Role of atrial natriuretic peptide in volume-expansion natriuresis

1986 ◽  
Vol 251 (2) ◽  
pp. R310-R313 ◽  
Author(s):  
T. R. Schwab ◽  
B. S. Edwards ◽  
D. M. Heublein ◽  
J. C. Burnett
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Right Atrial ◽  
Fractional Excretion Of Sodium

Studies were performed to investigate the role of circulating atrial natriuretic peptide (ANP) in acute volume-expansion natriuresis. Sham-operated (SHAM, n = 6) and right atrial appendectomized (ATRX, n = 12) anesthetized rats underwent acute volume expansion with isoncotic albumin. After equilibration and control periods, volume expansion increased urine flow rate, urinary sodium excretion, fractional excretion of sodium, and circulating ANP. Absolute increases in urine flow rate (delta 46 +/- 4 SHAM; delta 25 +/- 5 microliter/min ATRX), urinary sodium excretion (delta 9.48 +/- 1.01 SHAM; delta 4.77 +/- 1.03 mueq/min ATRX), fractional excretion of sodium (delta 3.16 +/- 0.53 SHAM; delta 1.65 +/- 0.32% ATRX), and ANP (delta 303.3 +/- 35.9 SHAM; delta 156.6 +/- 26.0 pg/ml ATRX) were significantly reduced by right atrial appendectomy. No significant differences in mean arterial pressure, central venous pressure, or glomerular filtration rate during volume expansion were observed between groups. These studies support the hypothesis that right atrial appendectomy in the rat attenuates acute volume expansion-induced increases in circulating ANP and urinary sodium excretion and that the natriuresis of acute volume expansion is mediated in part by an increase in circulating ANP.

Activation of histamine H3 receptors inhibits renal noradrenergic neurotransmission in anesthetized dogs

2001 ◽  
Vol 280 (5) ◽  
pp. R1450-R1456 ◽  
Author(s):  
Tomoyuki Yamasaki ◽  
Isao Tamai ◽  
Yasuo Matsumura
Keyword(s):  
Receptor Antagonist ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Renal Nerve ◽  
Anesthetized Dogs ◽  
Induced Changes ◽  
Antidiuretic Action

To investigate the possible involvement of histamine H3 receptors in renal noradrenergic neurotransmission, effects of (R)alpha-methylhistamine (R-HA), a selective H3-receptor agonist, and thioperamide (Thiop), a selective H3-receptor antagonist, on renal nerve stimulation (RNS)-induced changes in renal function and norepinephrine (NE) overflow in anesthetized dogs were examined. RNS (0.5–2.0 Hz) produced significant decreases in urine flow and urinary sodium excretion and increases in NE overflow rate (NEOR), without affecting renal hemodynamics. When R-HA (1 μg · kg−1 · min−1) was infused intravenously, mean arterial pressure and heart rate were significantly decreased, and there was a tendency to reduce basal values of urine flow and urinary sodium excretion. During R-HA infusion, RNS-induced antidiuretic action and increases in NEOR were markedly attenuated. Thiop infusion (5 μg · kg−1 · min−1) did not affect basal hemodynamic and excretory parameters. Thiop infusion caused RNS-induced antidiuretic action and increases in NEOR similar to the basal condition. When R-HA was administered concomitantly with Thiop infusion, R-HA failed to attenuate the RNS-induced antidiuretic action and increases in NEOR. However, in the presence of pyrilamine (a selective H1-receptor antagonist) or cimetidine (a selective H2-receptor antagonist) infusion, R-HA attenuated the RNS-induced actions, similarly to the case without these antagonists. Thus functional histamine H3 receptors, possibly located on renal noradrenergic nerve endings, may play the role of inhibitory modulators of renal noradrenergic neurotransmission.

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

1987 ◽  
Vol 253 (5) ◽  
pp. F969-F975 ◽  
Author(s):  
T. A. Fried ◽  
M. A. Ayon ◽  
G. McDonald ◽  
A. Lau ◽  
T. Inagami ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Excretion Rate ◽  
Balloon Catheter ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Right Atrial

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.

