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Biomedical subjects

N H Holstein-Rathlou

Publications and source records attributed to N H Holstein-Rathlou.

At least 37 records · Page 2Linked to original sources

Long-range correlations of serial FEV1 measurements in emphysematous patients and normal subjects.

In obstructive lung disease the annual change in lung function is usually estimated from serial measurements of forced expiratory volume in 1 s (FEV1). Frequent measurements in each patient may not improve this estimate because data are not statistically independent; i.e., the measurements are autocorrelated. The purpose of this study was to describe the correlation structure in time series of FEV1 measurements. Nineteen patients with severe alpha1-antitrypsin deficiency (phenotype PiZ) and moderate to severe emphysema and two subjects with normal lungs were followed for several years with daily self-administered spirometry. FEV1 measurements fulfilling standard criteria were detrended, and the autocorrelation profile and the power spectrum were calculated. On average the subjects were followed for >3 yr and performed >1,000 acceptable spirometries. The autocorrelation of FEV1 measurements in the emphysematous patients was approximately 0.35 for short intervals and decreased almost exponentially with a half time of 38 days. Between 3 and 4 mo, the autocorrelation function became negative. It reached a minimum of -0.1 at approximately 8 mo and then increased toward zero over the following 12 mo. The autocorrelation function in the two normal subjects showed a similar pattern, but with a faster decay toward zero. In the patients, the power spectrum had a peak at 1 cycle/wk and showed a 1/f pattern, where f is frequency, with a slope of -0.88 at lower frequencies. We conclude that serial spirometric measurements show long-range correlations. The practical implication is that FEV1 need not be measured more often than once every 3 mo in studies of the long-term trends in lung function.

Adult↗

Urinary excretion of Tamm-Horsfall protein and epidermal growth factor in chronic nephropathy.

Tamm-Horsfall protein (THP) and epidermal growth factor (EGF) are both synthesized by tubular cells in the distal part of the nephron and excreted with the urine. The present study examines the urinary excretion rates of the two peptides in relation to functional tubular markers in patients with chronic nephropathy. Four groups of patients with moderate to severely reduced renal function were studied: glomerulonephritis (n = 10), diabetic nephropathy (n = 11), tubulointerstitial nephropathy (n = 13), and polycystic kidney disease (n = 8). The renal function was evaluated by glomerular filtration rate (GFR) as an indicator for the general renal function, lithium clearance (C(Li)) as an indicator for proximal tubular function, and absolute distal reabsorption of sodium (ADR(Na)) as an indicator for distal tubular function. The excretion rate of EGF was rather closely correlated with GFR, C(Li) and ADR(Na) (Spearman coefficients of variation 0.88, 0.69, and 0.74, respectively). The correlations between the excretion rate of THP and GFR, C(Li) and ADR(Na) were weaker (Spearman coefficients of variation 0.68, 0.42, and 0.44). When the effect of GFR had been accounted for by multiple variance analyses, the excretion rates of the two peptides were still associated with ADR(Na) but not with C(Li). In conclusion, the urinary excretion rates of especially EGF but also those of THP were correlated with renal function and distal tubular reabsorption of sodium in patients with chronic nephropathy.

Adjuvants, Immunologic↗

The cytochrome P-450 inhibitor cobalt chloride prevents inhibition of renal Na,K-ATPase and redistribution of apical NHE-3 during acute hypertension.

Acute systolic arterial hypertension provokes a rapid decrease in proximal tubule sodium reabsorption and diuresis associated with inhibition of renal cortex Na,K-ATPase activity and redistribution of apical membrane Na/H exchanger (NHE-3) to heavier density membranes containing markers of intermicrovillar cleft and endosomes. Because cytochrome P-450-dependent arachidonate metabolites participate in the regulation of renal sodium transport and BP, this study tested the hypothesis that these renal responses to acute hypertension would be prevented if cytochrome P-450 metabolism were inhibited by cobalt chloride (CoCl2). Four groups of rats (n = 4 to 5) were studied: (1) sham-operated; (2) 50 mg of CoCl2/kg subcutaneously for 2 d; (3) acute hypertension by constricting arteries for 5 min; and (4) acute hypertension after CoCl2 treatment as in group 3. Renal cortex was analyzed after sorbitol density gradient fractionation. CoCl2 treatment alone did not significantly affect the rate of urine output, endogenous lithium clearance (an inverse measure of proximal tubule sodium reabsorption), maximal activity of Na,K-ATPase, or subcellular distribution of NHE-3-containing membranes. In non-CoCl2-treated animals, acute hypertension provoked a three- to fourfold increase in urine output and endogenous lithium clearance, 33% inhibition of renal cortex Na,K-ATPase activity, and redistribution of NHE-3 out of the apical membrane peak. In CoCl2-treated animals, acute urine output and endogenous lithium clearance increased only twofold during acute hypertension, there was no inhibition of Na,K-ATPase activity, and there was no redistribution of NHE-3 immunoreactivity to higher density membranes. These findings demonstrate that CoCl2 treatment both attenuates the inhibition of proximal tubule sodium reabsorption and diuresis and abolishes Na,K-ATPase inhibition and NHE-3 redistribution during acute hypertension, evidence that these responses may be mediated by cytochrome P-450 arachidonate metabolites.

