Nitric oxide is involved in phosphorus deficiency-induced cluster-root development and citrate exudation in white lupin.

*White lupin (Lupinus albus) forms specialized cluster roots characterized by exudation of organic anions under phosphorus (P) deficiency. Here, the role of nitric oxide (NO) in P deficiency-induced cluster-root formation and citrate exudation was evaluated. *White lupin plants were treated with the NO donor sodium nitroprusside (SNP) and scavenger or inhibitor of NO synthase under conditions of P deficiency (0 muM) or P sufficiency (50 muM). *Phosphorus deficiency enhanced NO production in primary and lateral root tips, with a greater increase in cluster roots than in noncluster roots. NO concentrations decreased with cluster root development from the pre-emergent stage, through the juvenile stage, to the mature stage. The P deficiency-induced increase in NO production was inhibited by antagonists of NO synthase and xanthine oxidoreductase, suggesting the involvement of these enzymes in NO production. SNP markedly increased the number of cluster roots. Citrate exudation from different root segments in P-deficient roots was positively correlated with endogenous root NO concentrations. *These findings demonstrate differential patterns of NO production in white lupin, depending on root zone, developmental stage and P nutritional status. NO appears to play a regulatory role in the formation of cluster roots and citrate exudation in white lupin under conditions of P deficiency.

[Changes in monoamine neurotransmitters in CSF during inhibition of defensive hypertensive reactions by inputs of deep peroneal nerve].

Our previous work has indicated that excitation of hypothalamic defence area (HDA) could lead to an increase in the release of central monoamine neurotransmitters, pressor and other defence responses. The present experiments showed that stimulation of deep peroneal nerve with a current of low frequency and low intensity could inhibit the pressor, abolish the increase of noradrenaline and its metabolite MHPG and attenuate that of 5-HIAA (a 5-HT metabolite), dopamine and its metabolites DOPAC and HVA in CSF. The data suggest that inputs of deep peroneal nerve may inhibit the increased release of central monoamine neurotransmitters, and then defence reactions; and inhibition of NA release in some nuclei of the brain is an important mechanism of inhibition of defence pressor by inputs of deep peroneal nerve.

Roles of opioid peptides of PAG in analogous electro-acupuncture inhibition of experimental arrhythmia: analyzed by specific antisera microinjection.

Using specific antisera microinjected into periaqueductal grey (PAG), we further studied the mechanism of the analogous electroacupuncture, deep peroneal nerve stimulation (DPNS), inhibition on the experimental arrhythmia, hypothalamic stimulation-induced ventricular extrasystoles (HVE). Neither normal serum nor anti-leu-enkephalin antiserum interfered with DPNS inhibition; anti-dynorphin A (1-8) tended to attenuate the inhibition; and anti-beta-endorphin antiserum blocked it. The results provided further evidence for the hypothesis that beta-endorphin in PAG plays an important role in the neural circuit of DPNS inhibition on HVE.

Inhibitory effect of analogous electro-acupuncture on experimental arrhythmia.

Rabbits were used to study the inhibitory effect of analogous electro-acupuncture on the experimental arrhythmias, i.e. hypothalamic stimulation-induced ventricular extrasystole (HVE). The result revealed that HVE, which was due to an increased cardiac sympathetic activity, could be inhibited by deep peroneal nerve stimulation with an electrical current of low frequency and low intensity. Such effect is related to endogenous opioid peptides and serotonin in the arcuatus area, the periaqueductal gray and and the medial medulla. The acupuncture correction of arrhythmias may have the same mechanism.

The effect of acupuncture on blood pressure: the interrelation of sympathetic activity and endogenous opioid peptides.

Experimental hypertension was produced by intravenous infusion of norepinephrine in 13 conscious dogs. Electroacupuncture at the dogs' "Tsu San-Li" (St. 36) points showed a significant decrease in blood pressure, while the heart rate was not affected. The depressor effect was naloxone (0.2 mg/kg iv) reversible, and accompanied by an increased blood flow at the mesenteric artery, so it is suggested that the depressor effect was due to inhibition of the sympathetic vasoconstrictor tone. This inhibition was mediated by endogenous opioid peptides released by acupuncture. The location of this mediation was further analyzed. The central mechanism was evidenced by the ineffectiveness of acupuncture in reducing blood pressure in anesthetized dogs. On the other hand, the demonstration of opiate receptors in the blood vessels by radio-receptor assay provided evidence of peripheral mediation of blood pressure by opioids. The blood vessel might be a target organ for the plasma opioids, which can also be increased by acupuncture.