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PubMed1996

FK-506 and rapamycin but not cyclosporin inhibit aldosterone-stimulated sodium transport in A6 cells.

The immunosuppressants cyclosporin A (CyA), FK-506, and rapamycin (RAP) have multiple actions on target cells that appear to be mediated by interaction of drug-binding protein complexes. Both FK-506 and CyA, but not RAP, inhibit the Ca2(+)-dependent phosphatase, calcineurin, and in so doing have been found to inhibit Na(+)-K(+)-ATPase activity in various nephron segments. Of interest, FK-506 and RAP, but not CyA, are bound by the steroid receptor-associated FK-506-binding heat shock protein of 56 kDa, HSP56. To determine the physiological effect of this interaction on a steroid-mediated phenomenon, the effect of these agents on steroid-mediated Na+ transport in A6 cells was investigated. Aldosterone stimulation of Na+ transport and Na(+)-K(+)-ATPase activity are significantly inhibited by prolonged incubation with FK-506 and RAP. Although CyA inhibits basal Na(+)-K(+)-ATPase activity, it has no effect on aldosterone-induced Na+ transport or the aldosterone-induced increase in Na(+)-K(+)-ATPase activity. FK-506 inhibits the aldosterone-induced synthesis of G alpha i-3 protein but has no effect on glucocorticoid receptor number as quantified by Western blotting. The results suggest that FK-506 and RAP inhibit steroid-mediated Na+ transport at some pretranslational site. The common interaction of these agents with the steroid receptor-associated HSP56 might account for these findings.

Aldosterone↗

PubMed1989

Sustained increases in plasma epinephrine concentration do not modulate renin release.

We examined the relationship between plasma renin activity (PRA) and renal arterial pressure (RAP) during 1) control conditions, 2) acute, and 3) chronic intravenous epinephrine (EPI) infusion (125 ng.kg-1.min-1). In eight conscious uninephrectomized dogs maintained on a normal sodium intake, the renin stimulus-response curve (RSRC) was determined by a stepwise reduction in RAP with an inflatable occluder around the renal artery controlled by a servo unit. The RSRC could be approximated by two lines intersecting at a threshold pressure (approximately 20 mmHg below control RAP). In the high-pressure range, PRA was relatively insensitive to changes in RAP, whereas, below threshold pressure, changes in RAP had large effects on PRA. During acute EPI infusion there was approximately a 40% increase in heart rate (control = 57 +/- 3 beats/min) and hematocrit (control = 30 +/- 1%) in association with a rise in plasma EPI concentration from 73 +/- 16 to 1,413 +/- 100 pg/ml; mean arterial pressure (MAP) was unchanged (94 +/- 3 mmHg). Moreover, EPI acutely increased basal PRA from 0.3 +/- 0.1 to 0.8 +/- 0.3 ng angiotensin I.ml-1.h-1 and shifted the RSRC to the right (increasing threshold pressure 7 mmHg) without altering the slope of the RSRC curve either above or below threshold pressure. In contrast, although plasma EPI concentration and hematocrit remained elevated during chronic EPI infusion, heart rate and basal PRA returned to preinfusion values. In addition, there were no significant long-term changes in MAP or in any of the parameters of the RSRC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2004

Direction-dependent conduction abnormalities in a canine model of atrial fibrillation due to chronic atrial dilatation.

Chronic rapid atrial pacing (RAP) leads to changes that perpetuate atrial fibrillation (AF). Chronic atrial dilatation due to mitral regurgitation (MR) also increases AF inducibility, but it is not clear whether the underlying mechanism is similar. Therefore, we have investigated atrial electrophysiology in a canine MR model (mitral valve avulsion, 1 mo) using high-resolution optical mapping and compared it with control dogs and with the canine RAP model (6-8 wk of atrial pacing at 600 beats/min, atrioventricular block, and ventricular pacing at 100 beats/min). At followup, optical action potentials were recorded using a 16 x 16 photodiode array from 2 x 2-cm left atrial (LA) and right atrial (RA) areas in perfused preparations, with pacing electrodes around the field of view to study direction dependency of conduction. Action potential duration at 80% repolarization (APD(80)) was not different between control and MR but was reduced in RAP atria. Conduction velocities during normal pacing were not different between groups. However, the MR LA showed increased conduction heterogeneity during pacing at short cycle lengths and during premature extrastimuli, which frequently caused pronounced regional conduction slowing. Conduction in the MR LA during extrastimulation also displayed a marked dependence on propagation direction. These phenomena were not observed in the MR RA and in control and RAP atria. Thus both models form distinctly different AF substrates; in RAP dogs, the decrease in APD(80) may stabilize reentry. In MR dogs, regional LA conduction slowing and increased directional dependency, allowing unidirectional conduction block and preferential paths of conduction, may account for increased AF inducibility.

