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PubMed1997

The mechanism of the initial natriuresis after transjugular intrahepatic portosystemic shunt.

BACKGROUND & AIMS: The pathogenesis of the delayed natriuresis after transjugular intrahepatic portosystemic shunt (TIPS) insertion is unknown. This was studied to elucidate the mechanism involved. METHODS: In 12 patients with cirrhosis and refractory ascites after TIPS, systemic and renal hemodynamics, renal sodium handling, central blood volume, neurohumoral factors, and hepatic function were studied weekly after the shunt with the patients receiving a diet of 20 mmol sodium/day. RESULTS: Two weeks after TIPS, the initial natriuresis (4 +/- 1 to 18 +/- 3 mmol/day; P < 0.05) was associated with significant reductions in corrected sinusoidal pressure (24.4 +/- 1.8 to 7.5 +/- 0.4 mm Hg; P < 0.001), proximal renal tubular reabsorption of sodium (P = 0.05), and renin-angiotensin-aldosterone activity (P < 0.05), but with significant systemic vasodilatation (P < 0.05). At 4 weeks, negative sodium balance was achieved (52 +/- 21 mmol/day; P < 0.01), despite continued systemic arterial vasodilatation, associated with significant increases in total central and cardiac volumes (P < 0.05) and normalization of serum aldosterone levels (P < 0.01). Four late responders were significantly older (P = 0.01) and had significantly lower baseline glomerular filtration rates (P = 0.02). CONCLUSIONS: In cirrhosis, sinusoidal portal hypertension and an activated renin-angiotensin-aldosterone system seem to be important in the pathogenesis of sodium retention. Systemic vasodilatation without arterial underfilling does not prevent natriuresis. Delayed natriuresis after TIPS is associated with increasing age and pre-TIPS renal impairment.

Adult↗
PubMed2006

Polynocturia in chronic kidney disease is related to natriuresis rather than to water diuresis.

BACKGROUND: Nocturnal polyuria has been well known in renal insufficiency. Recently, we found that as renal function deteriorated in chronic kidney disease (CKD), natriuresis was enhanced during the night with nocturnal blood pressure elevation. In the present study, we investigated whether nocturnal polyuria in CKD was due to the inability to concentrate urine, as previously proposed, or based on osmotic diuresis mainly by natriuresis. METHODS: In 27 CKD patients, circadian rhythms of urinary sodium, potassium, urea and osmolar excretion rates (U(Na)V, U(K)V, U(urea)V, U(osm)V) as well as of urinary volume (V) and free-water clearance (C(H(2)O)) were estimated during both daytime (6:00 to 21:00) and nighttime (21:00 to 6:00). Then, the night/day ratios of these parameters were analysed in relation to creatinine clearance (C(cr)) as a marker of glomerular filtration rate. RESULTS: C(cr) had significantly negative relationships with night/day ratios of V (R = -0.69; P < 0.0001), U(osm)V (R = -0.54; P = 0.004) and U(Na)V (R = -0.63; P = 0.0005), but no correlation with night/day ratios of C(H(2)O) (R = -0.33; P = 0.1), U(K)V (R = -0.29; P = 0.1) or U(urea)V (R = -0.31; P = 0.1). Linear and multiple regression analysis identified nocturnal natriuresis rather than urea excretion as an independent determinant of nocturia. CONCLUSION: As renal function deteriorated, nocturnal polyuria was seen, being consistent with classical recognition. Furthermore, this increase in nocturnal urine volume seemed related to osmotic diuresis mainly by natriuresis rather than to water diuresis or urea excretion.

Blood Pressure↗
PubMed1987

Dopamine blockade abolishes the exaggerated natriuresis of essential hypertension.

