PubMed · 2679821
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Y Nomura, K Kitamura. 1989. [Recent information concerning the inner ear structure].. https://pubmed.ncbi.nlm.nih.gov/2679821/
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Central command, which is a neural drive originating in the brain during exercise, regulates the sympathetic nervous system and evokes cardiovascular responses to exercise. To examine the role of the central command on sympathetic regulation of renal circulation, we compared responses in renal cortical blood flow and vascular conductance to electrical stimulation of mesencephalic locomotor region (MLR) for 30 s in decerebrate and paralyzed rats between renal nerves that were intact (n=8) and denervated (n=8). In rats with renal nerves intact, stimulation of the MLR at 40 microA current intensity significantly (p<0.05) decreased renal cortical blood flow (-17+/-5%, means+/-S.E.M.) and vascular conductance (-43+/-4%) and the decrease in renal vascular conductance was dependent on current intensity (between 20 and 60 microA). In renal denervated rats, in contrast, there were no significant changes in either renal cortical blood flow or vascular conductance during stimulation at all current intensities. In a subset of rats (n=8), the response in renal sympathetic nerve activity to 30 s stimulation of the MLR was investigated. Stimulation of the MLR significantly increased renal sympathetic nerve activity (+57+/-14% at 40 microA) and the response was dependent on current intensity (between 20 and 60 microA). These data provide evidence that central command induces renal vasoconstriction by increasing sympathetic activity, depending on central command intensity.
This study was designed to clarify the alpha(1)-adrenoceptor subtypes mediating the vasoconstrictor response to tyramine in isolated and perfused canine splenic artery. It was shown that tyramine potentiated the nerve stimulation-induced second peaked vasoconstriction that was readily suppressed by prazosin treatment. A bolus injection of tyramine (0.01-0.3 micromol) caused a vasoconstriction in a dose-related manner. The tyramine-induced vasoconstriction was inhibited by WB 4101 (10 and 100 nM), an alpha(1A)-and alpha(1D)-adrenoceptor antagonist, in a concentration-related manner. Neither BMY 7378 (100 nM), a selective alpha(1D)-adrenoceptor antagonist, nor chloroethylclonidine (60 microM), an alpha(1B)- and alpha(1D)-adrenoceptor antagonist, affected the tyramine-induced response. The results indicate that the noradrenaline released by tyramine may diffuse to the extrajunctional cleft, and thus it activates the extrajunctional alpha(1A)-adrenoceptors, because nerve stimulation-evoked second peaked vasoconstrictions were markedly inhibited by chloroethylclonidine but not by WB 4101.
Group III metabotropic glutamate receptors (mGluRs; mGluR4, 6, 7, and 8) couple to the Galpha(i/o)-containing G protein heterotrimers and act as autoreceptors to regulate glutamate release, probably by inhibiting voltage-gated Ca(2+) channels. Although most mGluRs have been functionally expressed in a variety of systems, few studies have demonstrated robust coupling of mGluR8 to downstream effectors. We therefore tested whether activation of mGluR8 inhibited Ca(2+) channels. Both L-glutamate (L-Glu) and l-2-amino-4-phosphonobutyric acid (L-AP4), a selective agonist for group III mGluRs, inhibited N-type Ca(2+) current in rat superior cervical ganglion neurons previously injected with a cDNA encoding mGluR8a/b. L-AP4 was approximately 100-fold more potent (IC(50) = 0.1 microM) than L-Glu ( approximately 10 microM), but it had efficacy similar to that of L-Glu ( approximately 50% maximal inhibition). The potency and efficacy of L-AP4 and L-Glu were similar for both splice variants. Agonist-induced inhibition was abolished by pretreatment with (R,S)-alpha-cyclopropyl-4-phosphonophenylglycine, a selective group III mGluR antagonist, and pertussis toxin. Deletion of either a calmodulin (CaM) binding motif in the C terminus or the entire C terminus of mGluR8 did not affect mGluR8-mediated response. Our studies indicate that both mGluR8a and 8b are capable of inhibiting N-type Ca(2+) channel, suggesting a role as presynaptic autoreceptors to regulate neuronal excitability. The studies also imply that the potential CaM binding domain is not required for the mGluR8-mediated Ca(2+) channel inhibition and the C terminus of mGluR8a is dispensable for receptor coupling to N-type Ca(2+) channels.