Renal Function in Saline-Loaded Dogs with Minimal Sodium Excretion

1973 ◽  
Vol 51 (2) ◽  
pp. 148-152 ◽  
Author(s):  
Mortimer Levy ◽  
Earle A. Lockhart
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Arterial Blood ◽  
Saline Loading ◽  
Blood Pressure Fall ◽  
Pressure Fall

In this laboratory, dogs acutely saline-loaded to 7–8% body weight and treated with large doses of antidiuretic hormone and deoxycorticosterone acetate will excrete on the average 400–700 μequiv/min of sodium. We have been able to study five dogs, similarly treated, which for no apparent cause showed a trivial natriuretic response following comparable volume expansion. Postexpansion sodium excretion varied from 30 to 150 μequiv/min. Glomerular filtration rate and arterial blood pressure remained constant, but in each case p-aminohippurate clearance rate (CPAH) fell in response to acute saline loading. Renal vasodilatation with acetylcholine and elevation of perfusion pressure with noradrenaline reversed the sodium retention. Fractional reabsorption in the proximal tubule was normal, and the loop of Henle appeared to be the major nephron site responsible for the augmented sodium reabsorption. Constancy of arterial blood pressure, fall in CPAH, and response to altered intrarenal hemodynamics seem to characterize these saline-loaded dogs with minimal sodium excretion as a unique population.

Pressure natriuresis during saline expansion in newborn and adult dogs

1984 ◽  
Vol 246 (6) ◽  
pp. F828-F834 ◽  
Author(s):  
L. I. Kleinman ◽  
R. O. Banks
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Renal Perfusion Pressure ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Glomerular Filtrate ◽  
Pressure Natriuresis

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.

Rhythmicity of urinary sodium excretion, mean arterial blood pressure, and heart rate in conscious dogs

1992 ◽  
Vol 262 (1) ◽  
pp. H149-H156 ◽  
Author(s):  
U. Palm ◽  
W. Boemke ◽  
H. W. Reinhardt
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Conscious Dogs ◽  
Arterial Blood ◽  
Infusion Regimen

The existence of urinary excretion rhythms in dogs, which is a matter of controversy, was investigated under strictly controlled intake and environmental conditions. In seven conscious dogs, 14.5 mmol Na, 3.55 mmol K, and 91 ml H2O.kg body wt-1.24 h-1 were either administered with food at 8:30 A.M. or were continuously infused at 2 consecutive days. During these 3 days, automatized 20-min urine collections, mean arterial blood pressure (MABP), and heart rate (HR) recordings were performed without disturbing the dogs. Fundamental and partial periodicities, the noise component of urinary sodium excretion (UNaV), MABP, and HR were analyzed using a method derived from Fourier and Cosinor analysis. Oral intake (OI) leads to powerful 24-h periodicities in all dogs and seems to synchronize UNaV. UNaV on OI peaked between 1 and 3 P.M. Under the infusion regimen, signs of nonstationary rhythms and desynchronization predominated. UNaV under the infusion regimen could be separated into two components: a rather constant component continuously excreted and superimposed to this an oscillating component. No direct coupling between UNaV and MABP periodicities could be demonstrated. On OI, an increase in HR seems to advance the peak UNaV in the postprandial period. HR and MABP signals were both superimposed with noise. We conclude that UNaV rhythms are present in dogs. They are considerably more pronounced on OI.

Increased synthesis and release of atrial peptide during DOCA escape in conscious dogs

1987 ◽  
Vol 252 (1) ◽  
pp. R188-R192
Author(s):  
C. H. Metzler ◽  
D. G. Gardner ◽  
L. C. Keil ◽  
J. D. Baxter ◽  
D. J. Ramsay
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Natriuretic Peptides ◽  
Messenger Rna ◽  
Conscious Dogs ◽  
Sodium Retention ◽  
Atrial Natriuretic Peptides ◽  
Escape Phenomenon ◽  
Arterial Blood

The escape from the sodium-retaining effects of prolonged mineralocorticoid treatment in animals and humans was first noted over 40 yr ago, but despite intense study the mechanisms responsible for the escape phenomenon have not been identified. Putative “natriuretic hormones” have been proposed to account for the escape phenomenon. To determine whether atrial natriuretic peptides (ANP) could participate in the escape phenomenon, the mineralocorticoid deoxycorticosterone acetate (DOCA) was administered to conscious dogs for 14 days. Escape was accompanied by a doubling of plasma ANP concentration and four- to sevenfold increases in cardiac ANP messenger RNA. There were also significant increases in mean arterial blood pressure during the last 8 days of DOCA treatment. Thus increases in the synthesis and secretion of ANP and increases in atrial pressure may represent mechanisms that contribute to the escape from mineralocorticoid-induced sodium retention.

scholarly journals Arterial Blood Pressure and Renal Sodium Excretion in Dopamine D3 Receptor Knockout Mice

2007 ◽  
Vol 30 (1) ◽  
pp. 93-101 ◽  
Author(s):  
Torsten STAUDACHER ◽  
Bärbel PECH ◽  
Michael TAPPE ◽  
Gerhard GROSS ◽  
Bernd MÜHLBAUER ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Knockout Mice ◽  
Sodium Excretion ◽  
Dopamine D3 Receptor ◽  
D3 Receptor ◽  
Arterial Blood ◽  
Renal Sodium Excretion ◽  
Dopamine D3

Hormonal regulation of renal sodium and water excretion during normotensive sodium loading in conscious dogs

