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Biomedical subjects

W J Fu

Publications and source records attributed to W J Fu.

8 recordsLinked to original sources
PubMed1995

Mechanisms of regulatory volume decrease in collecting duct cells.

The mechanisms of cell volume regulation upon osmotic cell swelling were examined in the inner stripe of the outer medullary collecting duct (OMCDi). Segments of OMCDi were dissected from rabbit kidney and perfused in vitro. Using an image processing system, the cross-sectional area of tubule cells was monitored as an index of the relative cell volume. In response to a decrease in extracellular osmolality (290 to 190 mOsm), the tubule cells swelled promptly and restored gradually their original cell volume by a mechanism termed regulatory volume decrease (RVD). The initial response of RVD (the rate of the decrease in cell volume during the first 10 min) was inhibited by 79% at a high concentration of basolateral K+ (50 mM). By contrast, the same concentration of luminal K+ did not affect the response. When basolateral Cl- was removed 30 min before the experiment, the initial response of RVD was decreased by 77%, whereas the response was not affected 30 min after removal of luminal Cl-. Addition of basolateral Ba2+ and basolateral anthracene-9-CO2H inhibited the response by 70 and 65%, respectively. RVD response was accompanied by a transient rise in intracellular Ca2+. The Ca2+ rise was abolished when intracellular Ca2+ was chelated by acetoxymethyl ester of 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM). In this condition, the initial RVD response was decreased by 68%. Our data suggest that the exit of basolateral K+ and Cl- via conductive pathways mainly mediates the RVD response in rabbit OMCDi cells, and that intracellular Ca2+ is involved in this response.

Animals↗
PubMed1994

[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.

Animals↗
PubMed1993

Mechanisms of regulatory volume increase in collecting duct cells.

To examine the mechanisms of cell volume regulation in response to hyperosmolality, segments of the inner stripe of rabbit outer medullary collecting duct (OMCDi) were perfused in vitro. The cross-sectional area of the tubule was monitored as an index of the relative cell volume. When luminal and basolateral osmolalities were increased from 290 to 390 mOsm simultaneously, the tubule cell shrank instantaneously and reswelled gradually, showing the so-called regulatory volume increase (RVI). Basolateral Na+ removal and addition of basolateral ethyl isopropyl amiloride (EIPA) decreased the RVI response by 76 and 66%, respectively. By contrast, apical Na+ removal had no effect on this response. RVI response was also inhibited by basolateral, but not luminal, Cl- removal (-63%), by total HCO3- removal (-74%), and by adding basolateral 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) (-62%). Intracellular pH did not change significantly during RVI. Vasopressin increased RVI response by 56%. However, this increase was abolished in the absence of basolateral Na+ and Cl-, and in the presence of basolateral EIPA and DIDS. These results suggest that major mechanisms responsible for RVI are Na(+)-H+ and Cl(-)-HCO3- exchange systems in the basolateral membrane, and that these systems are stimulated by vasopressin in rabbit OMCDi.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1992

[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.

Animals↗
PubMed1991

Insect resistance of transgenic tobacco plants expressing delta-endotoxin gene of Bacillus thuringiensis.

The initiative B.thuringiensis delta-endotoxin (Bt toxin) gene clones TH12 and TH48 contain two different classes of homologous genes, the 5.3 kb class and 6.6 kb class, respectively. Bt toxin genes of both classes, modified at the 5'-end and truncated at the 3'-end, can still be expressed to produce the insecticidal, truncated toxin proteins in E. coli. The modified Bt toxin genes were inserted into the plant binary expression vector pBin 437 (a derivative plasmid of pBin 19) and were transferred into tobacco by Ti plasmid-mediated gene transfer system. Southern blot and DNA slot blot analysis indicate that the Bt toxin genes have been integrated into tobacco genome at a copy number of 1 to 5. Northern blot analysis of polyA+ RNAs from progeny of the transgenic plants revealed that Bt toxin genes of both 5.3 kb and 6.6 kb classes were expressed in transgenic plants, though the transcripts were degraded to RNAs of lower molecular weights. In insecticidal test, 5 plants from the progeny of 5.3 kb class gene-transformed SR1 tobacco plants and 3 plants from those of 6.6 kb class gene-transformed plants were found to be toxic to the testing larvea of H.assulta. In comparison with the control, mortality of the insects fed on transgenic plants reached 40-50% and the growth of the survived insects was remarkably inhibited. These results indicate that the modified Bt genes of the 5.3 kb and 6.6 kb classes were expressed in transgenic plants and could confer on the transgenic plants a new character of insect resistance.

Animals↗
PubMed1991

[Effects of stimulation of locus coeruleus on cardiac contractility and renal nerve activity].

Experiments were performed on 64 cats anesthetized with chloralose-urethane, paralyzed and artificially ventilated. Electrical stimulation of locus coeruleus (LC) elicited increases in BP, HR, LVSP, dP/dt max and RNA. Buffer nerve section had no effect on the increase of these parameters, but could prolong the time of rise of BP and recovery phases. Injection of L-glutamate into LC, on the other hand, could decrease BP, HR, LVSP and dP/dt max. Intra-LC injection of kainic acid could also decrease BP. When the LC neurons showed degeneration or depolarization block after kainic acid injection, electrical stimulation of the LC could still elicit marked pressor response. The results suggest that the pressor response induced by electrical stimulation of LC might be mediated by the fibers passing through LC, while activation of LC neurons themselves would result in the depressor response.

Animals↗
PubMed1989

[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.

Animals↗