Acute Disease↗

Detection of chaotic determinism in time series from randomly forced maps.

Time series from biological system often display fluctuations in the measured variables. Much effort has been directed at determining whether this variability reflects deterministic chaos, or whether it is merely "noise". Despite this effort, it has been difficult to establish the presence of chaos in time series from biological sytems. The output from a biological system is probably the result of both its internal dynamics, and the input to the system from the surroundings. This implies that the system should be viewed as a mixed system with both stochastic and deterministic components. We present a method that appears to be useful in deciding whether determinism is present in a time series, and if this determinism has chaotic attributes, i.e., a positive characteristic exponent that leads to sensitivity to initial conditions. The method relies on fitting a nonlinear autoregressive model to the time series followed by an estimation of the characteristic exponents of the model over the observed probability distribution of states for the system. The method is tested by computer simulations, and applied to heart rate variability data.

Algorithms↗

Influence of forced respiration on nonlinear dynamics in heart rate variability.

Although it is doubtful whether the normal sinus rhythm can be described as low-dimensional chaos, there is evidence for inherent nonlinear dynamics and determinism in time series of consecutive R-R intervals. However, the physiological origin for these nonlinearities is unknown. The aim of this study was to test whether the known nonlinear input from spontaneous respiration is a source for the nonlinearities in heart rate variability. Twelve healthy subjects were examined in supine position with 3-h electrocardiogram recordings during both spontaneous and forced respiration in accordance with a metronome set to 12 min(-1). Nonlinear dynamics were measured as the correlation dimension and the nonlinear prediction error. Complexity expressed as correlation dimension was unchanged from normal respiration, 9.1 +/- 0.5, compared with forced respiration, 9.3 +/- 0.6. Also, nonlinear determinism expressed as the nonlinear prediction error did not differ between spontaneous respiration, 32.3 +/- 3.4 ms, and forced respiration, 31.9 +/- 5.7. It is concluded that the origin of the nonlinear dynamics in heart rate variability is not a nonlinear input from the respiration into the cardiovascular oscillator. Additional studies are needed to elucidate the mechanisms behind the nonlinear dynamics in heart rate variability.

Adolescent↗

Effect of angiotensin II receptor blockade on proximal tubular fluid reabsorption.

The effect of physiological concentrations of angiotensin II on proximal tubular fluid reabsorption remains controversial. To investigate the effect of blockade of intratubular AT1 receptors on tubular reabsorption, losartan (10(-5) M) was administered by microperfusion into an early proximal convolution of halothane-anesthetized Sprague-Dawley rats. Four parameters that depend on the rate of proximal fluid reabsorption were measured: proximal intratubular pressure (Pprox), early and late proximal flow rate, and early distal NaCl concentration. Pprox decreased by 0.5 +/- 0.1 mmHg, late proximal flow rate decreased by 2.0 +/- 0.8 nl/min, and early distal NaCl concentration decreased by 4.3 +/- 0.8 mM (mean +/- SE). No changes were observed after microperfusion with saline. Because the tubuloglomerular feedback mechanism was operating in the closed-loop mode, the decreased NaCl load to the macula densa will be compensated by an increase in the single-nephron glomerular filtration rate. In agreement with this, the early proximal flow rate, measured proximal to the site of losartan administration, increased by 5.7 +/- 1.3 nl/min. The increase in the rate of proximal reabsorption between the early and late proximal convolutions was estimated to be 7.8 nl/min (approximately 36%). It is concluded that a decrease in local luminal angiotensin II levels and/or AT1 receptor activity under free flow conditions increases the rate of proximal tubular fluid reabsorption.

