[Effect of endothelin-1 injected into rostral ventrolateral medulla on cardiovascular responses in cats].

AIM: To study the effect of endothelin-1 (ET-1) in the rostral ventrolateral medulla (rVLM) on cardiovascular responses in cats. METHODS: The stereotatic technique and microinjection method were used. RESULTS: ET-1 (4 mumol.L-1 0.5 microL) microinjected into rVLM induced mean arterial pressure (MAP) increasing (3.7 +/- 1.3) kPa, heart rate (HR) accelerating (29 +/- 7) beats.min-1, and renal nerve activity (RNA) intensifying 45% +/- 10%. The effects were dose-dependent. Before and after bilateral vagotomy, there was no significant difference in the reaction of MAP, HR, and RNA. After intravenous injection with phentolamine (5 mg.kg-1, alpha-blocker), ET-1 did not induce significant change of MAP. ET-1 raised the content of peripheral plasma argipressin (Arg) from (12.4 +/- 6.5) to (70.3 +/- 24.2) ng.L-1 with radioimmunoassay, and showed a correlation with MAP changes. ET-1 induced heart rhythm disorder (HRhD) in acute myocardiac ischemia, the occur time of HRhD was (4.8 +/- 2.9) min, and the score was 4.4 +/- 1.6, and it was significantly different from control. CONCLUSION: ET-1 microinjected into rVLM could involve with control regulation of cardiovascular and sympathetic nerve activity.

[Influence of endothelin-1 on ventricular fibrillation threshold in acute myocardial ischemic rats].

The influence of endothelin-1 on ventricular fibrillation threshold was studied in acute myocardial ischemic rats. Endothelin-1 (1.5-3.0 micrograms.kg-1 i.v.) given 5 min before ischemia reduced the ventricular fibrillation threshold in a dose- and time-dependent manner. Its effect lasted at least 60 min. A marked increase of spontaneous ventricular tachycardia and myocardial infarct size was seen and the arterial blood pressure was at a higher level (18.5-20.1/14.4-15.8 kPa) after 3.0 micrograms.kg-1. Diltiazem prevented partially from reduction of ventricular fibrillation threshold, eliminated completely the vasopressor response and limited the extension of myocardial necrosis induced by endothelin-1.

[Changes in cardiac contractility induced by stimulation of hypothalamic ventromedial nucleus].

Experiments were performed on anesthetized cats to observe the effect of electrical stimulation of the hypothalamic ventromedial nucleus (VMH) on cardiac contractility as judged by the change in LVSP, dp/dtmax, Vmax, P-dp/dt, P-lndp/dt. Electrical stimulation of VMH induced an augment response in cardiac force, while stimulation of an area between VMH and the third ventricle led only to a decrease in cardiac contractile force. All these changes were not accompanied by significant changes in heart rate and unaffected by bilateral vagotomy. The present experiment indicates that the inotropic and chronotropic regulation centers of cardiac function exist in different hypothalamic areas.

[Inhibition of renal sympathetic efferent activities induced by stimulation of the paraventricular nucleus of the hypothalamus(PVH) in rabbits].

Experiments were performed on rabbits anesthetized with chloralose-urethane mixture, paralyzed with gallamine triethiodide, and ventilated artificially. Bilateral vagi, aortic and carotid sinus nerves were severed. Renal sympathetic efferent discharge (RSED) and its histogram were recorded, while the blood pressure (BP) of the femoral artery was monitored. When PVH was strongly stimulated, a transient increase of RSED was observed, which was followed by an inhibition of RSED. The inhibition of RSED was divided into two phases: the initial inhibitory phase without change in BP and the late inhibitory phase with an increase of BP. It was found that both the duration of total inhibition and the late, but not initial, inhibitory phase were positively correlated with the alterations of BP. When PVH was weakly stimulated, no change in BP was observed, but the inhibition of RSED still appeared. The inhibition duration was shortened remarkably following cutting of baroreceptor nerves. In some experiments, the RSED inhibition was not accompanied by a definite excitatory response. The present results indicate that 1) an inhibitory mechanism of PVH-renal sympathetic efferent system is present in the central nervous system; 2) the initial inhibitory phase of RSED originates from central mechanisms, while the late inhibitory phase is associated with the baroreceptor reflex and a direct action of the central nervous system; 3) the inhibition of RSED seems not to be a post-excitation depression, but an active inhibition exerted by the PVH on the spinal sympathetic preganglionic neurons.