We studied natriuresis during central hypervolaemia by immersing eight normal subjects and eight patients with uncomplicated essential hypertension up to the neck in water, either in the absence (study 1) or presence (study 2) of dopamine blockade by metoclopramide. Water immersion without metoclopramide induced an exaggerated natriuresis in hypertensives compared with normotensives (P less than 0.001). This occurred in the presence of identical hormonal (plasma renin activity, plasma aldosterone and prolactin), renal (creatinine clearance) and pressor responses in both groups (study 1). The marked natriuresis seen during water immersion alone in normotensives was significantly blunted (P less than 0.02) but not abolished during water immersion with addition of metoclopramide. On the other hand, the exaggerated natriuresis found in hypertensives during water immersion alone was completely abolished during water immersion plus dopamine blockade by metoclopramide (study 2). Similar hormonal, renal and pressor changes were detected in both normotensive and hypertensive subjects during water immersion plus metoclopramide administration. Our data demonstrate that metoclopramide abolishes the exaggerated natriuretic response seen in hypertensives during volume expansion produced by water immersion, and suggest that dopamine may play a critical role in mediating the hypernatriuresis of essential hypertension.

Adult↗
PubMed1997

Implications of the linear pressure-natriuresis relationship and importance of sodium sensitivity in hypertension.

Although the concept of the pressure-natriuresis curve is very clear, considerable confusion concerning its importance and utility in understanding the pathophysiology of hypertension persists. We recently showed that the pressure-natriuresis curve could be considered linear. In this brief review, we would like to stress the advantages of treating it as a line. Its linear approximation simplifies understanding of the sodium sensitivity of the blood pressure and mechanisms of hypertension. The blood pressure can be expressed as the sum of two components: the non-sodium-sensitive component determined by the x intercept of the pressure-natriuresis curve and the sodium sensitive one determined by the product of the reciprocal of the slope and the amount of sodium intake. Theoretically, it can be affected in two different ways to cause hypertension; either a parallel shift along the blood pressure axis toward a higher blood pressure level due to the increase in the x intercept or a decrease in the slope. The parallel shift induces non-sodium-sensitive hypertension, whereas the decrease in slope induces sodium-sensitive hypertension. Thus, the linear approximation makes the definition of the sodium sensitivity of the blood pressure very clear and, furthermore, suggests that mechanisms of hypertension can be clarified if the determinants of the x intercept and the slope of the pressure-natriuresis curve are known. A clear definition of sodium sensitivity allows us to study its importance as a marker of a greater risk of renal and cardiovascular complications.

Animals↗
PubMed1988

Dose-dependent effects of felodipine on diuresis and natriuresis in healthy subjects.

We compared the effects of various acute doses of felodipine and placebo on diuresis and natriuresis in healthy men. The subjects were given felodipine, 1 and 3 mg as an intravenous infusion, and 5, 15, and 40 mg as an oral solution on 5 separate days. On each day blood pressure and heart rate were recorded and urine was collected for analysis of volume and sodium for 24 h. Felodipine induced a dose-dependent increase in heart rate and a dose-dependent decrease in diastolic blood pressure. These effects were maximal within 30 min of drug administration. Felodipine induced a maximal increase in diuresis of about 150% compared with placebo and a maximal increase in natriuresis of about 240%. The renal effects were most pronounced during the first 4 h after dose intake. During the 8-24 h interval, diuresis and natriuresis were lower than after placebo, but when the whole 24-h period was considered, no significant differences were found between felodipine and placebo in regard to sodium and water excretion. The most pronounced effects on diuresis and natriuresis were seen after moderate doses (3 mg i.v. and 15 mg orally). The response to the highest dose (40 mg orally) was somewhat less probably due to the excessive drop in diastolic blood pressure.

Adult↗
PubMed1997

Validation study of a central venous pressure-based protocol for the management of neurosurgical patients with hyponatremia and natriuresis.

