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PubMed1979

Nonpressor mechanisms in CNS-induced natriuresis.

Ventriculocisternal perfusion was performed in pentobarbital-anesthetized dogs. Perfusion of high Na (300 mM NaCl) artificial cerebrospinal fluid (CSF) (E) for 2 h was preceded by 2 h of control (C) and was followed by 2 h of recovery (R) during which normal (150 mM NaCl) artificial CSF was perfused. A time-control group was perfused with normal artificial CSF throughout C, E, and R. High sodium perfusion resulted in a marked natriuresis in each of nine animals and suppression of plasma renin activity. Theere were no simultaneous changes in mean arterial pressure, glomerular filtration rate, or renal plasma flow. Sodium excretion and plasma renin activity showed a slight gradual rise in the time-control group, but no significant differences were observed between the C and E periods; sodium excretion and plasma renin activity were similar in the high Na and time-control groups during C and R, but significantly different during E. It is concluded that when CSF sodium is elevated by perfusing artificial CSF, the resulting natriuresis and suppression of plasma renin activity are not caused by hemodynamic changes.

Animals↗
PubMed1984

Efferent role of ADH in CNS-induced natriuresis.

Ventriculocisternal perfusion (VCP) of artificial cerebrospinal fluid (CSF) was performed in pentobarbital-anesthetized dogs. Renal function was studied in protocols consisting of a 1-h experimental period in which the animals received either CSF with an elevated sodium concentration (300 mM, high Na) via VCP or antidiuretic hormone (ADH) intravenously, bracketed by 1-h control and recovery periods. High Na VCP caused an increase in plasma ADH measured by radioimmunoassay (to 176% of control) that coincided with a natriuresis (to 180% of control). In a second set of experiments, these changes in endogenous ADH were mimicked experimentally with intravenous infusions of synthetic ADH in animals receiving continuous VCP with normal sodium artificial CSF. The dose-response relationship between log ADH and urinary sodium excretion for the intravenous ADH experiments was not different from the relationship for those experiments in which ADH was elevated as a consequence of high Na VCP. These results suggest that ADH causes part, if not all, the natriuresis induced by high Na VCP.

Animals↗
PubMed1984

Attenuated pressure natriuresis in the early phases of two-kidney Goldblatt hypertension.

We studied the effect of changing perfusion pressure on the excretory function of isolated perfused nonclipped kidneys from the two-kidney Goldblatt hypertensive rat ( GHR ). Kidneys were studied from newly hypertensive rats about 8 days after contralateral renal artery clipping [blood pressure (BP) 138 +/- 4.3 mmHg] and before onset of hypertension 3 days following surgery (BP 111 +/- 1.9 mmHg). In addition, nonclipped kidneys from adrenalectomized Goldblatt rats were also examined approximately 9 days following surgery (BP 114 +/- 4.7 mmHg). Kidneys from sham-operated rats served as controls. We noted no differences in GFR in kidneys from newly hypertensive rats and sham controls above a perfusion pressure of 120 mmHg. In response to increasing perfusing pressure, perfusate flow and fractional sodium excretion were significantly lower in newly hypertensive rats than in sham-operated controls. No differences in glomerular filtration rate, perfusate flow, or sodium excretion were noted in kidneys from sham-operated rats or Goldblatt rats 3 days following surgery. After clipping, adrenalectomized (ADX) Goldblatt rats had less of a rise in blood pressure than did rats with intact adrenal glands. No attenuation of natriuresis was noted in the ADX-clipped group in response to increasing perfusion pressure. Isolated perfused kidneys from ADX rats had greater sodium excretion at all levels of pressure than kidneys from rats with intact adrenal glands. Deoxycorticosterone acetate replacement returned sodium excretion to that approaching intact rats. We conclude that nonclipped kidneys of newly hypertensive Goldblatt rats exhibit blunted pressure natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1984

Pressure natriuresis during saline expansion in newborn and adult dogs.