Atrial natriuretic peptide – cyclic GMP coupling and urinary sodium excretion during acute volume expansion in man

1990 ◽  
Vol 68 (4) ◽  
pp. 535-538 ◽  
Author(s):  
Giuseppe A. Sagnella ◽  
Donald R. J. Singer ◽  
Nirmala D. Markandu ◽  
Graham A. MacGregor ◽  
David G. Shirley ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cyclic Gmp ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Saline Infusion ◽  
Atrial Natriuretic

The present study examines hormonal and renal responses to acute volume expansion in normal man, with particular emphasis on the atrial natriuretic peptide (ANP) – cyclic GMP coupling. Two liters of isotonic saline were infused into eight normotensive male subjects over a 1-h period. Plasma and urinary measurements were made before, during, and up to 300 min after the start of the saline infusion. With the initial increase in urinary sodium excretion there were increases in plasma ANP and plasma cyclic GMP, which reached maximum levels at 15 min after the end of the saline infusion. Urinary cyclic GMP increased gradually during saline infusion up to approximately 60 min after the end of the infusion. Plasma ANP and plasma and urinary cyclic GMP excretion gradually declined thereafter. By contrast, urinary sodium excretion remained elevated up to the end of the observation period. The saline infusion was associated with marked reductions in plasma renin activity and aldosterone, which persisted up to the end of the study. These results suggest a coupling between the increases in plasma ANP, the production of cyclic GMP, and urinary sodium excretion, in particular during the initial renal response to acute volume expansion. However, other mechanisms including the suppression of the rennin–angiotensin–aldosterone system may become increasingly important in the later natriuretic response to acute volume expansion.Key words: atrial natriuretic peptide, cyclic GMP, sodium, renal, human.

Cardiovascular and renal effects of adrenomedullin in rats with heart failure

1999 ◽  
Vol 276 (1) ◽  
pp. R213-R218 ◽  
Author(s):  
Noritoshi Nagaya ◽  
Toshio Nishikimi ◽  
Takeshi Horio ◽  
Fumiki Yoshihara ◽  
Akio Kanazawa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Intravenous Infusion ◽  
Sodium Excretion ◽  
Systolic Pressure ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Right Atrial ◽  
High Dose ◽  
Renal Effects

Plasma adrenomedullin (AM), a novel hypotensive peptide, has been shown to increase in heart failure (HF). This study sought to examine the cardiovascular and renal effects of intravenous infusion of AM in HF rats and sham-operated rats (control) using two doses of AM that would not induce hypotension. Rat AM-(1—50) was intravenously administered at rates of 0.01 (low) and 0.05 (high) μg ⋅ kg body wt−1 ⋅ min−1. Low-dose AM increased urine flow (+21% in HF, +29% in control) and urinary sodium excretion (+109% in HF, +123% in control) without changes in any hemodynamic variables. In contrast, high-dose AM slightly decreased mean arterial pressure (−3% in HF, −5% in control) and significantly increased cardiac output (+20% in HF, +12% in control). Infusion of high-dose AM resulted in significant decreases in right ventricular systolic pressure (−11%) and right atrial pressure (−28%) only in HF rats. High-dose AM significantly increased glomerular filtration rate (+10% in HF, +16% in control) and effective renal plasma flow (+25% in HF, +46% in control) as well as urine flow and urinary sodium excretion. In summary, intravenous infusion of AM exerted diuresis and natriuresis without inducing hypotension and, in the higher dose, produced beneficial hemodynamic and renal vasodilator effects in rats with compensated HF.

Evidence supporting a physiological role for proANP-(1–30) in the regulation of renal excretion

2001 ◽  
Vol 280 (5) ◽  
pp. R1510-R1517 ◽  
Author(s):  
John R. Dietz ◽  
Dionne Y. Scott ◽  
Carol S. Landon ◽  
Stanley J. Nazian
Keyword(s):  
Sodium Excretion ◽  
Volume Expansion ◽  
Renal Excretion ◽  
Physiological Role ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Potassium Excretion ◽  
Fractional Excretion Of Sodium