OBJECTIVE: We had previously suggested a protocol for the management of neurosurgical patients with hyponatremia and natriuresis that was based on their volume status as determined by actual blood volume measurements. All patients in that study were found to be hypovolemic or normovolemic and responded, within 72 hours, to salt and fluid replacement. In the present study, the validity of that protocol was tested using central venous pressure as the sole measure of volume status of patients with hyponatremia and natriuresis. METHOD: Twenty-five consecutive patients (26 cases) who fulfilled the inclusion criteria typically used to diagnose the syndrome of inappropriate secretion of antidiuretic hormone were included in the study. Central venous pressure was used to classify patients as hypovolemic (< 5 cm of water), normovolemic (6-10 cm of water), or hypervolemic (> 11 cm of water). Hypovolemic patients were given fluids (50 ml/kg/d) and salt (12 g/d). Normovolemic patients were given normal fluid with 12 g of salt per day. In addition, patients with anemia (hematocrit, < 27%) were administered whole blood. The end point was a serum sodium of more than or equal to 130 mEq/L measured in two consecutive samples 12 hours apart or 72 hours after entry into the study. If the serum sodium was less than 130 mEq/L at the end of 72 hours, the clinical condition of the patient determined further management. RESULTS: Nineteen of 25 patients (26 cases) were hypovolemic, the rest were normovolemic. No patient was hypervolemic. Nineteen of 25 patients (26 cases) attained normal serum sodium values within 72 hours, and an additional 3 responded within the next 36 hours (108 h after entry into the study). One patient who was discharged on request had normalized her serum sodium a week later. Among the three nonresponders, who were severely hypovolemic, as revealed by blood volume measurement, and responded to increased fluid and salt administration. One was normovolemic and responded to increased salt administration. There were no complications related to the therapy. CONCLUSION: Hyponatremia with natriuresis in the neurosurgical setting responds to salt and fluid replacement guided by the patients' volume status as determined by the central venous pressure. This study also offers further indirect evidence to suggest that the syndrome of hyponatremia with natriuresis is most often caused by "cerebral salt wasting" rather than by the syndrome of inappropriate secretion of antidiuretic hormone.

Adolescent↗
PubMed1977

Influence of glucagon on natriuresis and glucose-induced sodium retention in the fasting obese subject.

The role which glucagon could play in the mechanism of fasting natriuresis and renal sodium retention associated with carbohydrate refeeding was studied in thirty-seven non-diabetic obese subjects. In nine obese subjects undergoing a 7 day fast without any additional treatment (control group), the renal sodium excretion exceeded intake through the whole experimental period, with maximal natriuresis on day 2 of the fast. Blood glucose and plasma insulin (IRI) levels fell rapidly from the first day of fast on, while pancreatic glucagon (IRG) titres rose from day 1 to day 4, declining slightly thereafter. When additional subjects received intravenous glucose on day 4 (n = 6), there was a rise in blood glucose concentration and in IRI associated with a rapid drop in IRG restricted to the period of glucose infusion. The resulting antinatriuresis occurred essentially during the following 36 h, while IRG and IRI levels had returned to fasting levels. A comparable glucose load on day 4 associated with 0.1 mg glucagon (n = 5) still led to the glucose-induced antinatriuresis while 1 mg glucagon added to a similar glucose infusion completely abolished its antinatriuretic effect (n = 6). Glucagon infused alone on day 4 of fast aggravated fasting natriuresis (n = 5) but was devoid of this effect when administered 24 h after the glucose load (n = 6). These data indicate that fasting hyperglucagonaemia or its reduction upon glucose refeeding, cannot be considered as directly involved in renal mechanism(s) responsible for fasting natriuresis of antinatriuretic effects of carbohydrate. It is suggested that the role of glucagon is indirect, possibly through its influence on ketogenesis which in turn may alter renal sodium handling.

Adult↗
PubMed2004

Guanylin and uroguanylin induce natriuresis in mice lacking guanylyl cyclase-C receptor.