Pressure natriuresis was studied in anesthetized saline-expanded adult (n = 10) and neonatal (n = 23) dogs. One group (protocol B) received ethacrynic acid and amiloride to block distal nephron function. Studies in the other group (protocol A) were done without diuretics. Renal arterial blood pressure was raised by bilateral carotid artery occlusion. Renal perfusion pressure was then lowered in steps by partially occluding the aorta proximal to the renal arteries. In protocol B carotid occlusion was associated with an increase in both absolute and fractional sodium excretion by adult and newborn dogs. Moreover, there was significant negative correlation (P less than 0.01) between absolute change in renal arterial pressure and change in tubular reabsorption of sodium per milliliter glomerular filtrate for both age groups. For each mmHg increase in blood pressure there was greater inhibition of sodium reabsorption in the puppy (0.55 mueq/ml glomerular filtrate) than in the adult (0.18 mueq/ml, P less than 0.05). In protocol A puppies, the inhibition of sodium reabsorption due to increases in renal perfusion pressure was less than that occurring in protocol B, indicating that some of the sodium escaping proximal nephron reabsorption was reabsorbed distally. Results of these studies indicate that during saline expansion pressure natriuresis is primarily a proximal tubular event, and the sensitivity of the proximal tubule to changes in renal arterial blood pressure is greater in the newborn than the adult kidney.

Aging↗
PubMed1984

Mechanism of furosemide-induced natriuresis by direct stimulation of renal prostaglandin E2.

Studies were conducted to investigate the interaction of renal prostaglandin E2 (PGE2) production and the renin-angiotensin system in the mechanism of furosemide-induced natriuresis. In conscious rabbits with permanent urinary bladder cannulation, furosemide in vivo (10 mg/kg) increased urinary water, sodium, and PGE2 excretion and plasma renin activity (PRA) over 50 min. Furosemide administered in vivo enhanced renal papillary but not cortical in vitro PGE2 biosynthesis. Prior administration of indomethacin at 2 mg/kg augmented the saluretic effect of furosemide, decreased its effect on UPGE2 V, abolished the rise in PRA, and reduced cortical but not papillary PGE2 biosynthesis. However, at 10 mg/kg, indomethacin reduced the saluretic effect of furosemide and eliminated the increase in UPGE2 V with continued suppression of PRA. Direct addition of furosemide in vitro to the incubation medium (10(-5) and 10(-3) M) markedly augmented papillary PGE2 synthesis. It is concluded that furosemide stimulates renal papillary PGE2 biosynthesis directly without mediation by angiotensin II, resulting in an increase in UPGE2 V, and the enhanced or inhibitory effect of indomethacin on furosemide-induced natriuresis is dose related and dependent on the degree of PGE2 synthesis inhibition in the presence of suppressed PRA, which occurred at all doses studied.

Angiotensin II↗
PubMed1985

Role of the pituitary in reflex natriuresis following acute unilateral nephrectomy.

We studied the role of altered pituitary function in the reflex natriuresis that occurs after acute unilateral nephrectomy (AUN). In normal rats, AUN increased both sodium (UNaV) and potassium excretion within 90 min. In hypophysectomized rats, no increase in cation excretion after AUN occurred, results which were duplicated in rats in which pituitary function was altered by prior treatment with dexamethasone (2 mg/kg ip for 3 days). In adrenalectomized rats, AUN led to increases in cation excretion similar to those seen in normal rats, indicating that intact adrenal function was not necessary for this excretory response following AUN. These changes in cation excretion were correlated with measurements in peripheral plasma of two peptides derived from the pituitary precursor molecule pro-opiomelanocortin (POMC). Radioimmunoassayable plasma beta-endorphin failed to change after AUN in any of the conditions studied. However, a sensitive radioimmunoassay for the N-terminal fragment (NTF) of POMC indicated that plasma NTF rose significantly after AUN in normal and adrenalectomized rats but did not change in hypophysectomized, steroid-pretreated, or shamoperated rats. The increase in NTF concentration correlated with the increase in UNaV after AUN. These results demonstrate that the reflex increase in cation excretion after AUN is dependent on an intact pituitary gland and is associated with an increase in peripheral plasma concentration of NTF. NTF, or some other peptide residing in the N-terminal portion of POMC, could promote the natriuresis after AUN; the importance of the pituitary gland in this response could be the secretion of this peptide.

Animals↗
PubMed1987

The contribution of atrial natriuretic factor to acute volume natriuresis in rats.