The experiments, performed in pentobarbital sodium-anesthetized rats, consisted of a 1-h equilibration period followed by two 30-min control periods. Subsequently, synthetic rat pro atrial natriuretic peptide (ANP) [proANP-(1–30)] ( n = 8) was given as a bolus of 10 μg in 1 ml of 0.9% saline followed by an infusion at 30 ng/min (20 μl/min) for six additional periods. Control rats ( n = 6) received only 0.45% saline in the appropriate volumes. Mean arterial pressure, renal blood flow, and glomerular filtration rate did not change significantly in either group during the proANP-(1–30) infusion. Urine flow and potassium excretion increased ∼50% in the proANP-(1–30)-infused group only ( P < 0.05). Sodium excretion and fractional excretion of sodium, expressed as the change from their own baselines, were significantly increased by the proANP-(1–30) infusion ( P < 0.05), whereas cGMP excretion was similar in both groups. These results suggest that the rat sequence of proANP-(1–30) produces a natriuresis in the rat independent of changes in hemodynamics and renal cGMP production. In a second study, rats ( n = 8) were prepared as above and pretreated with 0.4 ml iv of rabbit serum containing an antibody directed against proANP-(1–30) (anti-proANP group). The rats were volume expanded with 3 ml of 6% albumin in Krebs and observed for 3 h to determine if the anti-proANP would attenuate the responses to volume expansion. Control rats ( n = 7) received 0.4 ml of normal rabbit serum. The elevation in potassium excretion in response to volume expansion was significantly attenuated in the anti-proANP group ( P < 0.05). Sodium excretion and urine flow responses also tended to be reduced but not significantly. These results suggest that in the rat, proANP-(1–30) plays a physiological role in regulating renal excretion.

Role of atrial appendages in modulating stimulated plasma atrial natriuretic peptide levels in conscious rats

1990 ◽  
Vol 259 (5) ◽  
pp. R1017-R1024
Author(s):  
A. Hoffman ◽  
E. Grossman ◽  
H. R. Keiser
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Levels ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Vena Cava ◽  
Urinary Sodium Excretion ◽  
Basal Plasma ◽  
Atrial Natriuretic

To evaluate the role of the atrial appendages in modulating plasma levels of atrial natriuretic peptide (ANP), we applied a series of both acute and chronic stimuli in conscious, chronic, bilaterally atrial-appendectomized (APP) and sham-operated control rats. Basal plasma ANP levels and urinary sodium excretion were normal in all rats after APP. The release of ANP was markedly blunted to acute volume expansion (+67% vs. +357% in controls, P less than 0.01) but was only moderately reduced after norepinephrine infusion (+106% vs. +212%, P less than 0.05) and was normal after acute salt load [+148% vs. +180% in controls, not significant (NS)]. Furthermore, plasma levels of ANP were increased normally in APP rats treated with deoxycorticosterone acetate (270 + 18 vs. 296 + 14 pg/ml in controls, NS) and in APP rats with congestive heart failure induced by a large arteriovenous (a-v) fistula between the aorta and the vena cava (306 +/- 18 vs. 302 +/- 12 pg/ml, NS). Sodium excretion patterns were similar in chronically stimulated APP and control rats. The results demonstrate that, although APP reduces the response of ANP release to acute volume expansion, it does not do so to other stimuli of either acute or chronic nature, suggesting that there is no permanent defect in the ability of APP rats to secrete ANP. These studies confirm that the atria are the major source for ANP release into the circulation after acute intravascular volume expansion. However, other tissue sources may contribute significantly to the levels of circulating ANP in response to this and other acute and chronic stimuli.

Lack of a Role for the Renal Nerves in Renal Sodium Reabsorption in Conscious Dogs

1978 ◽  
Vol 54 (5) ◽  
pp. 567-572 ◽  
Author(s):  
M. D. Lifschitz
Keyword(s):  
Body Weight ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Fractional Sodium Excretion ◽  
Renal Sodium Reabsorption

1. Studies in anaesthetized animals suggest that the renal nerves have a role in the regulation of sodium excretion. Urinary sodium excretion decreases when the renal nerves are stimulated and increases after renal denervation or ganglionic blockade. In order to define the role of the renal nerves in the regulation of urinary sodium excretion in awake animals, dogs were prepared with one kidney denervated and the other intact and the bladder split so that urine could be collected from each kidney. Denervation was confirmed by kidney noradrenaline analysis (1·72 ± 0·29 vs 0·18 ± 0·12 nmol/g). 2. These dogs were studied awake with one of two protocols on each of two separate days. In protocol VH, volume expansion (5% body weight) was followed by haemorrhage of 2% body weight. Fractional sodium excretion fell from 4·7 ± 0·5 to 1·1 ± 0·2% on the denervated side and from 5·6 ± 0·6 to 1·4 ± 0·3% on the intact side. Inulin and p-aminohippurate clearance fell similarly on both sides. 3. In protocol HV, haemorrhage of 2% body weight was followed by blood replacement and volume expansion of 5% body weight. In this second protocol fractional sodium excretion during haemorrhage was 0·23 ± 0·07 and 0·24 ± 0·09% for denervated and intact kidneys respectively and increased to 2·04 ± 0·32 and 2·78 ± 0·60 after volume expansion. 4. In both protocols the denervated kidney was able to reabsorb sodium as well as the innervated kidney during haemorrhage and was able to increase fractional sodium excretion as well as the denervated kidney during volume expansion. These results suggest that the renal nerves do not have a significant role in the regulation of sodium excretion in conscious animals.