BACKGROUND: Guanylin (GN) and uroguanylin (UGN) are intestinally derived peptide hormones that are similar in structure and activity to the diarrhea-causing Escherichia coli heat-stable enterotoxins (STa). These secretagogues have been shown to affect fluid, Na+, K+, and Cl- transport in both the intestine and kidney, presumably by intracellular cyclic guanosine monophosphate (cGMP)-dependent signal transduction. However, the in vivo consequences of GN, UGN, and STa on renal function and their mechanism of action have yet to be rigorously tested. METHODS: We hypothesized that intravenous administration of GN, UGN, or STa would cause an increase in natriuresis in wild-type mice via cGMP and guanylyl cyclase-C (GC-C, Gucy2c), the only known receptor for these peptide-hormones, and that the peptide-induced natriuresis would be blunted in genetically altered mice devoid of GC-C receptors (GC-C(-/-) null). RESULTS: In wild-type mice using a modified renal clearance model, GN, UGN, and STa elicited significant natriuresis, kaliuresis, and diuresis as well as increased urinary cGMP levels in a time- and dose-dependent fashion. Absolute and fractional urinary sodium excretion levels were greatest approximately 40 minutes following a bolus infusion with pharmacologic doses of these peptides. Unexpectedly, GC-C(-/-) null mice also responded to the GN peptides similarly to that observed in wild-type mice. Glomerular filtration rate (GFR), blood pressure, and plasma cGMP in the mice (wild-type or GC-C(-/-) null) did not significantly vary between the vehicle- and peptide-treatment groups. The effects of UGN may also influence long-term renal function due to down-regulation of the Na+/K+ ATPase gamma-subunit and the Cl- channel ClC-K2 by 60% and 75%, respectively, as assessed by differential display polymerase chain reaction (PCR) (DD-PCR) and Northern blot analysis of kidney mRNA from mice treated with UGN. CONCLUSION: GN, UGN, and STa act on the mouse kidney, in part, through a cGMP-dependent, GC-C-independent mechanism, causing significant natriuresis by renal tubular processes. UGN may have further long-term effects on the kidney by altering the expression of such transport-associated proteins as Na+/K+ ATPase and ClC-K2.

Animals↗
PubMed2004

Nocturnal blood pressure is elevated with natriuresis and proteinuria as renal function deteriorates in nephropathy.

BACKGROUND: We reported that patients with sodium sensitive type of hypertension exhibited the lack of nocturnal fall in blood pressure with enhanced natriuresis during night. Sodium sensitivity is caused by diminished glomerular filtration capability and/or augmented tubular reabsorption of sodium, and seems tightly linked with glomerular capillary hypertension. In the present study, we investigated the relationship between glomerular filtration rate and circadian rhythms of these parameters in patients with glomerulopathy. METHODS: Twenty six patients (15 men and 11 women; aged 17 to 72 years; mean age 47 +/- 3 years), whose diagnosis was confirmed as glomerulopathy with renal biopsy, were studied during hospitalization. Ambulatory blood pressure for 24 hours was monitored, while urinary samples were collected for both daytime (6:00 a.m. to 9:00 p.m.) and nighttime (9:00 p.m. to 6:00 a.m.) to estimate circadian rhythms of urinary sodium and protein excretion rates (UNaV, UproV). Then night/day ratios of mean arterial blood pressure (MAP), UNaV, and UproV were analyzed in relation to 24-hour creatinine clearance as a marker of glomerular filtration rate. RESULTS: Serum creatinine and creatinine clearance were 1.1 +/- 0.1 mg/dL and 89 +/- 7 mL/min/1.73 m2. There were significant day-night differences in MAP (96 +/- 2 mm Hg vs. 92 +/- 2 mm Hg; P= 0.006), UNaV (6.7 +/- 0.9 mmol/hour vs. 3.6 +/- 0.3 mmol/hour; P= 0.003), and UproV (161 +/- 27 mg/hour vs. 128 +/- 28 mg/hour; P= 0.02). Creatinine clearance had significantly negative relationships with night/day ratios of MAP (r=-0.49; P= 0.01), UNaV (r=-0.43; P= 0.03,) and UproV (r=-0.41; P= 0.04). In addition, night/day ratio of MAP had significantly positive relationships with night/day ratios of UNaV (r= 0.49; P= 0.01) and UproV (r= 0.45; P= 0.02). CONCLUSION: Our results show that as renal function deteriorates in glomerulopathy the nocturnal dip in blood pressure is lost, resulting in enhanced urinary sodium and protein excretions during night. These findings are compatible with our proposal that impaired natriuresis during daytime makes nocturnal blood pressure elevated to compensate for diminished natriuresis by pressure natriuresis. We speculate that nocturnal glomerular capillary hypertension contributes, at least in part, to enhanced urinary sodium and protein excretions during night.

