Effect of intracisternal thyrotropin-releasing hormone on hepatic blood flow in rats

Abstract

Central neuropeptides play a role in many physiological regulatory processes through the autonomic nervous system. Thyrotropin-releasing hormone (TRH) is distributed in the central nervous system and acts as a neurotransmitter to regulate gastric functions through vagal-muscarinic pathways. The central effect of the TRH analog on hepatic blood flow was investigated in urethan-anesthetized rats. Hepatic blood flow was determined by the hydrogen gas clearance technique. Intracisternal injection of the stable TRH analog RX-77368 (5–100 ng) dose dependently increased hepatic blood flow with peak response at 15 min after the peptide was administered (net change from basal for vehicle and 5, 10, 100, and 500 ng RX-77368 was 2.0 ± 0.2, 8.9 ± 0.8, 19.4 ± 2.6, 32.6 ± 3.3, and 28.5 ± 6.8 ml ⋅ min−1 ⋅ 100 g−1, respectively), and this stimulatory effect returned to baseline at 90 min. The stimulation of hepatic blood flow by the intracisternally administered TRH analog was abolished by atropine methyl nitrate (0.15 mg/kg ip), indomethacin (5 mg/kg ip), N G-nitro-l-arginine methyl ester (10 mg/kg iv), and hepatic branch vagotomy but not by cervical spinal cord transection (C6 level). Intravenous injection of RX-77368 did not have any effect on hepatic blood flow. These results indicate that TRH acts in the central nervous system to stimulate hepatic blood flow through vagal-muscarinic and indomethacin- and nitric oxide-dependent pathways.

The effect of vagal cooling on canine hepatic glucose metabolism in the presence of hyperglycemia of peripheral origin

“…Studies of the effect of the hepatic vagal nerves on HBF are limited and the results are controversial; Bobbioni et al [58] showed that there was an increase in HBF in rats when the vagus nerve was electrically stimulated. Most other studies, however, have reported no change in HBF after vagal nerve stimulation [30,[59][60][61] or hepatic vagotomy [62]. It is unclear why there was an increase in hepatic arterial blood flow in response to vagal cooling in the present study because we did not observe such an effect in our earlier bcoolingQ studies [24,34,63].…”

Effect of central corticotropin releasing factor on hepatic circulation in rats: the role of the CRF2 receptor in the brain

“…To date, we have shown that central neuropeptide Y stimulates bile secretion through vagal nerves, and central thyrotropin releasing hormone enhances the hepatic circulation and proliferation, and also induces hepatic cytoprotection. [30][31][32][33][34] It is interesting to note that several neuropeptides act in the central nervous system and play significant roles in the physiological and pathophysiological regulation of hepatic functions involving different autonomic nervous pathways.…”

Involvement of endogenous CRF in carbon tetrachloride-induced acute liver injury in rats

“…Although a little is revealed about central neuropeptides as a neurotransmitter inducing modulation of hepatic function (5,31,(33)(34)(35)(36)(37), nothing is known about the role of endogenous neuropeptides in hepatic physiological and pathophysiological regulations. In the present study, we found that central administration of CRF receptor antagonist induces a partial hepatic cytoprotection against experimental liver injury through sympathetic-noradrenergic pathways and speculated that endogenous CRF acts in the brain as neurotransmitter to induce central modulation of experimental acute liver injury.…”