Salt-induced hypertension in the dog

Ja, Visconti

doi:10.1152/ajplegacy.1966.210.1.186

Cited by 23 publications

(7 citation statements)

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“…As obesity was induced by increasing the amount of the same feed, sodium intake was most likely higher during the weight gain phase of the weigh-change group (S2 Table). While an increase in blood pressure, volume and flow after receiving a diet containing high amounts of sodium (4 g/kg body weight) have been seen in an experimental study using dogs, the sodium content was considerably higher than what the dogs received in our study [74]. Dogs are able to tolerate a wide range of sodium concentrations in the diet as long as access to water remains available [75].…”

Section: Plos Onecontrasting

confidence: 46%

Weight-gain induced changes in renal perfusion assessed by contrast-enhanced ultrasound precede increases in urinary protein excretion suggestive of glomerular and tubular injury and normalize after weight-loss in dogs

et al. 2020

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Early detection of obesity-related glomerulopathy in humans is challenging as it might not be detected by routine biomarkers of kidney function. This study's aim was to use novel kidney biomarkers and contrast-enhanced ultrasound (CEUS) to evaluate the effect of obesity development and weight-loss on kidney function, perfusion, and injury in dogs. Sixteen healthy lean adult beagles were assigned randomly but age-matched to a control group (CG) (n = 8) fed to maintain a lean body weight (BW) for 83 weeks; or to a weight-change group (WCG) (n = 8) fed the same diet to induce obesity (week 0-47), to maintain stable obese weight (week 47-56) and to lose BW (week 56-83). At 8 time points, values of systolic blood pressure (sBP); serum creatinine (sCr); blood urea nitrogen (BUN); serum cystatin C (sCysC); urine protein-to-creatinine ratio (UPC); and urinary biomarkers of glomerular and tubular injury were measured. Glomerular filtration rate (GFR) and renal perfusion using CEUS were assayed (except for week 68). For CEUS, intensity-and time-related parameters representing blood volume and velocity were derived from imaging data, respectively. At 12-22% weight-gain, cortical time-to-peak, representing blood velocity, was shorter in the WCG vs. the CG. After 37% weight-gain, sCysC, UPC, glomerular and tubular biomarkers of injury, urinary immunoglobulin G and urinary neutrophil gelatinase-associated lipocalin, respectively, were higher in the WCG. sBP, sCr, BUN and GFR were not significantly different. After 23% weight-loss, all alterations were attenuated. Early weight-gain in dogs

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Section: Plos Onecontrasting

confidence: 46%

Weight-gain induced changes in renal perfusion assessed by contrast-enhanced ultrasound precede increases in urinary protein excretion suggestive of glomerular and tubular injury and normalize after weight-loss in dogs

et al. 2020

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“…Herein, we refer to salt-induced changes of this time course as 'acute' to distinguish them from much slower salt-induced effects discussed in subsequent sections. Acute salt sensitivity of blood pressure has been demonstrated in experiments involving a number of species including chickens, 19,20 dogs, [21][22][23][24] green monkeys, 25 mice, 26 pigs, 27 rabbits, 28,29 rats [30][31][32][33][34] and spider monkeys. 25,35 An example of the time course of the blood pressure response to a high-salt diet in regular Sprague-Dawley rats is shown in Figure 2.…”

Section: Acute Salt Sensitivity Of Blood Pressurementioning

confidence: 99%

“…21,22,24 In other species, the long-term effects of excess salt have not been investigated in detail in the few studies that have appeared, conclusions are limited because of the short duration of salt exposure, the lack of time course data or the reliance on special measures to induce or amplify salt sensitivity of blood pressure. In rabbits, for example, addition of 5 g day À1 NaCl for 8 months was associated with significant increases in blood pressure, but the time course data presented suggest that the increase in blood pressure was not progressive, with blood pressure stabilizing within the first 6 weeks or so.…”