Adult↗
PubMed1995

Responses to reduced water intake, including dehydration natriuresis, in sheep excreting sodium predominantly in urine or in faeces.

Sheep which were predominantly urinary excretors (U) or faecal excretors (F) of sodium were exposed to a 75% reduction of water intake for 72 h. The experiment was performed on moderate, low or high sodium intakes (0.4, 0.05 or 1.2 mmol kg-1 day-1) to test the hypothesis that dehydration natriuresis was not a cause of sodium depletion but a defence against hypernatraemia. Dehydration caused elevation of plasma sodium concentration, osmolality, antidiuretic hormone (ADH) and oxytocin but, as in other experiments, a fall in haematocrit. The two higher levels of sodium intake were associated with dehydration natriuresis but also a smaller increase in faecal sodium excretion in both U and F sheep. On low sodium intake, however, neither urinary nor faecal sodium excretion increased in either group of sheep although the rise in plasma sodium concentration caused by dehydration was similar. Thus, when there is a risk of sodium depletion, due to low sodium intake, dehydration natriuresis does not occur, consistent with the hypothesis. Active sodium transport inhibitor (ASTI) and atrial natriuretic peptide (ANP) fell rather than rose during dehydration. Since aldosterone is suppressed by the higher levels of sodium intake, none of these hormones is likely to mediate dehydration natriuresis in sheep. F sheep showed more effective renal and faecal water conservation when dehydrated. During water restriction, the urinary potassium excretion of U sheep was significantly reduced, unlike that of F sheep; moreover, the latter maintained an identical plasma potassium concentration between baseline and restriction period, whereas in U sheep it was 0.3 mmol l-1 higher during water restriction. Increased drinking rather than reduced urine output was the basis of rehydration when ad lib. water intake was restored.

Animals↗
PubMed1996

Neuropeptide Y-enhanced diuresis and natriuresis in anaesthetized rats is independent of renal blood flow reduction.

1. Neuropeptide Y (NPY) has been reported to enhance diuresis and natriuresis in anaesthetized rats although it is a potent renal vasoconstrictor in vitro in vivo in several species. Therefore, we have investigated anaesthetized rats to see whether reduction in renal blood flow (RBF) and enhancement of diuresis and natriuresis can occur concomitantly, and how diuresis and natriuresis might be enhanced despite reduced RBF. 2. Systemic or intrarenal NPY infusion (0.03-3 micrograms kg-1 min-1) had only a small effect on mean arterial pressure (maximal increase 15-20 mmHg) and heart rate (maximal decrease 30 beats min-1) but dose-dependently reduced RBF (maximal peak reduction 3 ml min-1) Endogenous creatinine clearance was not significantly altered. 3. In anaesthetized rats systemic infusion of 1 or 3 micrograms kg-1 min-1 NPY enhanced urine formation and sodium and calcium excretion by a maximum of 110, 110 and 45%, respectively, but did not alter potassium excretion. Enhancement of diuresis was also detectable in conscious rats. 4. The diuretic and natriuretic effects of systemically infused NPY were at least partly maintained in rats with decapsulated kidneys and in rats where NPY-induced increase of renal perfusion pressure was excluded mechanically by an adjustable clamp placed on the abdominal aorta. 5. Intrarenal infusion of 0.3 or 1 microgram kg-1 min-1 NPY reduced RBF to a greater extent than systemic infusion (maximal peak reduction 4 ml min-1) but caused a smaller enhancement or even a reduction of urine formation and sodium excretion. 6. We conclude that systemic infusion of NPY reduces RBF by a direct effect on the renal vasculature. Systemic NPY infusion enhances urine formation and sodium and calcium excretion. This occurs independently (at least in part) of pressure natriuresis by formation and/or release of an extrarenal factor which might act on distal tubules and/or collecting ducts.

