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Kay-Pong Yip

Publications and source records attributed to Kay-Pong Yip.

17 recordsLinked to original sources
PubMed2006

Parameter estimation of feedback gain in a stochastic model of renal hemodynamics: differences between spontaneously hypertensive and Sprague-Dawley rats.

Proximal tubular pressure shows periodic self-sustained oscillations in normotensive rats but highly irregular fluctuations in spontaneously hypertensive rats (SHR). Although we have suggested that the irregular fluctuations in SHR represent low-dimensional deterministic chaos in tubuloglomerular feedback (TGF), they could also arise from other mechanisms, such as intrinsic instabilities in preglomerular vessels or inputs from neighboring, coupled nephrons. To test this possibility, we applied a parameter estimation procedure to a model of TGF, where a stochastic process was added to represent mechanisms not included explicitly in the model. In its deterministic version, the model can have chaotic dynamics arising from TGF. The model introduces random fluctuations into a parameter that determines the gain of TGF. The model shows a rich variety of dynamics ranging from low-dimensional deterministic oscillations and chaos to high-dimensional random fluctuations. To fit the data from normotensive rats, the model must introduce only a small variation in the feedback gain, and its estimates of that gain agree well with experimental values. These results support the use of the deterministic model of nephron dynamics in normotensive rats. In contrast, the irregular tubular pressure fluctuations in SHR were best described by a model dominated by random parameter fluctuations. The results point to the failure of simple mathematical models of nephron dynamics adequately to describe processes that are important for the irregular tubular pressure fluctuations and the need to consider other factors, such as differences in vascular function or nephron-nephron interactions, in further work on this problem.

Animals↗
PubMed2006

Integrin ligands mobilize Ca2+ from ryanodine receptor-gated stores and lysosome-related acidic organelles in pulmonary arterial smooth muscle cells.

Extracellular matrix (ECM) protein receptors, or integrins, participate in vascular remodeling and the systemic myogenic response. Synthetic ligands and ECM fragments regulate the vascular smooth muscle cell contractile state by altering intracellular Ca2+ levels ([Ca2+]i). Information on the Ca2+ effect of integrins in vascular smooth muscle cells is limited, but nonexistent in pulmonary arterial smooth muscle cells (PASMCs). We therefore characterized integrin expression in endothelium-denuded pulmonary arteries, and explored [Ca2+]i mobilization pathways induced by soluble ligands in rat PASMCs. Reverse transcriptase-PCR showed mRNA expression of integrins alpha1, alpha2, alpha3, alpha4, alpha5, alpha7, alpha8, alpha(v), beta1, beta3, and beta4, and immunoblots of alpha5, alpha(v), beta1, and beta3 confirmed protein expression. Exposure of PASMCs to integrin-binding peptides (0.5 mM) containing the arginine-glycine-aspartate (RGD) motif elicited [Ca2+]i responses with an order of potency of GRGDNP > GRGDSP > GRGDTP = cyclo-RGD. Pharmacological analysis revealed that the GRGDSP-induced Ca2+ response was unrelated to Ca2+ influx and the inositol triphosphate receptor-gated Ca2+ store, but partially blocked by ryanodine or inhibition of lysosome-related acidic organelles with bafilomycin A1. Simultaneous inhibition of both pathways was necessary to abolish the response. GRGDSP treatment increased cyclic ADP-ribose, the endogenous activator of ryanodine receptors, by 70%. GRGDSP also rapidly reduced Lysotracker Red accumulation, confirming direct modulation of acidic organelles. These data are the first demonstration of integrin-mediated Ca2+ regulation in PASMCs. The presence of an array of integrins, and activation of ryanodine-sensitive Ca2+ stores and lysosome-like organelles by GRGDSP suggest important roles for integrin-dependent Ca2+ signaling in regulating PASMC function.

Animals↗
PubMed2006

Epac-mediated Ca(2+) mobilization and exocytosis in inner medullary collecting duct.

