
Abstract
In urethane-anesthetized rats, intrathecal administration of endothelin-1 (ET-1), endothelin-3 (ET-3) (3-100 pmol/rat) or the C-terminal hexapeptide ET(16-21) (10-100 nmol/rat) dose-dependently increased mean blood pressure (MBP) and suppressed the supraspinal micturition reflex (SMR). ET(16-21), at 100 nmo-, produced a pressor response comparable to that induced by ET-1 at 100 pmol. Guanethidine and hexamethonium pretreatment significantly reduced the increase of MBP induced by ET-1 but was inactive in antagonizing inhibition of SMR. Neither naloxone nor adrenalectomy were effective in preventing the responses to ET-1. The high degree of lethality (60-100%), observed with ET-1 (10-100 pmol), was not reduced by guanethidine, naloxone, adrenalectomy or by hexamethonium. ET-3, at 100 pmol or 1 nmol, induced death in about 50% of cases. The symptoms before death were reduction of the respiratory rate followed by respiratory arrest. These findings indicate that the pressor response to intrathecally-administered endothelins involves activation of sympathetic preganglionic elements; induction of secretion of catecholamines from adrenal glands was excluded. Lethality and inhibition of SMR does not involve opioids, sympathetic activation or release of catecholamines from the adrenal glands.I documenti in FLORE sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.