Renal tubular function in horses during submaximal exercise

Exercise-induced changes in renal function were examined during steady-state submaximal treadmill exercise in six unfit mares. Horses were randomly assigned to either an exercise or parallel control (no exercise) trial on day 1 and the alternate trial 1 wk later. The mares ran on a treadmill, set at a 6 degrees incline, for 1 h at 55-60% of maximal heart rate. Exercise significantly (P less than 0.05) increased plasma osmolality, plasma [K+], urine flow (+ 45%), Na+ excretion (+ 371%), K+ excretion (+ 57%), osmotic clearance (+ 32%), Na+ clearance (+ 391%), K+ clearance (+ 33%), and fractional Na+ excretion (+ 320%) and significantly decreased plasma [Cl-], Cl- excretion (-46%), Cl- clearance (-41%), and fractional Cl- excretion (-47%). Glomerular filtration rate, fractional K+ excretion, and free water clearance did not change during exercise. Atrial natriuretic peptide increased during exercise from 11 +/- 1 pg/ml at rest to a peak of 40 +/- 9 pg/ml (264%, P less than 0.05) at 40 min. Increases in plasma renin activity (66%, P less than 0.05) were accompanied by increases in plasma aldosterone concentration (760%, P less than 0.05). Vasopressin concentration increased (P less than 0.05) steadily over the 60-min period of exercise. It was concluded that, in horses, submaximal exercise-induced increases in urine flow and sodium excretion are associated with a concurrent increase in the plasma concentration of atrial natriuretic peptide.

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Atrial natriuretic peptide response to rapid atrial pacing in cardiac-denervated dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1989.257.1.r162 ◽

1989 ◽

Vol 257 (1) ◽

pp. R162-R167 ◽

Cited By ~ 1

Author(s):

T. D. Williams ◽

K. P. Walsh ◽

R. Canepa-Anson ◽

M. I. Noble ◽

A. J. Drake-Holland ◽

...

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Flow Rate ◽

Free Water ◽

Urine Flow ◽

Urine Flow Rate ◽

Right Atrial ◽

Atrial Pacing ◽

Cardiac Denervation ◽

Atrial Natriuretic

The effects of rapid atrial pacing on central hemodynamics, plasma hormones, and renal function were investigated in eight control and nine cardiac-denervated dogs under chloralose anesthesia. Pacing at approximately 250 ppm for 60 min caused similar increases in pulmonary wedge and right atrial pressures, systemic vascular resistance, and plasma atrial natriuretic peptide (ANP) in both groups. In control dogs, pacing produced a fall in both plasma vasopressin (AVP) and plasma renin activity (PRA) and a rise in urine flow rate associated with an increase in free water but not sodium clearance. In contrast, in cardiac-denervated dogs, both plasma AVP and PRA increased during pacing; urine flow rate did not change, and marked sodium retention occurred. This study supports the concept that the increase in urine flow during rapid atrial pacing is mediated by inhibition of renin and AVP secretion through intact cardiac nerves. The secretion of ANP is unaffected by cardiac denervation. The natriuretic and vasodilator actions of high plasma ANP concentrations during rapid atrial pacing can be inhibited either by neurally mediated cardiorenal effects in normal animals or by stimulation of the renin-angiotensin system after cardiac denervation.

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Central oxytocin and ANP receptors mediate osmotic inhibition of salt appetite in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1995.269.2.r245 ◽

1995 ◽

Vol 269 (2) ◽

pp. R245-R251 ◽

Cited By ~ 23

Author(s):

R. E. Blackburn ◽

W. K. Samson ◽

R. J. Fulton ◽

E. M. Stricker ◽

J. G. Verbalis

Keyword(s):

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Osmolality ◽

Plasma Sodium ◽

Salt Appetite ◽

Saline Ingestion ◽

A Chain ◽

Anp Receptors ◽

Atrial Natriuretic

These studies evaluated the involvement of central oxytocin (OT) and atrial natriuretic peptide (ANP) receptors in the osmotic inhibition of hypovolemia-induced salt appetite. Rats were pretreated centrally with the A chain of the cytotoxin ricin conjugated to OT (rAOT) or ANP (rAANP) to selectively inactivate cells bearing these respective receptors, or rats were pretreated with the unconjugated A chain (rA) as a control. Hypovolemia was induced with subcutaneous colloid injections, and rats then were given either 2 M mannitol, which raises plasma osmolality but lowers plasma sodium, or 1 M NaCl, which raises both. Hypertonic mannitol inhibited saline ingestion in rA-treated control rats but stimulated ingestion in rAOT- and rAANP-treated rats, whereas hypertonic NaCl blunted saline ingestion in rA- and rAOT-treated rats but stimulated ingestion in rAANP-treated rats. Angiotensin II-induced saline intake was similarly potentiated in rAOT- and rAANP-treated rats, indicating that this treatment also activates central inhibitory OT and ANP pathways. These data suggest that central ANP receptors mediate both Na(+)- and osmolality-induced inhibition of NaCl ingestion, whereas central OT receptors primarily mediate osmolality-induced inhibition of NaCl ingestion in rats.