Action Potentials↗

PubMed1991

Limited cardiac preload reserve in conscious cirrhotic rats.

In conscious rats with experimental cirrhosis without ascites, we have studied whether there is a limited cardiac preload reserve by performing cardiac output (CO) curves. CO was determined by thermodilution at basal, 5, 7.5, and 10 cmH2O of right atrial pressure (RAP). RAP was elevated by dextran infusion (1 ml/min iv, 30 min). CO curves were performed by plotting changes in CO with changes in RAP. In the basal state, cirrhotic rats showed a hyperdynamic circulation defined by increased CO and stroke volume, decreased total peripheral resistances, and normotension without changes in heart rate. Blood volume was also elevated in cirrhotic rats compared with the control animals. Between the limits of RAP studied, the CO curve of control rats presented a typical ascending limb. In contrast, the CO curve of the cirrhotic animals showed first an ascending shifted upward limb and afterward a descending limb. These alterations were accompanied by changes in the inotropic state as measured as left ventricular (LV) peak dP/dt in hexamethonium-pretreated animals submitted to the same volume loads described above. With the same increases in RAP, LV dP/dt changed, in every group, in a manner similar to CO. The results of the present study indicate that cirrhotic rats with high blood volume and hyperdynamic circulation show, in the steady state, a limited preload reserve. The partial utilization of the preload reserve can make the cirrhotic heart unable to modulate cardiac performance with changes in loading conditions, thus determining a state of heart failure.

Animals↗

PubMed1994

Reduced collateral perfusion is a direct consequence of elevated right atrial pressure.

In the present study we determined quantitatively the effects of increased right atrial pressure (RAP) on coronary and collateral flows. In an isolated, blood-perfused, maximally vasodilated dog heart preparation in which the left ventricle was vented, we used the retrograde flow method to assess collateral flow. When RAP was elevated from 5 +/- 1 (control) to 13 +/- 1 and 23 +/- 1 mmHg, retrograde flow from the left circumflex coronary artery (which was open to atmospheric pressure) increased 29 +/- 8 and 97 +/- 21% relative to control while left anterior descending flow decreased 5 +/- 1 and 14 +/- 2%, respectively (P < 0.01; n = 7). The increase in retrograde flow could be due to 1) an increase in collateral flow due to increased pressure at the origin of the collaterals or 2) the elevated RAP (venous outflow pressure), which forces the antegrade collateral flow component in the retrograde direction. To distinguish between these possibilities we embolized the circumflex with 30-microns spheres to eliminate the antegrade flow component. After embolization there was no significant change in retrograde flow with elevated RAP, indicating that the second supposition was correct. We conclude that increased RAP 1) results in a reduction of flow to the collateral-dependent myocardium and 2) reduces perfusion of the unoccluded coronary vessel. Furthermore, we found that under conditions of varying venous outflow pressure, retrograde flow may not serve as a reliable index of collateral flow.

Animals↗

PubMed1995

Determinants of respiratory sinus arrhythmia in the vagotomized rabbit.

After cardiac denervation, a small-amplitude respiratory sinus arrhythmia (RSA) has been described in animals and humans. Its mechanical and chemical determinants were investigated in 19 urethan-anesthetized, vagotomized, and mechanically ventilated rabbits. We measured the influence on RSA of arterial blood gases, beta-adrenergic blockade, and phasic and steady changes in right atrial pressure (RAP) induced by changes in tidal volume (VT, 20, 40, 60 ml), respiratory frequency (RF, 10, 20, 30 cycles/min), and dextran-induced RAP increases. Phasic changes in RAP during each recording were quantified as standard deviation of the first derivative of the RAP signal (dRAP) as a measure of magnitude of variations of the rate of change due to respiration. RSA was assessed by combined autoregressive power spectral analysis of R-R interval and respiration on sequences of 256 heart-beats. Despite vagotomy, RSA was present in all recordings in all animals. During room air breathing, RSA changes were dependent on RF and VT (P < 0.025 and P < 0.001, respectively) and correlated with dRAP (P < 0.001) and arterial PO2 (P < 0.001). beta-Adrenergic blockade did not change the amplitude of this residual RSA or its dependence on ventilatory mechanics. Dextran-induced increase in mean RAP from 2.9 to 11.9 mmHg did not modify RSA or dRAP. During 100% O2 inhalation, RSA changes were no longer significantly linked to RF and VT, and also the correlation of RSA with dRAP was reduced (P < 0.05). Changing the arterial PCO2 from 28 to 79 mmHg (induced by increasing dead space at fixed ventilation) did not modify RSA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