To explore the role of atrial natriuretic factor (ANF) in acute volume-expansion natriuresis, right atrial pressure (RAP), mean arterial pressure (MAP), rate of urinary sodium excretion (UNaV), and plasma immunoreactive ANF (IR-ANF) were measured in anesthetized, open-chest rats. All groups received 33% blood volume expansion with whole blood in 15 min. RAP was not allowed to increase in one group by using a caval snare. MAP was controlled in a second group with the use of an aortic snare. A third group (RAP-controlled ANF) with control of RAP received rat ANF (99-126) at doses designed to mimic the IR-ANF measured in the MAP-controlled rats. IR-ANF was similar 5 min after blood infusion in rats exhibiting increased RAP (490 +/- 111 pg/ml) and in those without increased RAP but receiving ANF infusion (447 +/- 44 pg/ml); this was also true at 45 min after blood infusion (232 +/- 44 vs. 263 +/- 27 pg/ml). IR-ANF in rats with constant RAP (without ANF infusion) remained low throughout the experiment (61 +/- 10 and 74 +/- 10 pg/ml). UNaV increased only in the MAP-controlled and ANF-infused groups, but peak responses occurred 15-30 min after the onset of volume expansion in the former, and 60-75 min in the latter. Thus, factors other than ANF mostly accounted for the immediate natriuresis after volume expansion, whereas ANF predominated after a delayed period. The results suggest that increased plasma ANF accounted for at least 34% of the observed natriuretic response to acute volume expansion in anesthetized rats.

Animals↗
PubMed1989

Modulation of natriuresis by sympathetic nerves and angiotensin II in conscious dogs.

The effects of renal perfusion pressure and reflex sympathetic nerve stimulation on sodium excretion were studied in six conscious foxhounds on a normal sodium diet. This was done before, during common carotid occlusion (CCO), and during a recovery period following CCO. Three protocols were used 1) control (n = 6), 2) converting-enzyme inhibition (CEI, n = 6), and 3) CEI combined with a constant renal artery pressure (RAP, n = 5). In protocol 1, CCO increased RAP markedly (140.5 +/- 5.1 vs. 103.0 +/- 4.4 mmHg; P less than 0.001) along with a considerable natriuresis (128.4 +/- 20.1 vs. 86.3 +/- 15.1 mumol Na+/min; P less than 0.05). In protocol 2, CEI increased control sodium excretion but did not impair the natriuresis by CCO. Maintaining RAP at control levels in protocol 3 lead to an antinatriuresis (53.1 +/- 16.8 vs. 128.3 +/- 32.2 mumol Na+/min; P less than 0.05). Creatinine clearance was unaffected by all procedures. In conclusion, a change in ANG II formation shifts but does not impair the natriuretic response to CCO. A moderate sympathetic activation has a pronounced pressure-independent antinatriuretic effect, which is not mediated by angiotensin II.

Angiotensin I↗
PubMed1992

Blockade of pressure natriuresis induced by inhibition of renal synthesis of nitric oxide in dogs.

To evaluate the participation of nitric oxide (NO) on pressure-induced natriuresis in pentobarbital-anesthetized dogs, renal perfusion pressure (RPP) was increased twice from 100 to 150 mmHg before and during the intrarenal administration of an NO-synthesis inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), while determining changes in glomerular filtration rate (GFR), renal blood flow (RBF), and urine sodium and water excretion. Before the inhibition of NO, the increase in RPP induced diuresis (5-fold) and natriuresis (4.2-fold) with no change in RBF or GFR. However, the intrarenal infusion of L-NAME (1 microgram.kg-1.min-1) blunted the diuretic and natriuretic responses without altering RBF or GFR. The infusion of the NO synthesis precursor L-arginine prevented the inhibitory effect that L-NAME exerted on the diuretic and natriuretic responses to the increase in RPP. These results indicate that the increase in RPP stimulates NO synthesis and suggest that NO might play an important role in the control of sodium and water excretion during acute changes in RPP.

Animals↗
PubMed1995

NaCl injections in brain induce natriuresis and blood pressure responses sensitive to ANG II AT1 receptors.