Absorption↗

Internephron coupling by conducted vasomotor responses in normotensive and spontaneously hypertensive rats.

We compared conducted vasomotor responses in juxtamedullary microcirculation in normotensive Sprague-Dawley (SD) and spontaneously hypertensive rats (SHR). The goals of the study were as follows: 1) decide whether internephron coupling is facilitated by conducted vasomotor responses; 2) determine whether the magnitude of induced vasoconstriction decreases with increasing distance from the stimulation site; and 3) determine whether the response is stronger in SHR than in SD rats. Microapplication of KCl to the distal afferent arteriole caused local vasoconstriction that was rapidly conducted (speed > 3.0 mm/s) into the cortical radial artery and neighboring afferent arterioles in SD and SHR. The strength of the response was significantly greater (approximately 40%, P < 0.025) in SHR than SD, and the magnitude decreased monotonically with increasing distance from the stimulation site in both strains. Mechanical length constants were similar in SD and SHR (approximately 325 microm), indicating that the signal responsible for the effect decays at the same rate in both strains. We conclude that internephron coupling strength is significantly greater in SHR and that internephron coupling is due to vascular events conducted along the preglomerular vasculature.

Animals↗

Dynamic autoregulation and renal injury in Dahl rats.

The Dahl salt-sensitive (Dahl S) rat develops hypertension and renal injuries when challenged with a high salt diet and has been considered to be a model of chronic renal failure. Renal injuries appear very early in life compared with the spontaneously hypertensive rat (SHR). During the course of hypertension, a gradual impairment of autoregulatory control of renal blood flow might expose the glomerular circulation to periods of elevated pressure, resulting in renal injuries in Dahl S rats. Dynamic autoregulatory capacity was assessed in Dahl S and Dahl salt-resistant (Dahl R) rats, SHR, and Sprague-Dawley rats by inducing broad-band fluctuations in the arterial blood pressure and simultaneously measuring renal blood flow. Dynamic autoregulation was estimated by the transfer function using blood pressure as the input and renal blood flow as the output. Renal morphological injuries were evaluated in Dahl S rats and SHR and were scored semiquantitatively. Dynamic autoregulation was efficient and comparable in the low-frequency range (<0.015 Hz) in Dahl R rats, SHR, and Sprague-Dawley rats. The response in Dahl S rats depended strongly on the initiation time of the high salt diet. Autoregulation was preserved during a low salt diet and in rats exposed to a late-onset hypertension of short duration, only partly preserved if the late-onset hypertension was of a longer duration, and abolished in early-onset hypertension. All Dahl S rats on a high salt diet showed severe morphological changes in the kidney. In conclusion, autoregulatory capacity in the kidney of Dahl S rats is gradually impaired when rats are rendered hypertensive with a high salt diet. Renal morphological injuries develop before loss of dynamic autoregulation. Impaired autoregulation appears to be the result, not the cause, of the process that ultimately leads to renal failure in the Dahl S rat.

Animals↗

Detection of "noisy" chaos in a time series.

Time series from biological system often displays fluctuations in the measured variables. Much effort has been directed at determining whether this variability reflects deterministic chaos, or whether it is merely "noise". The output from most biological systems is probably the result of both the internal dynamics of the systems, and the input to the system from the surroundings. This implies that the system should be viewed as a mixed system with both stochastic and deterministic components. We present a method that appears to be useful in deciding whether determinism is present in a time series, and if this determinism has chaotic attributes. The method relies on fitting a nonlinear autoregressive model to the time series followed by an estimation of the characteristic exponents of the model over the observed probability distribution of states for the system. The method is tested by computer simulations, and applied to heart rate variability data.

Algorithms↗

The influence of angiotensin-converting enzyme inhibition on renal tubular function in progressive chronic nephropathy.