PubMed1991

Hormonal and circulatory responses to chronically controlled increments in right atrial pressure.

To study the time-dependent changes in the secretion of atrial natriuretic peptide (ANP) in response to chronic stimulation by controlled increments in atrial pressure, we developed methodology for precise control of right atrial pressure (RAP) in dogs by employing an externally adjustable occluder around the pulmonary artery and a servo-control system. During 7 days of servo-control of RAP at 6.3 +/- 0.1 mmHg above control levels (1.3 +/- 0.1 mmHg), the 24-h coefficient of variation in RAP was 1/45 the variation that occurred under control conditions. After 30 min of increased RAP, mean arterial pressure (MAP) was reduced from 101 +/- 4 to 84 +/- 3 mmHg in association with increments in plasma renin activity (PRA) from 0.6 +/- 0.1 to 2.5 +/- 0.9 ng angiotensin I (ANG I).ml-1.h-1 and in the plasma concentrations of ANP, arginine vasopressin (AVP), and epinephrine from 93 +/- 18 to 484 +/- 61 pg/ml, from 0.5 +/- 0.1 to 9.2 +/- 2.4 pg/ml, and from 82 +/- 27 to 585 +/- 133 pg/ml, respectively. In comparison, on day 7 of servo-control of RAP, sodium balance was achieved and MAP remained depressed (82 +/- 4 mmHg) along with sustained increments in both plasma ANP concentration (482 +/- 67 pg/ml) and PRA (1.7 +/- 0.6 ng ANG I.ml-1.h-1); on the other hand, the plasma concentrations of AVP and epinephrine returned to control levels. This quantitative study indicates that ANP secretion does not chronically adapt to stimulation by increased atrial pressure and suggests that the plasma levels of ANP achieved in heart failure markedly increase renal excretory capability and allow fluid balance to be achieved at a substantial fall in renal perfusion pressure.

Angiotensin I↗

PubMed1995

Effect of loading right atrial and ventricular receptors on stimulated AVP, ACTH, and renin secretion in awake dogs.

The goal of this study was to test the hypothesis that increasing or decreasing the load on baroreceptors in the right heart influenced the secretion of arginine vasopressin (AVP), adrenocorticotropic hormone (ACTH), and renin during a state of sustained arterial hypotension. The hypothesis was tested in chronically instrumented conscious dogs prepared with inflatable cuffs around the pulmonary artery (PA) and the thoracic inferior vena cava (IVC). In one protocol (n = 5), mean arterial pressure was reduced 10 or 20% below control by constriction of the PA, a maneuver that caused a fall in left atrial pressure (LAP) and an increase in right atrial pressure (RAP). Plasma AVP, ACTH, atrial natriuretic peptide (ANP), and plasma renin activity (PRA) all increased (P < 0.05) in response to constriction of the PA. Reducing RAP to control by constriction of the IVC during maintained constriction of the PA had no effect on MAP, LAP, plasma AVP, ACTH, or PRA, but plasma ANP fell significantly. In a separate protocol (n = 4), constriction of the IVC was used to reduce MAP 10 or 20% below control, and this led to significant decreases in both LAP and RAP and increases in plasma AVP, ACTH, and PRA. RAP was then increased above control by constriction of the PA without altering either MAP or LAP. Raising RAP from a level that was 6.3 +/- 1.3 mmHg below control to 3.5 +/- 1.0 mmHg above control had no effect on plasma AVP, ACTH, or PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1977

Dissociation of renal blood flow and filtration rate autoregulation by renin depletion.