2000 ◽  
Vol 278 (1) ◽  
pp. R11-R18 ◽  
Author(s):  
Niels C. F. Sandgaard ◽  
Jens Lundbæk Andersen ◽  
Peter Bie
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Plasma Osmolality ◽  
Conscious Dogs ◽  
Ang Ii ◽  
Water Excretion ◽  
Arterial Blood ◽  
Sodium Loading

.—Saline was infused intravenously for 90 min to normal, sodium-replete conscious dogs at three different rates (6, 20, and 30 μmol ⋅ kg− 1 ⋅ min− 1) as hypertonic solutions (HyperLoad-6, HyperLoad-20, and HyperLoad-30, respectively) or as isotonic solutions (IsoLoad-6, IsoLoad-20, and IsoLoad-30, respectively). Mean arterial blood pressure did not change with any infusion of 6 or 20 μmol ⋅ kg− 1 ⋅ min− 1. During HyperLoad-6, plasma vasopressin increased by 30%, although the increase in plasma osmolality (1.0 mosmol/kg) was insignificant. During HyperLoad-20, plasma ANG II decreased from 14 ± 2 to 7 ± 2 pg/ml and sodium excretion increased markedly (2.3 ± 0.8 to 19 ± 8 μmol/min), whereas glomerular filtration rate (GFR) remained constant. IsoLoad-20 decreased plasma ANG II similarly (13 ± 3 to 7 ± 1 pg/ml) concomitant with an increase in GFR and a smaller increase in sodium excretion (1.9 ± 1.0 to 11 ± 6 μmol/min). HyperLoad-30 and IsoLoad-30 increased mean arterial blood pressure by 6–7 mmHg and decreased plasma ANG II to ∼6 pg/ml, whereas sodium excretion increased to ∼60 μmol/min. The data demonstrate that, during slow sodium loading, the rate of excretion of sodium may increase 10-fold without changes in mean arterial blood pressure and GFR and suggest that the increase may be mediated by a decrease in plasma ANG II. Furthermore, the vasopressin system may respond to changes in plasma osmolality undetectable by conventional osmometry.

Control of renin secretion in the anesthetized dog

1964 ◽  
Vol 207 (3) ◽  
pp. 537-546 ◽  
Author(s):  
Arthur J. Vander ◽  
Richard Miller
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Blood Pressure Reduction ◽  
Renin Secretion ◽  
Aortic Clamping ◽  
Arterial Blood ◽  
Pressor Activity ◽  
Intrarenal Pressure ◽  
Venous Plasma

Renin concentrations of renal venous plasma were indirectly measured by bio-assaying the pressor activity produced by plasma incubation under standardized conditions. Pressor activity was detectable in 85% of control dogs, was reciprocally related to sodium excretion, but did not correlate with arterial blood pressure. Reduction of mean renal arterial pressure to 90 mm Hg by an aortic clamp decreased sodium excretion and produced sustained increases in renin secretion and arterial blood pressure proximal to the clamp. Release of the aortic clamp resulted in gradual return of these variables toward control values. Induction of diuresis (osmotic diuretics, chlorothiazide, or acetazolamide) prior to aortic clamping minimized or completely prevented the usual clamp-induced rises in renin secretion and proximal blood pressure. Induction of diuresis during aortic clamping returned the elevated renin secretion and proximal blood pressure toward control values. These effects of diuretics could not be explained by changes in renal hemodynamics or plasma composition. Elevation of ureteral pressure in nondiuretic dogs also increased renin secretion and arterial blood pressure. We conclude that renin secretion is not controlled by blood pressure, per se, or intrarenal pressure, but by the flow or composition of intratubular fluid, probably at the level of the macula densa.

Blood Pressure Variability and Optimal Cerebral Perfusion Pressure—New Therapeutic Targets in Traumatic Brain Injury

Neurosurgery ◽  
2019 ◽  
Vol 86 (3) ◽  
pp. E300-E309 ◽  
Author(s):  
Teodor Svedung Wettervik ◽  
Timothy Howells ◽  
Anders Lewén ◽  
Per Enblad
Keyword(s):  
Blood Pressure ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Perfusion Pressure ◽  
Arterial Blood Pressure ◽  
Blood Pressure Variability ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Arterial Blood ◽  
Optimal Cerebral Perfusion Pressure

Abstract BACKGROUND Optimal cerebral perfusion pressure (CPPopt) is an autoregulatory-oriented target in the neurointensive care (NIC) of patients with traumatic brain injury (TBI), and deviation from CPPopt is associated with poor outcome. We recently found that blood pressure variability (BPV) is associated with deviation from CPPopt. OBJECTIVE To evaluate BPV and other variables related to deviation from CPPopt and to evaluate challenges and strategies for autoregulatory-oriented treatment in TBI. METHODS Data including arterial blood pressure and intracranial pressure (ICP) from 362 TBI patients treated at the NIC unit, Uppsala University Hospital, Sweden, between 2008 and 2016, were retrospectively analyzed day 2 to 5. RESULTS Higher BPV was a strong predictor of both CPP deviation below and above CPPopt after multiple regression analyses. There was no other explanatory variable for CPP deviation above CPPopt, whereas also higher ICP and worse autoregulation (higher pressure reactivity index) were associated with CPP deviation below CPPopt. A higher BPV was, in turn, explained by older age, lower ICP, higher mean arterial blood pressure, and higher slow arterial blood pressure amplitude (0.018-0.067 Hz). CONCLUSION BPV was strongly associated with deviation from CPPopt. High age is a risk factor for high BPV and hence CPP insults. Our treatment protocol is focused on avoiding CPP below 60 mm Hg. It is possible that a more restrictive upper level could generate more stable blood pressure and less deviation from CPPopt.

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