The influence of angiotensin-converting enzyme (ACE) inhibition on renal tubular function in progressive chronic nephropathy was investigated in 69 patients by the lithium clearance (C(Li)) method. Studies were done repeatedly for up to 2 years during a controlled trial on the effect of enalapril on progression of renal failure. The pattern of proteinuria was followed over the first 9 months. At baseline, the glomerular filtration rate (GFR) was 5 to 68 mL/min. Absolute proximal tubular reabsorption rate of fluid (APR), estimated as the difference between GFR and C(Li), was 1 to 54 mL/min. Calculated fractional proximal reabsorption (FPR) was moderately subnormal. During the study, GFR decreased and sodium clearance was unchanged; fractional excretion of sodium therefore increased. In the group of patients randomized to treatment with enalapril (n = 34), GFR at 1 month was 83% (P < 0.001) and C(Li) was 88% (P < 0.01) of the baseline values, APR and FPR had not changed significantly, and potassium clearance was significantly decreased. Through the rest of the study period, APR remained nearly unchanged and FPR even increased in the enalapril group. In the group of patients randomized to treatment with conventional antihypertensive drugs (n = 35), C(Li) was unchanged until severe reduction in GFR, APR and FPR decreased gradually, and potassium clearance was almost unchanged. These differences in tubular function between the two treatment regimens were significant (P < 0.05). An unchanged or increased APR in either treatment regimen was associated with a long-term slower progression of renal failure. Over 9 months, the 24-hour fractional clearance of albumin decreased in the ACE inhibitor group (P < 0.01), whereas the clearances of immunoglobulin G and retinol-binding protein were unchanged in this group. In the conventional group, the fractional clearances of these three plasma proteins all increased. It is concluded that in progressive chronic nephropathy ACE-inhibitor treatment was associated with different adaptive tubular changes in the handling of sodium, water, and protein compared with conventional antihypertensive therapy. During ACE inhibition, the reabsorptive capacity of the proximal tubule appeared to be better preserved, which might be of importance for the beneficial effect of this treatment in chronic renal disease.

Absorption↗

Endothelial Ca2+ in afferent arterioles during myogenic activity.

We measured endothelial Ca2+ concentration ([Ca2+]) in juxtamedullary afferent arterioles in response to step changes in perfusion pressure. Measurements were made with fura 2 using a fluorescence-imaging system designed to measure Ca2+ in whole tissues and minimize potentially harmful effects of ultraviolet illumination. The system yielded the typical sigmoidal relationship between fluorescence-emission ratio and [Ca2+] in vitro and was sensitive to endothelial Ca2+ transients elicited by bradykinin. Our goal was to determine whether changes in endothelial Ca2+ trigger events that cause myogenic vasoconstriction. Bradykinin, acting via endothelial cells, and sodium nitroprusside (SNP), acting independently, triggered vasodilation; bradykinin but not SNP increased endothelial Ca2+. Increased perfusion pressure caused vasoconstriction and a modest rise in endothelial Ca2+. Because the rise in Ca2+ with bradykinin initiates the vasodilation, the small rise in Ca2+ with pressure cannot cause vasoconstriction. Our results suggest that myogenic constriction is triggered from within vascular smooth muscle cells and that some other phenomenon, most likely increased shear stress, increases endothelial Ca2+ and modulates the myogenic reaction.

Animals↗

Rapid redistribution and inhibition of renal sodium transporters during acute pressure natriuresis.

Acute arterial hypertension provokes a rapid decrease in proximal tubule (PT) Na+ reabsorption, increasing flow to the macula densa, the signal for tubuloglomerular feedback. We tested the hypothesis, in rats, that Na+ transport is decreased due to rapid redistribution of apical Na+/H+ exchangers and basolateral Na+ pumps to internal membranes. Arterial pressure was increased 50 mmHg by constricting various arteries. We also tested whether transporter internalization occurred when PT Na+ reabsorption was inhibited with the carbonic anhydrase inhibitor benzolamide. Five minutes after initiating either natriuretic stimuli, cortex was removed, and membranes were fractionated by density gradient centrifugation. Urine output and endogenous lithium clearance increased threefold in response to either stimuli. Acute hypertension provoked a redistribution of apical Na+/H+ exchanger NHE3, alkaline phosphatase, and dipeptidyl peptidase IV to higher density membranes enriched in the intracellular membrane markers. Basolateral membrane Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) activity decreased 50%, 25-30% of the alpha 1-and beta 1-subunits redistributed to higher density membranes, and the remainder is attributed to decreased activity of the transporters. Benzolamide did not alter Na+ transporter activity or distribution, implying that decreasing apical Na+ uptake does not initiate redistribution or inhibition of basolateral Na(+)-K(+)-ATPase. We conclude that PT natriuresis provoked by acute arterial pressure is mediated by both endocytic removal of apical Na+/H+ exchangers and basolateral Na+ pumps as well as decreased total Na+ pump activity.

Acute Disease↗

The inner ear produces a natriuretic hormone.