In the present study we tested the hypothesis that the natriuretic and pressor effects of intracerebroventricularly (icv) injected hypertonic saline involve a central angiotensinergic pathway. All experiments were performed in conscious Wistar rats. Bolus injections of hypertonic saline (0.19, 0.23, 0.30, and 0.60 M icv; injection volume 5 microliters) induced a concentration-dependent increase of renal sodium excretion without affecting urinary flow. The increase in renal sodium excretion after the two highest saline concentrations was accompanied by significant increases in mean arterial blood pressure (MAP). Pretreatment with the angiotensin (ANG) AT1 receptor antagonist, losartan (5 micrograms icv), reduced the natriuretic effect of 0.23 and 0.30 M saline but did not affect the natriuresis induced by 0.60 M saline. The increase in MAP after 0.30 and 0.60 M saline icv was markedly attenuated by intracerebroventricular pretreatment with losartan. Our results demonstrate the involvement of a central angiotensinergic mechanism in the natriuretic and pressor responses to hypertonic saline. In addition to the ANG II-mediated natriuresis, an additional natriuretic mechanism, independent of ANG II and associated with the saline-induced pressor effect, seems to be recruited with increasing concentrations of saline in the cerebrospinal fluid.

Angiotensin II↗
PubMed2000

Renal interstitial hydrostatic pressure and pressure natriuresis in pregnant rats.

The objective of this study was to test the hypothesis that a decrease in renal interstitial hydrostatic pressure (RIHP) accounts for the blunted pressure natriuresis during pregnancy. RIHP was measured in nonpregnant (NP; n = 9), midterm pregnant (MP; 12-14 days after conception; n = 10), and late-term pregnant (LP; 18-21 days after conception; n = 12) female Sprague-Dawley rats at two renal perfusion pressure (RPP) levels (99 and 120 mmHg). At the lower RPP level, RIHP was 5.9 +/- 0.3 mmHg for NP, 3.4 +/- 0.4 mmHg for MP (P < 0.05 vs. NP), and 2.9 +/- 0.1 mmHg for LP (P < 0.05 vs. NP) rats. The increase in RPP from 99 to 120 mmHg resulted in pressure natriuretic and diuretic responses in all groups; however, the increases in fractional excretion of sodium (DeltaFE(Na)), urine flow rate (DeltaV), and DeltaRIHP were significantly greater (P < 0. 05) in NP compared with both MP and LP rats. DeltaFE(Na), DeltaV, and DeltaRIHP were 2.06 +/- 0.28%, 81.44 +/- 14.10 microl/min, and 3. 0 +/- 0.5 mmHg for NP; 0.67 +/- 0.13%, 28.03 +/- 5.28 microl/min, and 0.5 +/- 0.2 mmHg for MP; and 0.48 +/- 0.12%, 18.14 +/- 4.70 microl/min, and 0.4 +/- 0.1 mmHg for LP rats. In conclusion, RIHP is significantly lower in pregnant compared with nonpregnant rats at similar RPP levels. Also, the ability of pregnant rats to increase RIHP in response to an increase in RPP is blunted. These changes in RIHP may play an important role in the blunted pressure natriuresis and contribute to the conservation of sodium and water that is critical for fetal growth and development during normal pregnancy.

Animals↗
PubMed1986

Morphological changes in the renal macula densa during natriuresis and diuresis.

Morphological changes in the macula densa have been studied during the infusion of diuretic agents into the renal artery of anesthetized dogs. The kidneys were fixed by rapid high pressure perfusion with glutaraldehyde. Large basolateral intercellular spaces were seen between macula densa cells in control kidneys, but the number and extent of these spaces were strikingly reduced during the natriuresis and diuresis induced by the infusion of frusemide, ethacrynic acid or mannitol. Natriuresis and diuresis produced by the intravenous infusion of large volumes of 0.9% NaCl solution also resulted in closure of these spaces. No simple relationship existed between changes in plasma renin activity and closure of the spaces between macula densa cells during these procedures. A distinctive, membrane-bound, vesicle-containing structure was identified between the basolateral processes of the cells of each macula densa; the function of this structure awaits elucidation. We suggest that changes in the size of the basolateral intercellular spaces of the macula densa reflect changes in fluid flux between the distal tubule and the interstitium of the juxtaglomerular apparatus.

Animals↗
PubMed1978

Natriuresis-induced protection in acute myohemoglobinuric renal failure without renal cortical renin content depletion in the rat.