PKA has traditionally been thought as the binding protein of cAMP for mediating arginine vasopressin (AVP)-regulated osmotic water permeability in kidney collecting duct. It is now known that cAMP also exerts its effects via Epac (exchange protein directly activated by cAMP) and that intracellular Ca(2+) mobilization is necessary for AVP-induced apical exocytosis in inner medullary collecting duct (IMCD). The role of Epac as an effector of cAMP action in addition to PKA was investigated using confocal fluorescence microscopy in perfused IMCD. PKA inhibitors (1 microM H-89 or 10 microM KT-5720) at concentrations known to inhibit aquaporin-2 (AQP2) phosphorylation did not prevent AVP-induced Ca(2+) mobilization and oscillations. Epac-selective cAMP agonist (8-pCPT-2'-O-Me-cAMP) mimicked AVP in triggering Ca(2+) mobilization and oscillations, which was blocked by ryanodine but not by Rp-cAMP (a competitive antagonist of cAMP binding to PKA). 8-pCPT-2'-O-Me-cAMP also triggered apical exocytosis in the presence of a PKA inhibitor. Immunolocalization of AQP2 in perfused IMCD demonstrated that 8-pCPT-2'-O-Me-cAMP induces apical targeting of AQP2 and that AQP2 is abundant in junctional regions of basolateral membrane. Immunofluorescence study also confirmed the presence of Epac (isoform I) in IMCD. These results indicate that activation of Epac by an exogenous cAMP analog triggers intracellular Ca(2+) mobilization and apical exocytotic insertion of AQP2 in IMCD.

Animals↗
PubMed2006

Phenol injury-induced hypertension stimulates proximal tubule Na+/H+ exchanger activity.

Injection of 50 microl 10% phenol into rat renal cortex activates renal sympathetic nerve activity which provokes acute hypertension that persists for weeks. We have previously shown with membrane fractionation that phenol injury caused a redistribution of the main proximal tubule (PT) apical transporter NHE3 (Na+/H+ exchanger isoform 3) to low density membranes enriched in apical microvilli. The aim of this study was to determine whether phenol injury increases PT apical Na+/H+ exchanger (NHE) activity. NHE activity was measured in vivo as the initial rate of change in intracellular pH (dpH(i)/dt) during luminal Na+ removal in PT preloaded with the pH-sensitive fluorescence dye BCECF. Injection of 50 microl 10% phenol increased blood pressure from 113 +/- 5.2 to 130 +/- 4.6 mmHg without changing glomerular filtration rate or urine output. NHE activity increased 2.6-fold by 70 min after phenol injury. The increase of NHE activity was accompanied with an increase of tubular reabsorption. Total NHE activity/NHE3 protein in cortical brush-border membrane (BBM) vesicles, measured by acridine orange quench and immunoblot, respectively, was unchanged by phenol injury. In conclusion, acute phenol injury provokes coincident increases in PT apical NHE activity, redistribution of NHE3 into low density apical membranes, and hypertension. The increase in NHE activity may contribute to the lack of pressure-diuresis and the maintenance of chronic hypertension in this model.

Animals↗
PubMed2005

Interactions between TGF-dependent and myogenic oscillations in tubular pressure and whole kidney blood flow in both SDR and SHR.

We previously showed that nonlinear interactions between the two renal autoregulatory mechanics (tubuloglomerular feedback and the myogenic mechanism) were observed in the stop flow pressure (SFP) and whole kidney blood flow data from Sprague-Dawley rats (SDR) using time-invariant bispectrum analysis (3, 4). No such nonlinear interactions were observed in either SFP or whole kidney blood flow data obtained from spontaneously hypertensive rats (SHR). We speculated that the failure to detect nonlinear interactions in the SHR data may be related to our observation that these interactions were not continuous and therefore had time-varying characteristics. Thus the absence of such nonlinear interactions may be due to an inappropriate time-invariant method being applied to data that are especially time varying in nature. We examine this possibility in this paper by using a time-varying bispectrum approach, which we developed for this purpose. Indeed, we found significant nonlinear interactions in SHR (n = 18 for SFP; n = 12 for whole kidney blood flow). Moreover, the duration of nonlinear coupling is found statistically to be longer (P = 0.001) in SFP data from either SDR or SHR than it is in whole kidney data from either type of rat. We conclude that nonlinear coupling is present at both the single nephron as well as the whole kidney level for SDR and SHR. In addition, SHR data at the whole kidney level exhibit the most transient nonlinear coupling phenomena.