Anesthesia, General↗
PubMed1976

Propranolol induces acute natriuresis by beta blockade and dopaminergic stimulation.

dl-Propranolol (0.8-1.6 mg/kg - h for 1 h) produced a transient two- to three-fold increase in sodium excretion in nondiuretic rats infused with Pitressin and aldosterone and in water diuretic rats. Sodium excretion increased more in rats depleted of renin by chronic Doca and salt administration than in rats maintained on a low salt diet. An angiotensin inhibitor (1,sarcosine-8,valine angiotensin II) decreased sodium excretion. Therefore the natriuresis was not mediated by antidiuretic hormone, aldosterone, or renin-angiotensin. d-Propranolol did not produce a natriuresis. Prior treatment with phenoxybenzamine did not prevent the natriuretic response but chlorisondamine pretreatment did. The natriuresis is produced by beta blockade and requires post ganglionic nerve function but is independent of alpha receptors. dl-Propranolol decreased heart rate and cardiac output but systemic pressure did not fall and renal blood flow increased. This suggests a dopamine-mediated renal vasodilation and natriuresis. Haloperidol and pimozide, both dopamine blocking agents with minimal beta blocking effects, prevented the natriuretic response. We conclude that propranolol may increase sodium excretion directly by blocking beta receptors in the distal nephron and indirectly by dopamine-mediated renal vasodilation.

Adrenergic beta-Antagonists↗
PubMed2002

Angiotensin II attenuates the natriuresis of water immersion in humans.

The hypothesis was tested that suppression of generation of ANG II is one of the mechanisms of the water immersion (WI)-induced natriuresis in humans. In one protocol, eight healthy young males were subjected to 3 h of 1) WI (WI + placebo), 2) WI combined with ANG II infusion of 0.5 ng. kg(-1). min(-1) (WI + ANG II-low), and 3) a seated time control (Con). In another almost identical protocol, 7-10 healthy young males were investigated to delineate the tubular site(s) of action of ANG II by the lithium clearance method (C(Li)) and were on an additional fourth study day subjected to infusion of ANG II at a rate of 1.5 ng. kg(-1). min(-1) (WI + ANG II-high). During WI + placebo, plasma concentration of ANG II decreased from 16 +/- 2 to 8 +/- 1 pg/ml (P < 0.05) and renal sodium excretion increased from 104 +/- 15 to 294 +/- 27 micromol/min (P < 0.05). During WI + ANG II-low, plasma ANG II was not suppressed by WI, and the natriuresis was blunted by 52 +/- 13% (P < 0.05). During WI + ANG II-low and WI + ANG II-high, an increase in C(Li) was prevented that was otherwise observed during WI, and fractional distal reabsorption of sodium was facilitated. In conclusion, maintaining plasma concentration of ANG II unchanged at the level of control attenuates the natriuresis of WI considerably in humans. Therefore, suppression of generation of ANG II is an important mechanism of the natriuresis of WI in humans. Furthermore, infusion of ANG II during WI prevents an otherwise induced increase in C(Li) and facilitates the fractional distal reabsorption of sodium, probably via an effect on aldosterone release.

Adult↗
PubMed1989

Atrial natriuretic peptide and pressure natriuresis: interactions with the renin-angiotensin system.

