The present experiments were designed to study effects of neural control mechanisms on renal sympathetic nerve activity during acute portal vein distension in anesthetized dogs. Following the inflation of a balloon placed into the main portal vein of animals with the neuraxis intact (intact group), portal vein pressure at a site of the splanchnic regions increased significantly. Mean blood pressure (MBP) fell significantly and then renal vascular resistance (RVR) increased significantly in parallel with changes in portal venous pressure. In animals with sinoaortic denervation (SAD group), changes in portal venous pressure during the inflation of a balloon did not differ from the intact group. However, decreases in MBP in the SAD group were greater than that in the intact group, and sinoaortic denervation did not alter increases in RVR. In animals with both sinoaortic denervation and cervical vagotomy (vagotomy group), portal vein distension produced more profound hypotension, and significant increases in RVR occurred. This increase in RVR, however, was abolished by renal nerve denervation. The results of the present study indicate that increases in RVR during the portal vein distension, which is associated with systemic hypotension, may be mediated by an activation of efferent sympathetic renal nerves and modified by at least two neural reflex mechanisms such as carotid sinus baroreceptors and cardiopulmonary baroreceptors. In addition, local reflex systems such as stretch receptors in the venous wall of the portal vein may be involved in excitatory response to renal sympathetic nerve, leading to renal vasoconstriction, during the portal vein distension.

In anesthetized dogs, intravenous injections of 30 µg/kg of leucine-and methionine-enkephalin (L-and M-enk respectively) produced a significant reduction of mean blood pressure (MBP) and heart rate (HR). The peak decreases in MBP and HR occurred within 1 min after injection and recoveries to pre-injection levels within 3 min. The depressor responses to both L-enk and M-enk were abolished by intracisternal pretreatment with yohimbine (0.5 mg/kg) but not with prazosin (0.1 mg/kg). Pretreatment with either drug did not alter the bradycardia. All cardiovascular effects of both L-enk and M-enk were prevented by intravenous pretreatment with naloxone (2 mg/kg). These results suggest that central cr2-adrenoceptors may participate in the central actions of enkephalins on blood pressure regulation. HR responses to enkephalins may be elicited by a different mechanism.

Summary Intravenous administration of leucine-enkephalin (30 pg/kg) caused significant decreases in mean blood pressure, cardiac output, and left ventricular dP/dt in intact dogs. However, cardiovascular effects of leucine-enkephalin (30-120 µg/kg) did not occur in the heartlung preparation uninfluenced by extracardiopulmonary factors. These results provide no evidence of a direct cardiac action of leucine-enkephalin.

Studies were conducted to determine the cardiovascular responses to leucine-enkephalin (L-enk) in three different species of animals; rabbit, dog and monkey. All animals were anesthetized with pentobarbital sodium after sedation with ketamine. Mean blood pressure (MBP) and heart rate (HR) were simultaneously monitored. The pressor and HR responses to bilateral carotid occlusion (BCO) were determined before injection of L-enk. Increased MBP and HR due to BCO in monkey were significantly greater than in the other two animal groups. Following i.v. injection of L-enk (5-30 micrograms/kg), a significant fall in MBP occurred in all groups in a dose-dependent manner; however, the time course of changes in MBP in rabbits was significantly shorter than that in the other animal groups. Significant decreases in HR after the injection of L-enk occurred in rabbits and dogs, whereas increases in HR occurred in monkeys. These results show that some cardiovascular responses to L-enk may be species dependent. These different cardiovascular responses to L-enk may be at least partly related to species differences in baroreceptor reflex sensitivity.

The purpose of this experiment was to evaluate the effects of the arterial baroreceptor buffering capacity on cardiovascular parameters during hypotension caused by E. coli endotoxin in anesthetized dogs. In the control group, mean blood pressure and cardiac output fell significantly from 104 + 10 mmHg to 63±7 mmHg and 1.17 + 0.16 l/min to 0.67 + 0.08 l/min, respectively, 60 min after intravenous injection of endotoxin (1 mg/kg). Central venous pressure also decreased significantly after the injection. Total peripheral resistance and portal vein pressure increased significantly immediately after the injection, and then returned toward baseline levels. The time course of changes in these five cardiovascular parameters after the injection of endotoxin was the same as that in dogs with sino-aortic denervation. Following the injection of endotoxin, stroke volume and left ventricular dP/dt fell significantly in both control and denervated dogs; however, these decreases in the denervated group were significantly greater. These findings suggest that the arterial baroreceptors may play a role in the poor compensatory response to hypotension induced by endotoxin, at least, in the cases of mean blood pressure, cardiac output, total peripheral resistance, central venous pressure, and portal vein pressure.