Animals↗
PubMed2005

Multiple ryanodine receptor subtypes and heterogeneous ryanodine receptor-gated Ca2+ stores in pulmonary arterial smooth muscle cells.

Ryanodine receptors (RyRs) of pulmonary arterial smooth muscle cells (PASMCs) play important roles in major physiological processes such as hypoxic pulmonary vasoconstriction and perinatal pulmonary vasodilatation. Recent studies show that three subtypes of RyRs are coexpressed and RyR-gated Ca2+ stores are distributed heterogeneously in systemic vascular myocytes. However, the molecular identity and subcellular distribution of RyRs have not been examined in PASMCs. In this study we detected mRNA and proteins of all three subtypes in rat intralobar PASMCs using RT-PCR and Western blot. Quantitative real-time RT-PCR showed that RyR2 mRNA was most abundant, approximately 15-20 times more than the other two subtypes. Confocal fluorescence microscopy revealed that RyRs labeled with BODIPY TR-X ryanodine were localized in the peripheral and perinuclear regions and were colocalized with sarcoplasmic reticulum labeled with Fluo-5N. Immunostaining showed that the subsarcolemmal regions exhibited clear signals of RyR1 and RyR2, whereas the perinuclear compartments contained mainly RyR1 and RyR3. Ca2+ sparks were recorded in both regions, and their activities were enhanced by a subthreshold concentration of caffeine or by endothelin-1, indicating functional RyR-gated Ca2+ stores. Moreover, 18% of the perinuclear sparks were prolonged [full duration/half-maximum (FDHM) = 193.3 +/- 22.6 ms] with noninactivating kinetics, in sharp contrast to the typical fast inactivating Ca2+ sparks (FDHM = 44.6 +/- 3.2 ms) recorded in the same PASMCs. In conclusion, multiple RyR subtypes are expressed differentially in peripheral and perinuclear RyR-gated Ca2+ stores; the molecular complexity and spatial heterogeneity of RyRs may facilitate specific Ca2+ regulation of cellular functions in PASMCs.

Animals↗
PubMed2005

Flash photolysis of caged nitric oxide inhibits proximal tubular fluid reabsorption in free-flow nephron.

A nonobstructing optical method was developed to measure proximal tubular fluid reabsorption in rat nephron at 0.25 Hz. The effects of uncaging luminal nitric oxide (NO) on proximal tubular reabsorption were investigated with this method. Proximal fluid reabsorption rate was calculated as the difference of tubular flow measured simultaneously at two locations (0.8-1.8 mm apart) along a convoluted proximal tubule. Tubular flow was estimated on the basis of the propagating velocity of fluorescent dextran pulses in the lumen. Changes in local tubular flow induced by intratubular perfusion were detected simultaneously along the proximal tubule, indicating that local tubular flow can be monitored in multiple sites along a tubule. The estimated tubular reabsorption rate was 5.52 +/- 0.38 nl.min(-1).mm(-1) (n = 20). Flash photolysis of luminal caged NO (potassium nitrosylpentachlororuthenate) was induced with a 30-Hz UV nitrogen-pulsed laser. Release of NO from caged NO into the proximal tubule was confirmed by monitoring intracellular NO concentration using a cell-permeant NO-sensitive fluorescent dye (DAF-FM). Emission of DAF-FM was proportional to the number of laser pulses used for uncaging. Photolysis of luminal caged NO induced a dose-dependent inhibition of proximal tubular reabsorption without activating tubuloglomerular feedback, whereas uncaging of intracellular cGMP in the proximal tubule decreased tubular flow. Coupling of this novel method to measure reabsorption with photolysis of caged signaling molecules provides a new paradigm to study tubular reabsorption with ambient tubular flow.