The aim of this study was to quantitate the effects of increases in atrial natriuretic peptide (ANP), within the pathophysiological range, on the acute pressure natriuresis mechanism and the role of the renin-angiotensin system (RAS) in modulating these effects. Renal hemodynamics and electrolyte excretion were measured in anesthetized dogs while renal perfusion pressure (RPP) was controlled at three levels (120-122, 100, and 75 mmHg) with and without intrarenal infusion of ANP at 5 ng.kg-1.min-1. Sodium excretion was significantly higher during ANP infusion at RPP of 122 +/- 3 mmHg, averaging 55.8 +/- 13.7 during control and 113.3 +/- 23.3 mueq/min during ANP infusion. AT RPP of 101 +/- 1 mmHg, sodium excretion was 51.8 +/- 17.4 during control and 93.0 +/- 17.6 mueq/min during ANP infusion, but at RPP of 75 +/- 0 mmHg there was no difference in sodium excretion between control and ANP infusion. In a second set of dogs, angiotensin II (ANG II) formation was blocked with captopril (20 micrograms.kg-1.min-1), circulating (5 ng.kg-1.min-1), and the above protocol was repeated. When the RAS was fixed, the renal responses to ANP infusion were abolished, even at the higher pressure levels. These data indicate that ANP increases the slope of pressure natriuresis; at higher levels of RPP, ANP potentiates pressure natriuresis but not at lower pressures. In addition, part of this effect may be due to suppression of the RAS, because the ANP-induced shift in the pressure natriuresis relationship was abolished when circulating ANG II was maintained constant.

Animals↗
PubMed1992

Pressure natriuresis and angiotensin II in reduced kidney mass, salt-induced hypertension.

In normal subjects, high sodium intake causes little change in mean arterial pressure (MAP). However, MAP is sodium sensitive after reduction of kidney mass. The present study examined the role of increased renal artery pressure and decreased angiotensin II (ANG II) formation in maintaining sodium balance during high sodium intake in dogs with reduced kidney mass. In seven dogs with pressure natriuresis intact, increasing sodium intake from 36 to 466 meq/day for 7 days raised MAP from 91 +/- 2 to 106 +/- 2 mmHg. Sodium excretion increased promptly and cumulative sodium balance increased by only 80 +/- 26 meq after 7 days of high sodium intake. When renal perfusion pressure was servo-controlled to prevent pressure natriuresis, comparable increases in sodium intake raised MAP from 88 +/- 2 to 128 +/- 4 mmHg after 7 days. Sodium excretion rose to match intake, but cumulative sodium balance increased by 226 +/- 34 meq after 7 days. In dogs in which ANG II levels were held constant by converting enzyme inhibition and constant ANG II infusion (2 ng.kg-1.min-1 iv), raising sodium intake for 7 days elevated MAP from 126 +/- 2 to 146 +/- 4 mmHg after 7 days while increasing cumulative sodium balance by 212 +/- 29 meq. When renal perfusion pressure was servo-controlled and ANG II levels held constant, raising sodium intake elevated MAP from 125 +/- 3 to 166 +/- 11 mmHg and increased cumulative sodium balance by 399 +/- 128 meq. These data indicate that pressure natriuresis and decreased ANG II formation are important in minimizing sodium retention and hypertension during high sodium intake. However, other mechanisms can increase sodium excretion independent of pressure natriuresis and suppression of ANG II during salt-induced hypertension.

Angiotensin II↗
PubMed1992

Renal interstitial hydrostatic pressure during verapamil-induced natriuresis.

Infusion of calcium antagonists results in significant increases in sodium excretion, an effect that is exacerbated in hypertensive animals. The mechanism responsible for the increase in sodium excretion has not been elucidated. The purpose of this study was to determine the role of renal interstitial hydrostatic pressure (RIHP) in mediating increases in sodium excretion produced by the calcium antagonist verapamil. Changes in renal hemodynamics and electrolyte excretion were examined in response to an intrarenal infusion of verapamil (100 micrograms/min) in normal dogs and in dogs with angiotensin II-induced hypertension. Infusion of verapamil in normal dogs increased renal blood flow by 18% and had no effect on glomerular filtration rate. Renal vascular resistance and filtration fraction both decreased in response to verapamil. Absolute (5.1 +/- 2.3 to 176 +/- 45.8 mueq/min) and fractional excretion of sodium (0.21 +/- 0.13 to 7.36 +/- 3.12%) also increased significantly. Despite renal vasodilation, the natriuresis was not associated with significant increases in RIHP (6.4 +/- 0.9 to 5.8 +/- 0.9 mmHg). Infusion of verapamil into dogs with angiotensin II hypertension resulted in a natriuresis (4.2 +/- 1.6 to 338.7 +/- 78.3 mueq/min) that was much greater than under normal conditions. Although the renal vasodilation was significantly higher in the angiotensin II-hypertensive dogs, the enhanced natriuresis in these animals was not associated with increases in RIHP. The results of this study indicate that increases in RIHP are not responsible for the natriuresis produced by verapamil in normal or angiotensin II-hypertensive dogs.