Cytoplasmic granules have been demonstrated in epithelial cells from the endolymphatic sac, an extraosseus part of the inner ear located in the posterior cranial fossa. Intravenously infused extracts from endolymphatic sacs in anesthetized rats elicited a potent natriuresis and diuresis without effects on blood pressure, glomerular filtration rate, or lithium clearance. Only a minor kaliuresis was observed. Extracts of dural tissue adjacent to the endolymphatic sacs had no effect. It is concluded that the endolymphatic sac contains as endogenous inhibitor of sodium reabsorption and could be the sensory organ/mediator of "cerebral" natriuresis. Furthermore, this substance, tentatively named saccin, may influence the homeostasis of the inner ear fluids and accordingly play a significant role in the pathogenesis of Mèniére's disease.

Absorption↗

Chaos and non-linear phenomena in renal vascular control.

Renal autoregulation of blood flow depends on the functions of the tubuloglomerular feedback (TGF) system and the myogenic response of the afferent arteriole. Studies of the dynamic aspects of these control mechanisms at the level of both the single nephron and the whole kidney have revealed a variety of non-linear phenomena. In halothane-anesthetized, normotensive rats the TGF system oscillates regularly at 2-3 cycles/min because of the non-linearities and the time delays within the feedback system. Oscillations are present in single nephron blood flow, tubular pressure and flow, and in the tubular solute concentrations. Nephrons deriving their afferent arteriole from the same cortical radial artery are entrained, and consequently oscillate at the same frequency. Experimental studies have shown that the synchronization is due to an interaction of the TGF between nephrons. A necessary condition for the interaction is that the nephrons derive their blood supply from the same cortical radial artery. Development of hypertension is associated with a shift from periodic oscillations of tubular pressure to random-like fluctuations. Numerical analyses indicate that these fluctuations are an example of deterministic chaos. Experimental studies show that the development of hypertension is associated with an increase in strength of the interaction between nephrons. Mathematical models suggest that an increased nephron-nephron interaction could cause a bifurcation in the dynamics of TGF from periodic oscillations to deterministic chaos. In addition to the TGF mediated oscillation, experimental studies have also demonstrated the presence of a faster oscillation, this having a frequency of 120-160 mHz. This is caused by a mechanism intrinsic to the vascular wall, and presumably represents the well-known phenomenon of vasomotion. Using newly developed non-linear analytical methods non-linear interactions between vasomotion and the TGF mediated oscillation were detected both in single nephron and in whole kidney blood flow. The physiological significance of these non-linear phenomena in renal vascular control is discussed.

Animals↗

Short- and long-term variations in non-linear dynamics of heart rate variability.

OBJECTIVES: The purpose of the study was to investigate the short- and long-term variations in the non-linear dynamics of heart rate variability, and to determine the relationships between conventional time and frequency domain methods and the newer non-linear methods of characterizing heart rate variability. METHODS: Twelve healthy subjects were investigated by 3-h ambulatory ECG recordings repeated on 3 separate days. Correlation dimension, non-linear predictability, mean heart rate, and heart rate variability in the time and frequency domains were measured and compared with the results from corresponding surrogate time series. RESULTS: A small significant amount of non-linear dynamics exists in heart rate variability. Correlation dimensions and non-linear predictability are relatively specific parameters for each individual examined. The correlation dimension is inversely correlated to the heart rate and describes mainly linear correlations. Non-linear predictability is correlated with heart rate variability measured as the standard deviation of the R-R intervals and the respiratory activity expressed as power of the high-frequency band. The dynamics of heart rate variability changes suddenly even during resting, supine conditions. The abrupt changes are highly reproducible within the individual subjects. CONCLUSIONS: The study confirms that the correlation dimension of the R-R intervals is mostly due to linear correlations in the R-R intervals. A small but significant part is due to non-linear correlations between the R-R intervals. The different measures of heart rate variability (correlation dimension, average prediction error, and the standard deviation of the R-R intervals) characterize different properties of the signal, and are therefore not redundant measures. Heart rate variability cannot be described as a single chaotic system. Instead heart rate variability consists of intertwined periods with different non-linear dynamics. It is hypothesized that the heart rate is governed by a system with multiple "strange" attractors.

Adult↗

A re-evaluation of the determinants of glomerular filtration rate.

