Renal nerves mediate blunted natriuresis to atrial natriuretic peptide in cirrhotic rats

1987 ◽  
Vol 252 (5) ◽  
pp. R1019-R1023 ◽  
Author(s):  
J. P. Koepke ◽  
S. Jones ◽  
G. F. DiBona
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sympathetic Nerve Activity ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Control ◽  
Renal Sympathetic ◽  
Atrial Natriuretic

The diuretic and natriuretic responses to atrial natriuretic peptide in conscious rats with cirrhosis (chronic bile duct ligation) were examined. Cirrhotic rats had sodium retention, ascites, and elevated liver weights. In conscious control rats, atrial natriuretic peptide increased urine flow rate and urinary sodium excretion. In conscious cirrhotic rats, atrial natriuretic peptide had no effect on urine flow rate or urinary sodium excretion. Renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide in cirrhotic rats. Renal sympathetic nerve activity increased in conscious cirrhotic rats during infusion of atrial natriuretic peptide but decreased in conscious control rats. Inhibition of the renin-angiotensin system with captopril had no effect on the diuretic or natriuretic responses to atrial natriuretic peptide in conscious control or cirrhotic rats. Mean arterial pressure, glomerular filtration rate, and renal plasma flow were affected similarly by atrial natriuretic peptide in control and cirrhotic rats. Increased renal sympathetic nerve activity, but not angiotensin II, mediates the blunted diuretic and natriuretic responses to atrial natriuretic peptide in conscious cirrhotic rats.

Renal sympathetic nerve activity and renal responses during head-up tilt in conscious dogs

1989 ◽  
Vol 257 (2) ◽  
pp. R337-R343 ◽  
Author(s):  
K. Miki ◽  
Y. Hayashida ◽  
F. Tajima ◽  
J. Iwamoto ◽  
K. Shiraki
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Urine Flow ◽  
Conscious Dogs ◽  
Functional Responses ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Head Up Tilt ◽  
Renal Sympathetic

Renal sympathetic nerve activity (RSNA) was measured in conjunction with functional responses of the kidney during head-up tilt in eight conscious female dogs. A 40 degree head-up tilt resulted in a sustained increase in RSNA by 53 +/- 10% (P less than 0.05) relative to control level. Urine flow and osmolal and sodium excretions decreased significantly to a nadir of -55 +/- 4, -42 +/- 7, and -59 +/- 10%, respectively, whereas free water clearance and creatinine clearance did not change significantly during head-up tilt. The systemic arterial pressure (at kidney level) increased significantly from 110 +/- 4 to 129 +/- 6 mmHg, and central venous pressure decreased significantly from -0.7 +/- 0.5 to -7.6 +/- 0.6 mmHg. The chronic bilateral renal denervation, which was performed 2-4 wk before the experiment, abolished both the antidiuretic and antinatriuretic responses to heald-up tilt. These results indicate that an increase in RSNA plays a significant role in the decrease in urine flow and sodium excretion induced by 40 degree head-up tilt in conscious dogs.

Atrial natriuretic peptide and mechanisms of cardiovascular control. Role of serotonergic receptors

1998 ◽  
Vol 274 (3) ◽  
pp. R711-R717 ◽  
Author(s):  
Robin Donna Deliva ◽  
Uwe Ackermann
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Renal Sympathetic Nerve Activity ◽  
Serotonergic Receptors ◽  
Arterial Blood ◽  
Cardiopulmonary Receptors ◽  
Type 3 ◽  
Renal Sympathetic ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) inhibits renal sympathetic nerve activity (RSNA), provided the vagi are intact. Afferents from chemosensitive cardiopulmonary receptors are specifically required. Such receptors produce the Bezold-Jarisch reflex, are prominent on the ventricular epicardium, and are richly supplied with 5-hydroxytryptamine type 3 (5-HT3) receptors. We tested the hypothesis that epicardial 5-HT3-sensitive neurons mediate depressor effects of ANP. Through a special catheter, anesthetized, sinoaortically denervated rats received pericardial test injections of ANP (28-amino acid rat ANP; 100 and 1,000 ng) in the presence or absence of 5-HT3 antagonist (Ondansetron, 20 μg/kg; n = 9). In other groups we observed the effects of systemic ANP while blocking either epicardial or systemic 5-HT3 receptors. Arterial blood pressure (ABP), heart rate, and RSNA were recorded continuously. Intravenous ANP (100 or 200 ng) decreased ABP and RSNA significantly. In contrast, intrapericardial ANP (100 or 1,000 ng) caused no significant fall in ABP or RSNA. Both intravenous and pericardial Ondansetron reduced the effects of intravenous ANP significantly, but the intravenous antagonism was significantly greater. We conclude that epicardial chemosensitive afferents are not sensitive to ANP and that sympathoinhibitory effects of ANP arise from a 5-HT3 agonist that cannot be produced when ANP is confined to the pericardial space.

Blunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders

1987 ◽  
Vol 252 (5) ◽  
pp. F865-F871 ◽  
Author(s):  
J. P. Koepke ◽  
G. F. DiBona
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Atrial Natriuretic

Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.

Baroreflexes prevent neurally induced sodium retention in angiotensin hypertension

2000 ◽  
Vol 279 (4) ◽  
pp. R1437-R1448 ◽  
Author(s):  
Thomas E. Lohmeier ◽  
Justin R. Lohmeier ◽  
Atif Haque ◽  
Drew A. Hildebrandt
Keyword(s):  
Sympathetic Nerve ◽  
Sodium Excretion ◽  
Sympathetic Nerve Activity ◽  
Urinary Sodium Excretion ◽  
Sodium Retention ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Recent studies indicate that renal sympathetic nerve activity is chronically suppressed during ANG II hypertension. To determine whether cardiopulmonary reflexes and/or arterial baroreflexes mediate this chronic renal sympathoinhibition, experiments were conducted in conscious dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separate 24-h urine collection from denervated (Den) and innervated (Inn) kidneys. Dogs were studied 1) intact, 2) after thoracic vagal stripping to eliminate afferents from cardiopulmonary and aortic receptors [cardiopulmonary denervation (CPD)], and 3) after subsequent denervation of the carotid sinuses to achieve CPD plus complete sinoaortic denervation (CPD + SAD). After control measurements, ANG II was infused for 5 days at a rate of 5 ng · kg−1 · min−1. In the intact state, 24-h control values for mean arterial pressure (MAP) and the ratio for urinary sodium excretion from Den and Inn kidneys (Den/Inn) were 98 ± 4 mmHg and 1.04 ± 0.04, respectively. ANG II caused sodium retention and a sustained increase in MAP of 30–35 mmHg. Throughout ANG II infusion, there was a greater rate of sodium excretion from Inn vs. Den kidneys ( day 5 Den/Inn sodium = 0.51 ± 0.05), indicating chronic suppression of renal sympathetic nerve activity. CPD and CPD + SAD had little or no influence on baseline values for either MAP or the Den/Inn sodium, nor did they alter the severity of ANG II hypertension. However, CPD totally abolished the fall in the Den/Inn sodium in response to ANG II. Furthermore, after CPD + SAD, there was a lower, rather than a higher, rate of sodium excretion from Inn vs. Den kidneys during ANG II infusion ( day 5 Den/Inn sodium = 2.02 ± 0.14). These data suggest that cardiac and/or arterial baroreflexes chronically inhibit renal sympathetic nerve activity during ANG II hypertension and that in the absence of these reflexes, ANG II has sustained renal sympathoexcitatory effects.

Differential effects of atrial natriuretic peptide and dopamine on urinary protein excretion in chronic glomerulonephritis

1991 ◽  
Vol 80 (2) ◽  
pp. 131-136 ◽  
Author(s):  
Yasunobu Hirata ◽  
Masao Ishii ◽  
Kazushige Fukui ◽  
Hiroshi Hayakawa ◽  
Etsu Suzuki ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Urinary Sodium Excretion ◽  
Urinary Protein Excretion ◽  
Urine Flow ◽  
Urinary Protein ◽  
Chronic Glomerulonephritis ◽  
Dopamine Infusion ◽  
Protein Excretion ◽  
Atrial Natriuretic

1. To examine whether or not atrial natriuretic peptide-induced proteinuria simply results from increases in urine flow or glomerular filtration rate, we infused dopamine (1 μg min−1 kg−1) and α-human atrial natriuretic peptide (0.025 μg min−1 kg−1) into nine patients with chronic glomerulonephritis and nine essential hypertensive patients without renal damage, and compared the effects of the two agents on renal function and urinary protein excretion. 2. In patients with chronic glomerulonephritis, dopamine infusion significantly increased urinary sodium excretion (+ 59%), renal blood flow (+ 20%) and creatinine clearance (+ 14%). However, urinary protein excretion was not changed. Addition of atrial natriuretic peptide to the dopamine infusion further increased urinary sodium excretion and maintained creatinine clearance at the same level. In contrast to the infusion of dopamine alone, atrial natriuretic peptide markedly increased urinary protein excretion (77 versus 229 mg min−1 m2, P < 0.02). Furthermore, the addition of atrial natriuretic peptide elevated the urinary protein/creatinine ratio (1.55 versus 5.35, P < 0.05), while dopamine alone did not(1.55 versus 1.45, not significant). 3. In essential hypertensive patients, dopamine and dopamine plus ANP showed renal effects similar to those of chronic glomerulonephritis; however, the urinary excretion of protein was not changed significantly. 4. These results suggest that atrial natriuretic peptide may increase urinary protein excretion mainly by increasing the permeability of the damaged glomeruli to protein rather than by simply increasing urine flow or glomerular filtration. Possible mechanisms underlying the proteinuria-increasing effects of atrial natriuretic peptide are discussed.

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