Animals↗
PubMed1993

Cardiac-renal-neural reflex plays a major role in natriuresis induced by left atrial distension.

The role of cardiac-renal-neural reflex in the natriuresis induced by left atrial balloon inflation was investigated in conscious dogs. Female mongrel dogs were assigned randomly to 1) sham-operated (n = 8), 2) cardiac-denervated (n = 6), and 3) renal-denervated (n = 8) groups. The dogs were chronically instrumented with a bipolar stainless steel wire electrode for measurement of renal sympathetic nerve activity (RSNA). Balloon inflation induced a step increase in left atrial pressure (Pla) by 7.7 +/- 1.7 mmHg, a step decrease in RSNA (-66.6 +/- 5.5%), and concomitant increases in urine flow (441 +/- 142%), osmolal excretion (60 +/- 12%), and sodium excretion (300 +/- 69%) in sham-operated dogs. Renal denervation abolished the diuresis and natriuresis during balloon inflation. Chronic cardiac denervation abolished also the diuresis and natriuresis in the face of a similar increase in Pla. RSNA did not change significantly throughout the experimental period in cardiac-denervated dogs. It is concluded that a sustained reduction of RSNA originating from left atrial mechanoreceptors plays a major role in the natriuresis during left atrial distension in conscious dogs.

Animals↗
PubMed1994

Altered pressure natriuresis in chronic angiotensin II hypertension in rats.

Angiotensin II (ANG II; 10 or 30 ng/min iv) was infused for 7-10 days in unilaterally adrenalectomized and nephrectomized Sprague-Dawley rats drinking 1% NaCl. The acute pressure-natriuresis relationship was studied under Inactin anesthesia in volume-expanded rats with fixed neurohumoral influences on the remaining kidney. Renal interstitial hydrostatic pressure (RIHP) was measured using a catheter implanted into the renal cortex. Arterial blood pressure before laparotomy was 149 +/- 3 (SE) mmHg (n = 6) and 152 +/- 6 mmHg (n = 16) for ANG II-infused rats (10 and 30 ng/min, respectively) and 123 +/- 5 mmHg (n = 6) and 123 +/- 7 mmHg (n = 16) for the respective control rats. Compared with values in control rats, ANG II-infused rats had significantly (P < 0.05) lower urine flow and absolute and fractional sodium excretion at renal artery pressures of 115-150 mmHg. There were no significant differences between RIHP measured in control and ANG II-hypertensive rats. The shift in the pressure-diuresis, pressure-natriuresis, and pressure-fractional sodium excretion relationships was similar with both doses of ANG II and was reversed by the acute administration of losartan (10 mg/kg iv). In all groups of rats, renal blood flow was autoregulated, whereas glomerular filtration rate was not autoregulated in ANG II-infused rats and was significantly lower than that in control rats at the lower level of renal artery pressure. The data indicate that rats with ANG II-induced hypertension have a rightward shift of the pressure-natriuresis curve caused primarily by a decrease in fractional excretion of sodium. The lack of effect of chronic ANG II infusion on filtration fraction and RIHP suggests that the increased tubular reabsorption was due to a direct action of ANG II on renal tubules. The reversal of these effects by losartan suggests that the shift in the pressure-natriuresis curve in ANG II-induced hypertension is mediated by the AT1-receptor subtype.

Angiotensin II↗