Renal blood flow (RBF) and glomerular filtration rate (GFR) autoregulation during changes in renal artery pressure (RAP) were examined in dogs fed a "normal" diet (group 1, n = 10) and in renin-depleted dogs (group 2, n = 11) which received a high-sodium diet and deoxycorticosterone acetate (DOCA) injections for a minimum of 21 days prior to the study. Renal venous plasma renin activity was undetectable in group 2 by radioimmunoassay of angiotensin I and did not increase even when RAP was reduced to less than 70 mmHg. Autoregulation of RBF was not impaired by renin depletion. However, GFR autoregulation, which was very effective in group 1 dogs, was markedly impaired in group 2. Average GFR in group 2 decreased progressively to 58 +/- 7% of the control value as RAP was reduced in steps from the control value of 137 +/- 3 to 69 +/- 1 mmHg. In normal dogs, the filtration fraction either increased slightly or did not change when RAP was reduced in steps, whereas in renin-depleted dogs the filtration fraction decreased progressively during reductions in RAP. Thus, chronic sodium loading and DOCA administration causes renin depletion and dissociates the autoregulation of RBF and GFR. These data are consistent with the hypothesis that the renin-angiotensin system participates in the control of GFR, possibly by an efferent arteriolar mechanism.

Animals↗

PubMed1987

Atrial natriuretic peptide, right atrial pressure, and sodium excretion rate in the rat.

This study examined the relationship between right atrial pressure (RAP), urine flow rate, sodium excretion rate, and plasma atrial natriuretic peptide (ANP) levels after an acute Ringer expansion. Two groups of rats had their RAP monitored and balloon catheters placed in their thoracic inferior venae cavae. In one group the balloon remained deflated, and in the second group the balloon was inflated during the volume expansion in an attempt to prevent the rise in RAP. The peak RAP was 7.3 +/- 0.8 mmHg when the balloon remained deflated and 3.5 +/- 0.6 mmHg in the group with the balloon catheter inflated (P less than 0.005). The corresponding peak ANP levels were 682 +/- 140 and 223 +/- 40 pg/ml. There was a significant correlation between the peak RAP and ANP levels (r = 0.754; P less than 0.05). The inflation of the balloon catheter significantly decreased the urine flow rate and the urine sodium excretion rate. A final group of animals had 200 microliters of rabbit serum containing antibody to ANP infused before the volume expansion. The antibody-treated animals had significantly lower urine flow and sodium excretion rates than nonantibody-treated control rats. We conclude that ANP is one of the factors which allows the rat to excrete an acute Ringer expansion.

Animals↗

PubMed1995

Changes in atrial natriuretic peptide and plasma renin activity following changes in right atrial pressure in patients with chronic renal failure.

Since it was first discovered in the early 1980s, the role of atrial natriuretic peptide (ANP) in the control of fluid and electrolyte balance and blood pressure has been extensively studied in both health and disease. We report here a study of ANP and its relationship to corresponding changes in right atrial pressure (RAP) in patients with chronic renal failure (CRF) on haemodialysis compared to healthy controls. Although there was a positive correlation between RAP and ANP in both groups, the changes in ANP following changes in RAP between the two groups were not statistically significant. A unique observation was the response of RAP to changes in posture, with RAP falling significantly as expected in healthy controls in contrast to the exceptional absence of a significant fall in patients with CRF. Healthy controls demonstrated appropriate postural changes in plasma renin activity (PRA) despite marked suppression of PRA levels due to salt loading, in complete contrast to patients with CRF who, despite chronic fluid overload and elevated levels of ANP, continued to have grossly elevated PRA levels that failed to change significantly in response to changes in posture.

Atrial Function, Right↗

PubMed1991

Effect of right atrial stimulation on both atrial pressure and atrial natriuretic peptide release in essential hypertension.