Absorption↗
PubMed2005

Frequency encoding in renal blood flow regulation.

With a model of renal blood flow regulation, we examined consequences of tubuloglomerular feedback (TGF) coupling to the myogenic mechanism via voltage-gated Ca channels. The model reproduces the characteristic oscillations of the two mechanisms and predicts frequency and amplitude modulation of the myogenic oscillation by TGF. Analysis by wavelet transforms of single-nephron blood flow confirms that both amplitude and frequency of the myogenic oscillation are modulated by TGF. We developed a double-wavelet transform technique to estimate modulation frequency. Median value of the ratio of modulation frequency to TGF frequency in measurements from 10 rats was 0.95 for amplitude modulation and 0.97 for frequency modulation, a result consistent with TGF as the modulating signal. The simulation predicted that the modulation was regular, while the experimental data showed much greater variability from one TGF cycle to the next. We used a blood pressure signal recorded by telemetry from a conscious rat as the input to the model. Blood pressure fluctuations induced variability in the modulation records similar to those found in the nephron blood flow results. Frequency and amplitude modulation can provide robust communication between TGF and the myogenic mechanism.

Animals↗
PubMed2005

Parameter estimation in a stochastic model of the tubuloglomerular feedback mechanism in a rat nephron.

A key parameter in the understanding of renal hemodynamics is the gain of the feedback function in the tubuloglomerular feedback mechanism. A dynamic model of autoregulation of renal blood flow and glomerular filtration rate has been extended to include a stochastic differential equations model of one of the main parameters that determines feedback gain. The model reproduces fluctuations and irregularities in the tubular pressure oscillations that the former deterministic models failed to describe. This approach assumes that the gain exhibits spontaneous erratic variations that can be explained by a variety of influences, which change over time (blood pressure, hormone levels, etc.). To estimate the key parameters of the model we have developed a new estimation method based on the oscillatory behavior of the data. The dynamics is characterized by the spectral density, which has been estimated for the observed time series, and numerically approximated for the model. The parameters have then been estimated by the least squares distance between data and model spectral densities. To evaluate the estimation procedure measurements of the proximal tubular pressure from 35 nephrons in 16 rat kidneys have been analyzed, and the parameters characterizing the gain and the delay have been estimated. There was good agreement between the estimated values, and the values obtained for the same parameters in independent, previously published experiments.

Animals↗
PubMed2004

Interactions of TGF-dependent and myogenic oscillations in tubular pressure.

We have previously shown that there are two oscillating components in spontaneously fluctuating single-nephron blood flow obtained from Sprague-Dawley rats (Yip K-P, Holstein-Rathlou NH, and Marsh DJ. Am J Physiol Renal Physiol 264: F427-F434, 1993). The slow oscillation (20-30 mHz) is mediated by tubuloglomerular feedback (TGF), whereas the fast oscillation (100 mHz) is probably related to spontaneous myogenic activity. The fast oscillation is rarely detected in spontaneous tubular pressure because of its small magnitude and the fact that tubular compliance filters pressure waves. We detected myogenic oscillation superimposed on TGF-mediated oscillation when ambient tubular flow was interrupted. Two well-defined peaks are present in the mean power spectrum of stop-flow pressure (SFP) centering at 25 and 100 mHz (n = 13), in addition to a small peak at 125-130 mHz. Bispectral analysis indicates that two of these oscillations (30 and 100 mHz) interact nonlinearly to produce the third oscillation at 125-130 mHz. The presence of nonlinear interactions between TGF and myogenic oscillations indicates that estimates of the relative contribution of each of these mechanisms in renal autoregulation need to account for this interaction. The magnitude of myogenic oscillations was considerably smaller in the SFP measured from spontaneously hypertensive rats (SHR, n = 13); consequently, nonlinear interactions were not observed with bispectral analysis. Reduced augmentation of myogenic oscillations in SFP of SHR might account for the failure in detecting nonlinear interactions in SHR.