Several factors are potentially able to change the glomerular filtration rate (GFR) and thereby participate in its regulation, but only a few factors seem to be physiologically important. The variable nature of proximal tubular pressure should be recognized as important in the regulation of GFR. It is argued that a distinction should be made between the terms 'autoregulation of GFR' and 'regulation of GFR'. The tubuloglomerular feedback mechanism (TGF) is an important factor for autoregulatory control of GFR. When perturbations result in major increases in tubular flow, the TGF saturates. Proximal tubular pressure then increases and becomes the major factor responsible for the stabilization of GFR. Changes in the proximal reabsorption rate (APR) are important for long-term variations in GFR (regulation of GFR). Small changes in the APR cause near parallel changes in the GFR mainly through the TGF mechanism, while larger changes in the APR cause near parallel changes in the GFR mainly because of the effect on tubular pressure. The hydraulic resistance in the distal nephron segments is an additional factor in regulating GFR, through its effect on proximal tubular pressure. The stimulus to the TGF mechanism also depresses renin release. The resulting local angiotensin II concentration has effects both on the arteriolar resistances and on the APR. The renin-angiotensin system and TGF are therefore considered to be integrated parts of a common control system regulating GFR. According to the hypothesis advocated here, TGF-mediated changes in afferent arteriolar resistance and angiotensin-mediated changes in efferent arteriolar resistance and APR cooperate in counteracting perturbations in proximal tubular pressure and Henle loop flow. However, because of the biphasic proximal effect of angiotensin II, a major unresolved question is whether physiological increases in endogenous local angiotensin II concentrations stimulate or inhibit proximal reabsorption.

Angiotensin II↗

Patterns of blood pressure variability in normotensive and hypertensive rats.

We sought patterns in mean arterial pressure of normotensive rats and alterations in chronic hypertension. Pressure was recorded for 4-6 days by telemetry from conscious, unrestrained rats and sampled digitally at 3 Hz, using normotensive Sprague-Dawley rats, spontaneously hypertensive rats (SHR), and Sprague-Dawley rats with two-kidney, one-clip renovascular hypertension (2K,1C). Time series analysis was by fast Fourier transform. Power spectra were divided into ultradian (frequencies > 1/day), circadian (frequency = 1/day), and infradian (frequencies < 1/day) domains. In the ultradian band from approximately 0.1 to 10 mHz the spectra were 1/f and without distinct peaks. The slopes were not significantly different among the groups and ranged from -1.03 to -1.61. At frequencies > 10 mHz, power continued to decrease but with a lower slope. A peak centered at approximately 100 mHz was present in both normotensive and 2K,1C rats but not in SHR. SHR had significantly more ultradian power than the others. The circadian rhythm modulated power in the ultradian band. Modulation was most prominent in normotensives, in which the ultradian activity was highest during the night when rats are active and lowest during the day; less pronounced in 2K,1C; and not detectable in SHR. There are regular patterns of blood pressure fluctuations and specific modifications to the patterns by different forms of hypertension.

Activity Cycles↗

Magnitude of TGF-initiated nephron-nephron interactions is increased in SHR.

We compared the tubuloglomerular feedback (TGF)-initiated nephron-nephron interaction in spontaneously hypertensive rats (SHR) and normotensive Sprague-Dawley (SD) rats. Interaction strength was assessed by measuring stop-flow pressure (delta SFP) responses in pairs of nephrons, where only one nephron of the pair was microperfused. The vascular connection was determined from casts of the nephrons and vessels; length of arteriolar separation between the two glomeruli was measured on the casts. When microperfusion rate was increased from 5 to 50 nl/min, delta SFP in perfused nephrons was 10.6 +/- 0.6 and 10.2 +/- 0.7 mmHg [not significant (NS)] in SD and SHR, respectively. In the matched unperfused nephrons from the same cortical radial artery, delta SFP was 1.3 +/- 0.2 and 2.9 +/- 0.7 mmHg (P < 0.05) in SD and SHR. When the perfused and unperfused nephron originated from different cortical radial arteries, delta SFP in the unperfused nephrons was -0.1 +/- 0.2 and 0.0 +/- 0.3 mmHg (NS) in SD and SHR, respectively. In both strains, interaction strength varied inversely with glomerular separation. When the dependence on distance was taken into account, interaction strength was about threefold greater in SHR than in SD. We conclude that the nephron-nephron interaction is significantly greater in SHR. The dependence of interaction strength on distance separating the glomeruli suggests that the interaction is propagated along the preglomerular vasculature.

Animals↗