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confidence: 99%

The time course of salt-induced hypertension, and why it matters

Vliet

Montani

2008

Int J Obes

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The epidemiology of salt-induced hypertension has been explored in detail in animal studies, in some cases involving exposures to excess dietary salt for much of the animal's lifespan. The results of these studies demonstrate the presence of two distinct time courses of the blood pressure response to a high salt intake: an acute (rapid) blood pressure response occurring over days to weeks, and a slow and progressive blood pressure response that develops over extremely long periods of time, amounting to a significant fraction of the lifespan in normal individuals. The acute form of salt sensitivity is well known in humans, having often been demonstrated as a fall in blood pressure during the period of salt restriction. The slow and progressive form of salt sensitivity has been demonstrated directly in rats and chimpanzees and is also evident in analyses of human cross-population data as a salt dependency of age-associated changes of blood pressure. This slow and progressive component of salt-induced hypertension may be attributable, at least in part, to a progressive rise in the acute salt sensitivity of blood pressure during sustained exposure to high salt. However, a progressively irreversible or 'self sustaining' component of salt-induced hypertension has also been demonstrated in rat studies. This irreversible component has not been completely characterized, but its presence raises the possibility that blood pressure responses to salt restriction may not fully reveal the contribution of salt to blood pressure or the epidemiology of hypertension. These various components of salt sensitivity (acute vs slow, reversible vs irreversible) should be considered in any comprehensive explanation of the effects of salt on blood pressure and especially in experimental studies of the genetic and physiological mechanisms underlying salt-induced hypertension.

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“…Most experimental studies on vascular responses have been performed on various strains of rats. However because other reports have shown that a high‐salt diet can result in a rise in blood pressure in the dog, 7 the present series of experiments was designed to investigate the reactivity of the pressurized mesenteric resistance artery of the dog to vasoactive agents following the feeding of different levels of salt in the diet.…”

Section: Introductionmentioning

confidence: 99%

High‐salt diet and responses of the pressurized mesenteric artery of the dog to noradrenaline and acetylcholine

Sofola

Knill

Myers

et al. 2004

Clin Exp Pharma Physio

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A high-salt diet in rats has been shown to result in enhanced vasoconstrictor and/or reduced vasodilator responses of isolated arteries to agonists. The present experiments were designed to investigate the effects of dietary salt on the responses of the pressurized mesenteric resistance artery of the dog to constrictor and dilator agents. Dogs were fed diets containing three different levels of salt with sodium concentrations (in mmol/kg per day) of 0.4 (low salt; LS), 3.0 (intermediate salt; IS) and 6.0 (high salt; HS) for a period of 4 weeks. At the end of the feeding period, animals were killed and lengths of third-order mesenteric artery were obtained and mounted in a perfusion myograph and changes in internal diameter were measured using a microscope and video-tracking device. The responses to noradrenaline (NA), acetylcholine (ACh) and sodium nitroprusside (SNP) were then determined. The vasoconstrictor responses to NA were identical in the three groups. However, the relaxation response of the vessels to ACh was attenuated in HS dogs compared with LS dogs (P < 0.05), but not with IS dogs. The application of N(G)-nitro-l-arginine methyl ester, an inhibitor of nitric oxide synthase, reduced the relaxation responses to ACh comparably in all three groups. The relaxation responses of the vessels to SNP were similar in all groups. These results indicate that, in the dog mesenteric resistance artery, a high-salt diet does not affect vasoconstrictor responses to NA, but does attenuate the vasorelaxant action of ACh, largely by inhibiting the production of endothelium-derived relaxing factor.

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Salt-induced hypertension in the dog

Cited by 23 publications

References 0 publications

Weight-gain induced changes in renal perfusion assessed by contrast-enhanced ultrasound precede increases in urinary protein excretion suggestive of glomerular and tubular injury and normalize after weight-loss in dogs

Weight-gain induced changes in renal perfusion assessed by contrast-enhanced ultrasound precede increases in urinary protein excretion suggestive of glomerular and tubular injury and normalize after weight-loss in dogs

The time course of salt-induced hypertension, and why it matters

High‐salt diet and responses of the pressurized mesenteric artery of the dog to noradrenaline and acetylcholine

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