UNLABELLED: Several reports indicated a direct relationship between atrial pacing and atrial natriuretic peptide (ANP) blood levels, but few controlled hemodynamic studies have been reported. In particular, the relationship between increase in heart rate, release of ANP and increase in right atrial pressure (RAP) are still uncertain. Moreover, the effect of accelerated heart rate on ANP secretion in patients with essential hypertension has not yet been fully elucidated. For this, we studied 12 untreated essential hypertensive (EH; WHO stage I-II) and 10 age-matched normotensive subjects (NO) as control by right atrial stimulation (parasinusal site) in consecutive steps of 110, 130 and 150 b.p.m., each step lasting for 5 min. Both before and during stimulation at each pacing rate (after 5 min) RAP and systolic blood pressure (SBP) were measured and blood was drawn from the right atrium for ANP measurements (radioimmunoassay method). During stimulation we observed significant differences in the ANP release in comparison to the initial values: at 130 (p less than 0.05) and at 150 b.p.m. (p less than 0.01) in EH; at 150 b.p.m. (p less than 0.005) in NO. RAP and SBP did not differ significantly at each pacing rate from initial values both in EH and NO. No significant differences in ANP and RAP were found between EH and NO. IN CONCLUSION: (a) ANP release increases in both EH and NO, even if beginning at 130 in EH and at 150 b.p.m. in NO; (b) in both EH and NO, there is no relationship between RAP or SBP values and ANP secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗

PubMed1999

Promotion of atrial fibrillation by heart failure in dogs: atrial remodeling of a different sort.

BACKGROUND: Studies of atrial fibrillation (AF) due to atrial tachycardia have provided insights into the remodeling mechanisms by which "AF begets AF" but have not elucidated the substrate that initially supports AF before remodeling occurs. We studied the effects of congestive heart failure (CHF), an entity strongly associated with clinical AF, on atrial electrophysiology in the dog and compared the results with those in dogs subjected to rapid atrial pacing (RAP; 400 bpm) with a controlled ventricular rate (AV block plus ventricular pacemaker at 80 bpm). METHODS AND RESULTS: CHF induced by 5 weeks of rapid ventricular pacing (220 to 240 bpm) increased the duration of AF induced by burst pacing (from 8+/-4 seconds in control dogs to 535+/-82 seconds; P<0.01), similar to the effect of 1 week of RAP (713+/-300 seconds). In contrast to RAP, CHF did not alter atrial refractory period, refractoriness heterogeneity, or conduction velocity at a cycle length of 360 ms; however, CHF dogs had a substantial increase in the heterogeneity of conduction during atrial pacing (heterogeneity index in CHF dogs, 2. 76+/-0.16 versus 1.46+/-0.10 for control and 1.51+/-0.06 for RAP dogs; P<0.01) owing to discrete regions of slow conduction. Histological examination revealed extensive interstitial fibrosis (connective tissue occupying 12.8+/-1.9% of the cross-sectional area) in CHF dogs compared with control (0.8+/-0.3%) and RAP (0. 9+/-0.2%) dogs. CONCLUSIONS: Experimental CHF strongly promotes the induction of sustained AF by causing interstitial fibrosis that interferes with local conduction. The substrates of AF in CHF are very different from those of atrial tachycardia-related AF, with important potential implications for understanding, treating, and preventing AF related to CHF.

Animals↗

PubMed1994

Blockade of distal nephron sodium transport attenuates pressure natriuresis in dogs.

The sodium excretory responses (UNaV) to acute changes in renal arterial pressure (RAP) during blockade of distal nephron sodium transport were evaluated in seven sodium-replete anesthetized dogs. The major distal sodium entry pathways were blocked by intrarenal infusion of amiloride (AM, 10(-5) mol/L) and bendroflumethiazide (BZ, 10(-6) mol/L). Infusion of AM plus BZ caused slight increases in renal blood flow (RBF, 4.1 +/- 0.5 to 4.6 +/- 0.4 mL.min-1.g-1; P < .001) but no changes in glomerular filtration rate (GFR, 0.96 +/- 0.05 to 1.01 +/- 0.07 mL.min-1.g-1; P = NS) or autoregulatory efficiency of RBF and GFR. There were significant increases in UNaV (2.7 +/- 0.7 to 5.2 +/- 0.6 mumol.min-1.g-1) and fractional excretion of sodium (FENa, 1.8 +/- 0.4% to 3.5 +/- 0.3%) and decreases in potassium excretion (0.59 +/- 0.10 to 0.35 +/- 0.06 mumol.min-1.g-1) during AM plus BZ infusion. During the control period and during repeat measurements in time control studies, decreases in RAP (150 to 100 mm Hg) elicited the usual decreases in UNaV (slope, 0.022 +/- 0.007 mumol.min-1.g-1.mm Hg-1; P < .01). After administration of AM plus BZ, there was a marked attenuation of the pressure-natriuretic responses, and the slopes of the RAP versus UNaV and RAP versus FENa relations at RAP levels above 100 mm Hg were not significantly different from zero. However, the pressure-natriuresis response was maintained at arterial pressure between 75 and 100 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗

PubMed1995

Relation between pressure natriuresis and urinary excretion of nitrate/nitrite in anesthetized dogs.