Animals↗
PubMed2004

Chronic hypoxia-induced upregulation of store-operated and receptor-operated Ca2+ channels in pulmonary arterial smooth muscle cells: a novel mechanism of hypoxic pulmonary hypertension.

Chronic hypoxic pulmonary hypertension is associated with profound vascular remodeling and alterations in Ca(2+) homeostasis in pulmonary arterial smooth muscle cells (PASMCs). Recent studies show that transient receptor potential (TRPC) genes, which encode store-operated and receptor-operated cation channels, play important roles in Ca(2+) regulation and cell proliferation. However, the influence of chronic hypoxia on TRPC channels has not been determined. Here we compared TRPC expression, and store- and receptor-operated Ca(2+) entries in PASMCs of normoxic and chronic hypoxic rats. Reverse-transcription polymerase chain reaction (RT-PCR), Western blot, and immunostaining showed consistently that TRPC1, TRPC3, and TRPC6 were expressed in intralobar pulmonary arteries (PAs) and PASMCs. Application of 1-oleoyl-2-acetyl-sn-glycerol (OAG) to directly activate receptor-operated channels, or thapsigargin to deplete Ca(2+) stores, caused dramatic increase in cation entry measured by Mn(2+) quenching of fura-2 and by Ca(2+) transients. OAG-induced responses were approximately 700-fold more resistant to La(3+) inhibition than thapsigargin-induced responses. siRNA knockdown of TRPC1 and TRPC6 specifically attenuated thapsigargin- and OAG-induced cation entries, respectively, indicating that TRPC1 mediates store-operated entry and TRPC6 mediates receptor-operated entry. In hypoxic PAs, there were 2- to 3-fold increases in TRPC1 and TRPC6 expression. They were accompanied by significant increases in basal, OAG-induced, and thapsigargin-induced cation entries in hypoxic PASMCs. Moreover, removal of Ca(2+) or inhibition of store-operated Ca(2+) entry with La(3+) and SK&F-96365 reversed the elevated basal [Ca(2+)](i) in PASMCs and vascular tone in PAs of chronic hypoxic animals, but nifedipine had minimal effects. Our results for the first time to our knowledge show that both store- and receptor-operated channels of PASMCs are upregulated by chronic hypoxia and contribute to the enhanced vascular tone in hypoxic pulmonary hypertension.

Animals↗
PubMed2003

Acute arterial hypertension inhibits proximal tubular fluid reabsorption in normotensive rat but not in SHR.

The effect of acute arterial hypertension on proximal tubular fluid reabsorption was investigated in Sprague-Dawley rats and spontaneously hypertensive rats (SHR) by measuring proximal tubular flow with a nonobstructive optical method. Under control conditions, spontaneous tubular flow was oscillating at 0.02-0.03 Hz in Sprague-Dawley rats. Acute hypertension induced an immediate increase of mean tubular flow (50% increase after 20 min of hypertension) and augmentation of oscillatory amplitude. Acute hypertension did not alter single-nephron blood flow as measured by laser-Doppler velocimetry (n = 12), suggesting that the increase of tubular flow was due to inhibition of reabsorption but not increase of filtration. By contrast, spontaneous tubular flow was fluctuating aperiodically in SHR. Acute hype tension did not induce a continuous increase of tubular flow or an increase in amplitude of fluctuations (n = 15). When apical Na(+)/H(+) exchange activity of proximal tubule was monitored, acute hypertension did not alter the activity in SHR (n = 8), while similar procedures had been shown to inhibit apical Na(+)/H(+) exchange activity of proximal tubules by more than 40% in Sprague-Dawley rats. These observations suggest that acute hypertension inhibits proximal tubular fluid reabsorption by inhibiting apical Na(+)/H(+) exchange activity in Sprague-Dawley rats and that this mechanism is impaired in SHR.