The interrelationships of renal cortical renin content RCRC, sodium chloride excreting and the severity of renal failure were studied in the glycerol-induced acute myohemoglobinuric renal failure model in the rat. Protocols were designed to increase sodium chloride excretion without necessarily resulting in RCRC depletion. Our data fail to demonstrate a relationship between RCRC and severity of renal failure, but they demonstrate an excellent inverse correlation between the sodium chloride excretion of the animals in the 24 h prior to glycerol administration and the severity of resulitng renal failure. The protection of long-term saline-drinking animals should properly be ascribed to the associated natriuresis which develops much before RCRC depletion during the time course of saline drinking. The exact mechanism by which natriuresis exerts its protective effect needs further elucidation, but our data argue against a major role for RCRC in the pathogenesis of acute experimental renal failure.

Acute Kidney Injury↗
PubMed1985

Sulindac and ibuprofen inhibit furosemide-stimulated renin release but not natriuresis in men on a normal sodium diet.

We compared the effect of two commonly prescribed nonsteroidal anti-inflammatory drugs, ibuprofen and sulindac, and placebo on intravenous furosemide-induced natriuresis and renin stimulation in 11 healthy male volunteers, consuming a 100 mEq sodium, 80 mEq potassium diet. Chronic (6-day) therapy with each agent was followed by a 1-week washout period. There were no significant treatment-related differences in either urine volume or sodium excretion for any of the designated collection periods or for the cumulative value for the 4 h after furosemide administration. Similarly, differences among groups were not observed for creatinine clearance, urinary potassium and urinary chloride excretion. Mean basal plasma renin activity levels prior to furosemide administration on day 6 were significantly lower in the presence of ibuprofen (1.5 +/- 2.0 ng/ml/h;p less than 0.01) and sulindac (2,3 +/- 0.9 ng/ml/h; p less than 0.05), compared with placebo (3.3 +/- 1.1 ng/ml/h); the difference between the two NSAIDs was also significant (p less than 0.05). Mean plasma renin activity levels in the 4 h after furosemide increased significantly at all time points in comparison to basal values, but were significantly less for ibuprofen and sulindac groups in the first hour. Our data suggest that the natriuresis following intravenous furosemide in men consuming a normal sodium intake is not prostaglandin-dependent. Furthermore, the observation that sulindac suppressed basal and stimulated plasma renin activity levels, albeit to a lesser extent than ibuprofen, questions the claim that sulindac "spares' the kidney and compels further evaluation of this issue.

Adult↗
PubMed1988

Dopamine blockade attenuates the natriuresis of saline loading in the adrenalectomized rat.

Dopamine blockade with the dopamine-1/dopamine-2 antagonist cis-flupenthixol (CF) attenuates sodium excretion associated with saline loading in both innervated and denervated kidneys of the rat. Blockade of adrenal dopamine-2 receptors prevents the decrease in aldosterone secretion associated with saline loading and may also be responsible for the reduction in sodium excretion induced by CF. Therefore, to determine the role of adrenal dopamine-2 receptors in the attenuated natriuresis induced by CF, the effect of CF or vehicle treatment was examined in two groups of saline-loaded rats 80 (group I) and 120 min (group II) after adrenalectomy. In both groups, CF decreased glomerular filtration rate and sodium excretion after adrenalectomy. It is concluded that dopamine blockade attenuates the natriuresis associated with sodium loading by a direct effect in the kidney.

Adrenalectomy↗
PubMed1992

Furosemide-induced natriuresis is augmented by ultra-low-dose captopril but not by standard doses of captopril in chronic heart failure.