Alterations in intrarenal nitric oxide (NO) formation during changes in renal arterial pressure (RAP) have been suggested as a mechanism mediating pressure natriuresis. To test this hypothesis further, we examined the relation between RAP and the urinary excretion rate of nitrate/nitrite (NO3-/NO2-; NO metabolites) in anesthetized sodium-replete dogs before (n = 9) and during (n = 6) intrarenal infusion of the NO synthesis inhibitor nitro-L-arginine (NLA; 50 micrograms.kg-1.min-1). Urinary NO3-/NO2- concentrations were measured with the Griess reaction and spectrophotometry methods after enzymatic reduction of NO3- to NO2- in the samples. During control conditions, there were decreases in the urinary NO3-/NO2- excretion rate in response to reductions in RAP (150 to 75 mm Hg; slope, 0.04 +/- 0.01 nmol.min-1.g-1.mm Hg-1) in association with decreases in urinary sodium excretion (UNaV). There was a positive correlation between changes in NO3-/NO2- excretion rate and changes in RAP (r = .48; P < .005) or UNaV (r = .59; P < .001). NLA infusion resulted in decreases in NO3-/NO2- excretion rate (4.8 +/- 1.4 to 1.0 +/- 0.3 nmol.min-1.g-1) in association with reductions in UNaV (4.3 +/- 0.3 to 0.7 +/- 0.2 microL.min-1.g-1), fractional excretion of sodium (2.9 +/- 0.2% to 0.5 +/- 0.1%), and renal blood flow (4.8 +/- 0.3 to 3.3 +/- 0.2 mL.min-1.g-1), without changes in glomerular filtration rate. Furthermore, there was a marked attenuation of the NO3-/NO2- and sodium excretory responses to alterations in RAP during NO synthesis inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗

PubMed1999

Impeded alveolar-capillary gas transfer with saline infusion in heart failure.

The microvascular pulmonary endothelium barrier is critical in preventing interstitial fluid overflow and deterioration in gas diffusion. The role of endothelium in transporting small solutes in pathological conditions, such as congestive heart failure (CHF), has not been studied. Monitoring of pulmonary gas transfer during saline infusion in CHF was used to probe this issue. Carbon monoxide diffusion (DL(CO)), its membrane diffusion (D(M)) and capillary blood volume (V(C)) subcomponents, and mean right atrial (rap) and mean pulmonary wedge (wpp) pressures after saline or 5% D-glucose solution infusions were compared with baseline in 26 moderate CHF patients. Saline was also tested in 13 healthy controls. In patients, 750 mL of saline lowered DL(CO) (-8%, P<0.01 versus baseline), D(M) (-10%, P<0.01 versus baseline), aldosterone (-29%, P<0.01 versus baseline), renin (-52%, P<0.01 versus baseline), and hematocrit (-6%, P<0.05 versus baseline) and increased V(C) (20%, P<0.01 versus baseline), without changing rap and wpp. Saline at 150 mL produced qualitatively similar results regarding DL(CO) (-5%, P<0.01 versus baseline), D(M) (-7%, P<0.01 versus baseline), V(C) (9%, P<0.01 versus baseline), rap, wpp, aldosterone (-9%, P<0.05 versus baseline), and renin (-14%, P<0.05 versus baseline). Glucose solution (750 mL), on the contrary, increased DL(CO) (5%, P<0.01 versus 750 mL of saline) and D(M) (11%, P<0.01 versus 750 mL of saline) and decreased V(C) (-9, P<0.01 versus 750 mL of saline); aldosterone (-40%), renin (-41%), hematocrit (-3%), rap, and wpp behaved as they did after saline infusion. In controls, responses to both saline amounts were similar to responses in CHF patients regarding aldosterone, renin, hematocrit, rap, and wpp, whereas DL(CO), D(M), and V(C) values tended to rise. Hindrance to gas transfer (reduced DL(CO) and D(M)) with salt infusion in CHF, despite an increase in V(C) and no variations in pulmonary hydrostatic forces, indicates an upregulation in sodium transport from blood to interstitium with interstitial edema. Redistribution of blood from the lungs, facilitating interstitial fluid reabsorption, or sodium uptake from the alveolar lumen by the sodium-glucose cotransport system might underlie the improved alveolar-capillary conductance with glucose.

