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Clonidine (10 micrograms X kg-1) reduced by almost 50% the increase in plasma neuropeptide (NPY)-like immunoreactivity (-LI) induced by preganglionic nerve stimulation at 8 Hz. This effect was reversed by yohimbine (1 mg X kg-1) which caused a three-fold increase of the plasma NPY-LI. Prazosin (1 mg X kg-1) had no such effect. Guanethidine (5 mg X kg-1) reduced the stimulation-evoked increase in plasma NPY-LI. It is concluded that the release of NPY-LI evoked by nerve stimulation from sympathetic nerve terminals is controlled by a presynaptic alpha 2-adrenoceptor-mediated mechanism. 相似文献
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INVOLVEMENT OF NON-NMDA AND NMDA RECEPTORS IN GLUTAMATE-INDUCED PRESSOR OR DEPRESSOR RESPONSES OF THE PONS AND MEDULLA 总被引:1,自引:0,他引:1
SY Chen WC Wu CJ Tseng JS Kuo CY Chai 《Clinical and experimental pharmacology & physiology》1997,24(1):46-56
1. Fifty-five intact and six baroreceptor denervated and vagotomized cats of either sex were anaesthetized intraperito-neally with urethane (400 mg/kg) and a-chloralose (40 mg/kg). Responses of the systemic arterial pressure (SAP), mean SAP (MSAP) and sympathetic vertebral nerve (VNA) and renal nerve activities (RNA) were recorded. 2. In intact animals, monosodium L-glutamate (Glu, 0.1 mol/L, 50 nL) was microinjected into pressor areas of the locus coeruleus (LC), gigantocellular tegmental field (GTF), rostral ventrolateral medulla (RVLM) and dorsomedial medulla (DM), and the depressor areas of caudal ventrolateral medulla (CVLM). The induced actions were compared before and after microinjection of either glutamate antagonists, glutamate diethylester (GDEE, 0.5 mol/L, 50–100nL), a competitive AMPA receptor blocker, or 2-amino-5-phosphonovaleric acid (D-AP5, 0.025 mol/L, 50–100 nL), a competitive N-methyl-D-aspartate (NMDA) receptor blocker. GDEE completely blocked the increases of SAP and VNA elicited from all pressor areas. D-AP5 only partially blocked the pressor but slightly blocked VNA and RNA responses from LC, GTF and DM, particularly those from RVLM. Neither GDEE nor D-AP5 blocked the depressor responses of SAP and two nerve activities elicited from CVLM. 3. In baroreceptor denervated animals, NMDA (2 mmol/L, 50–100 nL) and AMPA (0.2 mmol/L, 50–100 nL) were micro-injected into the same pressor areas of GTF, RVLM and DM and the depressor area of CVLM responsive to Glu activation (0.1 mol/L, 30 nL). In RVLM, DM and CVLM, the results of either NMDA or AMPA were similar to those induced by Glu. However, in GTF, microinjection of either NMDA or AMPA did not induce similar responses to Glu. This suggests that the nature of GTF may differ from RVLM and DM. 4. The above results suggest that the Glu-induced pressor responses from LC, GTF, DM and especially RVLM, are primarily mediated through AMPA receptors. The Glu-induced depressor responses from CVLM may not be predominantly mediated by either AMPA or NMDA receptors. 5. In both baroreceptor-intact and -denervated cats stimulation of the pressor areas often produced an increase of VNA and a decrease of RNA, while in the depressor CVLM decreased both VNA and RNA. The VNA, but not RNA were positively correlated with the pressor responses, while both VNA and RNA were positively correlated with the depressor responses. This may suggest that neurons of the sympathetic vertebral and renal nerves are topographically organized in the brain. 相似文献
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Occurrence of anti-C1q antibodies in IgA nephropathy 总被引:1,自引:0,他引:1
Gunnarsson I; Ronnelid J; Lundberg I; Jacobson S 《Nephrology, dialysis, transplantation》1997,12(11):2263-2268
Background: The pathogenic mechanisms and the antigens
involved in the establishment and progress of IgA nephropathy are unknown.
As antibodies against C1q have been reported to correlate with SLE
nephritis, we analysed the occurrence of these antibodies in IgA
nephropathy in order to investigate the possibility of pathogenetic
similarities in these renal disorders. Methods: The
occurrence of IgA- and IgG anti-C1q antibodies (anti-C1q) were determined
by ELISA in patients with IgA nephropathy (n=36) and SLE nephritis (n=37),
diseases both known to be associated with circulating immune complexes.
Levels of these antibodies were also determined in two other glomerular
diseases, i.e. idiopathic membranous glomerulo-nephritis (n=7) and minimal
change disease (n=2), in which circulating immune complexes are usually not
present, and in 40 healthy controls. Results: IgA
anti-C1q was observed in increased titres in 11/36 of the patients with IgA
nephropathy, in 2/37 of the patients with SLE nephritis (both with
proliferative disease) and in 1/9 of the patients with membranous and
minimal change disease (P<0.001). Increased titres of IgG anti-C1q
were observed in 1/36 of the patients with IgA nephropathy, in 17/37 of the
patients with SLE nephritis and in 0/9 of the patients with membranous and
minimal change disease (P<0.001). There were no correlations between
the levels of anti-C1q antibodies and clinical parameters such as degree of
proteinuria, haematuria, or renal function. Nor was there any correlation
to the concentration of C3a and the terminal complement complex (TCC) in
patients with IgA nephropathy. Conclusions: The
occurrence of anti-C1q antibodies in both IgA nephropathy and SLE
nephritis, albeit of different predominating isotypes, indicates the
possibility of a similar pathogenic mechanism involved in these renal
disorders. The occurrence of IgA anti-C1q antibodies in patients with IgA
nephropathy has to our knowledge not previously been reported. 相似文献