BACKGROUND: Ten chronic heart failure patients were studied on three occasions in randomized double-blind fashion to compare the acute hemodynamic, neurohormonal, and renal sodium-handling responses to 1 mg captopril versus 25 mg captopril, both in the absence of loop diuretic therapy and during furosemide-stimulated natriuresis. METHODS AND RESULTS: Compared with placebo, 1 mg captopril caused nonsignificant decreases in mean arterial pressure and circulating angiotensin II level and had no effect on glomerular filtration rate as determined by 51Cr-EDTA elimination. Captopril (25 mg) produced marked suppression of serum angiotensin II with or without oral furosemide (both p less than 0.002), a marked decrease in mean arterial pressure (p less than 0.001) that was accentuated by furosemide (p less than 0.00001), and a decrease in glomerular filtration rate (p = 0.0007). No difference from placebo in renal sodium excretion was noted with either 1 or 25 mg captopril in the absence of furosemide. In contrast, while 25 mg captopril caused slight attenuation of the natriuretic response to furosemide, 1 mg captopril significantly enhanced furosemide-induced natriuresis (p less than 0.05). No correlation was found in our patients between the natriuretic effect of furosemide and either absolute mean arterial pressure or change in mean arterial pressure during the furosemide phase of each study session. This suggests that blood pressure is not the important factor mediating the divergent renal responses to furosemide of the two captopril dosage regimens. CONCLUSIONS: We propose that in the face of furosemide-induced postglomerular vasodilatation in chronic heart failure, captopril at a starting dose of 1 mg (but not 25 mg) preserves enough circulating angiotensin II to maintain efferent arteriolar tone and thus glomerular filtration, while offsetting the antinatriuretic renal tubular effects of angiotensin II.

Aged↗
PubMed2002

Impaired stress-induced pressure natriuresis is related to left ventricle structure in blacks.

The mechanisms through which stress may contribute to the racial difference in the prevalence of essential hypertension and associated target organ damage remain unclear. This study examined differences in stress-induced pressure natriuresis in 69 black and 52 white normotensives age 14 to 27 years, all with a positive family history of hypertension. Urine samples for sodium excretion were collected before and after a series of tasks (video game challenge, forehead cold stimulation). The average blood pressure across the 2 tasks and the average increase in blood pressure to the 2 tasks were calculated. Blacks had higher mean systolic (131+/-12 versus 126+/-12 mm Hg, P<0.02) and diastolic (77+/-8 versus 72+/-9 mm Hg, P<0.001) blood pressure and a greater average change in systolic blood pressure (15+/-9 versus 11+/-7 mm Hg, P<0.04). This was associated with a smaller change in sodium excretion (2+/-6 versus 7+/-10 mEq/h, P<0.002). The change in sodium excretion was related to the change in systolic (r=0.31, P<0.03) and diastolic (r=0.27, P<0.05) blood pressure in whites but not in blacks. Relative wall thickness was greater in blacks (0.31+/-0.04 versus 0.29+/-0.03, P<0.002). In conclusion, impaired stress-induced pressure natriuresis in blacks may contribute to racial differences in essential hypertension and its sequelae.

Adolescent↗
PubMed2005

Diuresis and natriuresis caused by activation of VR1-positive sensory nerves in renal pelvis of rats.

To test the hypothesis that activation of the vanilloid receptor 1 (VR1) expressed in sensory nerves innervating the renal pelvis leads to diuresis and natriuresis, a selective VR1 receptor agonist, capsaicin (2.4 nmol), or vehicle was perfused intravenously or into the left renal pelvis of anesthetized rats at a rate without changing renal perfusion pressure. Mean arterial pressure was not altered by capsaicin administered intravenously or into the renal pelvis. Capsaicin perfusion into the left renal pelvis but not intravenously caused significant increases in urine flow rate and urinary sodium excretion bilaterally in a dose-dependent manner, which were abolished by capsazepine, a selective VR1 receptor antagonist, given ipsilaterally to the renal pelvis or by ipsilateral renal denervation. Capsaicin given intravenously or into the left renal pelvis increased plasma calcitonin gene-related peptide levels to the same extent. Increased plasma calcitonin gene-related peptide levels induced by capsaicin (68.9+/-2.8 pg/mL) perfusion into the renal pelvis was prevented either by capsazepine (22.5+/-10.1 pg/mL) given ipsilaterally into the renal pelvis or by ipsilateral renal denervation (25.9+/-2.3 pg/mL). Taken together, our data show that unilateral activation of VR1-positive sensory nerves innervating the renal pelvis leads to bilateral diuresis and natriuresis via a mechanism that is independent of plasma calcitonin gene-related peptide levels. These data suggest that VR1-positive sensory nerves in the kidney enhance renal excretory function, a mechanism that may be critically involved in sodium and fluid homeostasis.

Animals↗