Absorption↗
PubMed2003

ET-1 activates Ca2+ sparks in PASMC: local Ca2+ signaling between inositol trisphosphate and ryanodine receptors.

Ca+ sparks originating from ryanodine receptors (RyRs) are known to cause membrane hyperpolarization and vasorelaxation in systemic arterial myocytes. By contrast, we have found that Ca2+ sparks of pulmonary arterial smooth muscle cells (PASMCs) are associated with membrane depolarization and activated by endothelin-1 (ET-1), a potent vasoconstrictor that mediates/modulates acute and chronic hypoxic pulmonary vasoconstriction. In this study, we characterized the effects of ET-1 on the physical properties of Ca2+ sparks and probed the signal transduction mechanism for spark activation in rat intralobar PASMCs. Application of ET-1 at 0.1-10 nM caused concentration-dependent increases in frequency, duration, and amplitude of Ca2+ sparks. The ET-1-induced increase in spark frequency was inhibited by BQ-123, an ETA-receptor antagonist; by U-73122, a PLC inhibitor; and by xestospongin C and 2-aminoethyl diphenylborate, antagonists of inositol trisphosphate (IP3) receptors (IP3Rs). However, it was unrelated to sarcoplasmic reticulum Ca2+ content, activation of L-type Ca2+ channels, PKC, or cADP ribose. Photorelease of caged-IP3 indicated that Ca2+ release from IP3R could cross-activate RyRs to generate Ca2+ sparks. Immunocytochemistry showed that the distributions of IP3Rs and RyRs were similar in PASMCs. Moreover, inhibition of Ca2+ sparks with ryanodine caused a significant rightward shift in the ET-1 concentration-tension relationship in pulmonary arteries. These results suggest that ET-1 activation of Ca2+ sparks is mediated via the ETA receptor-PLC-IP3 pathway and local Ca2+ cross-signaling between IP3Rs and RyRs; in addition, this novel signaling mechanism contributes significantly to the ET-1-induced vasoconstriction in pulmonary arteries.

Animals↗
PubMed2002

Coupling of vasopressin-induced intracellular Ca2+ mobilization and apical exocytosis in perfused rat kidney collecting duct.

Arginine vasopressin (AVP) regulates the osmotic water permeability of the kidney collecting duct by inducing exocytotic insertion of aquaporin-2 into apical membrane. The coupling between AVP-induced intracellular Ca2+ mobilization and apical exocytosis was investigated in isolated perfused rat inner medullary collecting duct (IMCD) segments using confocal fluorescence microscopy. Changes of [Ca2+]i in IMCD cells were measured with fluo-4. A novel confocal imaging technique using a styryl dye, FM1-43, was developed to monitor real-time exocytosis induced by arginine vasopressin. AVP (0.1 nM) triggered a rapid increase of [Ca2+]i in IMCD cells, followed by sustained oscillations. Ratiometric measurement of [Ca2+]i confirmed that the observed [Ca2+]i oscillation was a primary event and was not secondary to changes in cell volume. The frequencies of [Ca2+]i oscillations in each IMCD cell were independent and time variant. 1-Deamino-8-D-arginine vasopressin (a V2 receptor agonist, 0.1 nM) simulated the effects of AVP by triggering [Ca2+]i oscillations. In the absence of extracellular Ca2+, ryanodine (0.1 mM) inhibited AVP-induced Ca2+ mobilization. AVP (0.1 nM) triggered accumulative apical exocytosis in IMCD cells within 20 s after application. Pre-incubating the IMCD with an intracellular Ca2+ chelator, BAPTA, prevented AVP-induced intracellular Ca2+ mobilization, apical exocytosis, and increase of osmotic water permeability. These results indicate that AVP, via the V2 receptor, triggers a calcium signalling cascade observed as [Ca2+]i oscillations in the IMCD and that intracellular Ca2+ mobilization is required for exocytotic insertion of aquaporin-2.