Aldosterone↗

PubMed1980

Importance of efferent arteriolar vascular tone in regulation of proximal tubule fluid reabsorption and glomerulotubular balance in the rat.

Micropuncture study was performed in 21 mildly volume-expanded Munich-Wistar rats before and during partial aortic constriction to examine the effects of endogenous prostaglandins (PG) and angiotensin II (AII) on single nephron glomerular filtration rate (SNGFR) and absolute proximal reabsorption rate (APR). Animals received either vehicle (group 1), indomethacin (group 2), or indomethacin plus saralasin (group 3). Before aortic constriction, these inhibitors were without effect on values of SNGFR and APR. In group 1 rats, reduction in mean renal arterial perfusion pressure (RAP) to approximately 65 mm Hg resulted in marked and proportional declines in SNGFR and APR. With equivalent reduction in RAP in group 2 rats, however, SNGFR fell to a lesser extent and APR tended to increase slightly above preconstriction values. Indomethacin administration was therefore associated with disruption of glomerulotubular balance. In view of the roughly equivalent declines in afferent arteriolar resistance measured in groups 1 and 2, the magnitude of increase in efferent arteriolar resistance (R(E)) appeared to be of major importance in determining the observed presence or absence of glomerulotubular balance. Thus, the lesser fall in SNGFR in group 2 than in group 1 was a result of the higher value for glomerular capillary hydraulic pressure in group 2, a consequence of the higher value of R(E). The higher average value for APR during reduced RAP in group 2 than in group 1 is also attributable to this pronounced rise in R(E), the effect of which was to augment the net reabsorptive pressure both by favoring higher postglomerular oncotic pressure and lower downstream (peritubular capillary) hydraulic pressure. Since intrarenal release of AII is enhanced when RAP declines, and because AII is known to raise R(E) selectively, it is likely that endogenous AII brought about the marked increase in R(E) in group 2, which was readily demonstrable only in indomethacin-treated rats, presumably because endogenous PG synthesis was suppressed. In keeping with this conclusion, when the action of endogenous AII was inhibited by saralasin in group 3 rats, reduction in RAP failed to induce a rise in R(E), so that net filtration and reabsorption pressures again declined proportionally, as did SNGFR and APR. The present evidence therefore suggests that glomerulotubular balance is influenced to an important extent by the prevailing vasomotor tone of the efferent arteriole.

Animals↗

PubMedDate not supplied

Combined surgical ablation and intravitreal triamcinolone acetonide for retinal angiomatous proliferation.

PURPOSE: Neovascular age-related macular degeneration (ARMD) with retinal angiomatous proliferation (RAP) has a poor natural history and the efficacy of any treatment has not yet been established. The authors describe a combined surgical treatment. METHODS: A 76-year-old woman presented with a best-corrected visual acuity (BCVA) of 20/600 in the right eye and macula with stage 3 RAP as identified by fluorescein angiography (FA), indocyanine green angiography (ICGA), and optical coherence tomography (OCT). After a standard three-port pars plana core vitrectomy (PPV), endodiathermy of the arteriolar and venous feeder vessels of each lesion was performed, intraretinal RAP feeder vessels were cut with manual vertical intraocular scissors, and 0.1 mL of triamcinolone acetonide (TAAC) was injected intravitreally. At 1 and 4 weeks and at the sixth month, the patient underwent a complete eye examination, FA, ICGA, and OCT to assess outcomes and complications. RESULTS: Six months later, BCVA was stable at 20/300, intraocular pressure was 15 mmHg, anterior segment and vitreous cavity were clear without evidence of TAAC granules, and retina was attached. FA and ICGA showed a complete occlusion of the RAP and absence of leakage or ischemia and OCT demonstrated decreased macular thickness with resolution of both intraretinal edema and pigment epithelium detachment, and the restoration of the normal macular profile. At the end of follow-up, the authors did not observe any ocular or systemic complication. CONCLUSIONS: Surgical approach to RAP stage 3 with intravitreal injection of 4 mg of TAAC was safe and anatomically effective.

Aged↗