Inhibition of nitric oxide synthesis attenuates pressure-induced natriuretic responses in anesthetized dogs

1993 ◽  
Vol 264 (1) ◽  
pp. F79-F87 ◽  
Author(s):  
D. S. Majid ◽  
A. Williams ◽  
L. G. Navar
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Sodium Excretion ◽  
Renin Angiotensin System ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Synthesis Inhibition ◽  
Fractional Excretion Of Sodium ◽  
Anesthetized Dogs ◽  
Pressure Natriuresis

Inhibition of nitric oxide (NO) synthesis by intrarenal administration of nitro-L-arginine (NLA) leads to decreases in urinary sodium excretion (UNaV) in association with the increases in renal vascular resistance (RVR). In the present study, we examined the ability of the kidney to alter its sodium excretion in response to acute changes in renal arterial pressure (RAP) in anesthetized dogs before and during intrarenal infusion of NLA (50 micrograms.kg-1.min-1). NO synthesis inhibition in 11 dogs increased RVR by 32 +/- 4% and decreased renal blood flow (RBF) by 25 +/- 3%, outer cortical blood flow by 25 +/- 6%, urine flow by 37 +/- 14%, UNaV by 71 +/- 5%, and fractional excretion of sodium (FENa) by 71 +/- 4%. Glomerular filtration rate was not significantly changed during NLA infusion. As previously reported, there was suppression of the RBF autoregulation plateau during NO synthesis inhibition. In addition, there was a marked attenuation of urine flow and UNaV responses to reductions in RAP (150 to 75 mmHg), with significant reductions in the slopes of the relationships between RAP vs. UNaV and RAP vs. FENa during NLA infusion. Similar responses were observed in nine other dogs treated with the angiotensin receptor antagonist losartan, indicating that an augmented activity of the renin-angiotensin system is not responsible for attenuation of the slope of the pressure-natriuresis relationship during NLA infusion. These data suggest that NO may participate in the mediation of the pressure-natriuresis response.

Direct renal interstitial volume expansion causes exaggerated natriuresis in SHR

1991 ◽  
Vol 261 (4) ◽  
pp. F567-F570 ◽  
Author(s):  
A. A. Khraibi
Keyword(s):  
Volume Expansion ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Renal Interstitium ◽  
Time Control ◽  
Arterial Blood ◽  
Interstitial Volume ◽  
Fractional Excretion Of Sodium ◽  
Wistar Kyoto ◽  
Second Period

In Okamoto spontaneously hypertensive rats (SHR), elevated arterial blood pressure is not transmitted to the renal interstitium, and therefore pressure natriuretic and diuretic responses are attenuated. The objective of this study was to determine the effect of increasing renal interstitial hydrostatic pressure (RIHP) by direct renal interstitial volume expansion (DRIVE) on natriuresis and diuresis of SHR and Wistar-Kyoto rats (WKY). Unilateral nephrectomy and implantation of two polyethylene (PE) matrices were performed 3-4 wk before the acute experiment. Four groups of rats, two experimental and two time control, were used. A control clearance period was taken in all groups. In experimental groups and at the beginning and middle of the second period DRIVE was accomplished by bolus injection of a solution of 2.5% human albumin in saline directly into interstitium through one of the PE matrices. In time-control groups saline was infused in renal interstitium at the beginning of the second period. The second PE matrix was used to continuously measure RIHP in all groups. In experimental groups, DRIVE produced a significant increase in RIHP from 3.8 +/- 0.4 to 5.7 +/- 0.8 mmHg (P less than 0.05) in SHR and 4.3 +/- 0.4 to 7.1 +/- 0.5 mmHg (P less than 0.05) in WKY. In both groups the significant increase in RIHP was associated with significant increases in urinary sodium excretion (UNaV), fractional excretion of sodium (FENa), and urine flow rate (V).(ABSTRACT TRUNCATED AT 250 WORDS)

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