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Beta-adrenoceptor blockade potentiates exercise-induced release of atrial natriuretic peptide

European Journal of Clinical Pharmacology ◽

10.1007/bf00315576 ◽

1990 ◽

Vol 38 (4) ◽

pp. 363-366 ◽

Cited By ~ 9

Author(s):

G. Deray ◽

I. Berlin ◽

G. Maistre ◽

F. Martinez ◽

S. Legrand ◽

...

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Beta Adrenoceptor ◽

Exercise Induced ◽

Atrial Natriuretic

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Atrial natriuretic peptide and exercise-induced fluid retention in man

Journal of Wilderness Medicine ◽

10.1580/0953-9859-2.2.94 ◽

1991 ◽

Vol 2 (2) ◽

pp. 94-101 ◽

Cited By ~ 2

Author(s):

J.S. Milledge ◽

S. McArthur ◽

A. Morice ◽

N. Luff ◽

R. Abrahams ◽

...

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Fluid Retention ◽

Exercise Induced ◽

Atrial Natriuretic

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Hemodynamic and renal effects of low-dose infusions of atrial peptide in awake dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1988.254.2.r161 ◽

1988 ◽

Vol 254 (2) ◽

pp. R161-R169 ◽

Cited By ~ 2

Author(s):

P. Bie ◽

B. C. Wang ◽

R. J. Leadley ◽

K. L. Goetz

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Sodium Excretion ◽

Plasma Renin ◽

Urine Flow ◽

Right Atrial ◽

Experimental Protocols ◽

Cardiac Filling ◽

Left And Right ◽

Atrial Natriuretic

The effects of alpha-human atrial natriuretic peptide (alpha-hANP) on cardiovascular and renal function in conscious dogs were evaluated in two experimental protocols. In one protocol, alpha-hANP was infused intravenously at increasing rates of 50, 100, and 200 ng.min-1.kg-1 (stepup infusion) during successive 20-min periods. The greatest responses occurred during the final 20-min period of the stepup infusion when the plasma concentration of immunoreactive atrial natriuretic peptide (irANP) was increased by 44-fold over preinfusion values; pressures in the aorta and both atria were decreased at this time, whereas glomerular filtration rate, urine flow, and sodium excretion were increased. In a second protocol, alpha-hANP was infused for 1 h at constant rates of either 12.5, 25, or 50 ng.min-1.kg-1; these constant infusions increased plasma irANP by 3-, 7-, and 12-fold, respectively. Each infusion rate decreased left and right atrial pressures and increased urine flow and sodium excretion. The two lowest infusion rates elevated plasma irANP to levels that would be expected to occur only during unusual physiological, or perhaps pathophysiological, conditions. The two highest infusion rates decreased plasma renin activity. Nevertheless, the accompanying maximal increases in sodium excretion were modest (41-72%). These data imply that small changes in circulating atrial peptides that presumably occur under normal physiological conditions would not have a dominant effect on the regulation of sodium excretion; the peptides may, however, play a modulatory role on sodium excretion under these conditions. It remains to be determined whether the ability of atrial peptides to lower cardiac filling pressures is of physiological significance.

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Atrial natriuretic peptide inhibits osmolality-induced arginine vasopressin release in man

Clinical Science ◽

10.1042/cs0750035 ◽

1988 ◽

Vol 75 (1) ◽

pp. 35-39 ◽

Cited By ~ 15

Author(s):

M. J. Allen ◽

V. T. Y. Ang ◽

E. D. Bennett ◽

J. S. Jenkins

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Arginine Vasopressin ◽

Plasma Osmolality ◽

Random Order ◽

Vasopressin Release ◽

Plasma Arginine ◽

Placebo Infusion ◽

Atrial Natriuretic

1. Eight normal volunteers were infused with 5% saline (5 g of NaCl/100 ml) at a rate of 0.06 ml min−1 kg−1 for 120 min to increase plasma osmolality and plasma arginine vasopressin. Human atrial natriuretic peptide (α-hANP; 100 μg) or placebo was given in random order in a double-bind cross-over design for the last 20 min of the saline infusion. 2. Compared with the placebo infusion, atrial natriuretic peptide (ANP) produced a 43% greater sodium excretion and a 34% greater urinary volume in the subsequent hour. 3. Mean plasma immunoreactive ANP did not increase in response to changes in osmolality and rose to a peak of 118 pg/ml during the α-hANP infusion. α-hANP produced significant suppression of mean plasma arginine vasopressin over the 60 min after the infusions. 4. We conclude that ANP is not released in response to increased osmolality in vivo, and that it inhibits osmolality-induced arginine vasopressin release in man.

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