Animals↗
PubMed2002

Apical H(+)/base transporters mediating bicarbonate absorption and pH(i) regulation in the OMCD.

The outer medullary collecting duct (OMCD) plays an important role in mediating transepithelial HCO transport [J(HCO(3)(-))] and urinary acidification. HCO absorption by type A intercalated cells in the OMCD inner stripe (OMCD(is)) segment is thought to by mediated by an apical vacuolar H(+)-ATPase and H(+)-K(+)-ATPase coupled to a basolateral Cl(-)-HCO exchanger (AE1). Besides these Na(+)-independent transporters, previous studies have shown that OMCD(is) type A intercalated cells have an apical electroneutral EIPA-sensitive, DIDS-insensitive Na(+)-HCO cotransporter (NBC3); a basolateral Na(+)/H(+) antiporter; and a basolateral Na(+)-K(+)-ATPase. In this study, we reexamined the Na(+) dependence of transepithelial Na(+) transport in the OMCD(is) and determined the role of apical NBC3 in intracellular (pH(i)) regulation in OMCD(is) type A intercalated cells. Control tubules absorbed HCO at a rate of approximately 13 pmol. min(-1). mm(-1). Lowering luminal Na(+) from 140 to 40 mM decreased [J(HCO(3)(-))] by approximately 15% without a change in transepithelial potential (V(te)). Furthermore, 50 microM EIPA (lumen) also decreased [J(HCO(3)(-))] by approximately 13% without a change in V(te). The effect of lowering luminal Na(+) and adding EIPA were not additive. These results demonstrate that [J(HCO(3)(-))] in the OMCD(is) is in part Na(+) dependent. In separate experiments, the pH(i) recovery rate after an NH prepulse was monitored in single type A intercalated cells with confocal fluorescence microscopy. The pH(i) recovery rate was approximately 0.21 pH/min in Na(+)-containing solutions and decreased to approximately 0.16 pH/min with EIPA (50 microM, lumen). In tubules perfused/bathed without Na(+), luminal Na(+) addition resulted in a pH(i) recovery rate of approximately 0.36 pH/min, whereas the Na(+)-independent recovery rate was approximately 0.16 pH/min. EIPA (50 microM, lumen) decreased the Na(+)-dependent pH(i) recovery rate to approximately 0.07 pH/min. The Na(+)-independent recovery rate was decreased to approximately 0.06 pH/min by bafilomycin (10 nM, lumen) and to approximately 0.10 pH/min using Schering 28080 (10 microM, lumen). These findings indicate that NBC3 contributes to pH(i) regulation in OMCD(is) type A intercalated cells and plays only a minor role in mediating [J(HCO(3)(-))] in the OMCD(is).

Acid-Base Equilibrium↗
PubMed2001

Synchronization phenomena in nephron-nephron interaction.

Experimental data for tubular pressure oscillations in rat kidneys are analyzed in order to examine the different types of synchronization that can arise between neighboring functional units. For rats with normal blood pressure, the individual unit (the nephron) typically exhibits regular oscillations in its tubular pressure and flow variations. For such rats, both in-phase and antiphase synchronization can be demonstrated in the experimental data. For spontaneously hypertensive rats, where the pressure variations in the individual nephrons are highly irregular, signs of chaotic phase and frequency synchronization can be observed. Accounting for a hemodynamic as well as for a vascular coupling between nephrons that share a common interlobular artery, we develop a mathematical model of the pressure and flow regulation in a pair of adjacent nephrons. We show that this model, for appropriate values of the parameters, can reproduce the different types of experimentally observed synchronization. (c) 2001 American Institute of Physics.

Journal Article↗