Angiotensin II in the renal excretory response to behavioral stress in conscious dogs

Koepke, J P; Obrist, P. A.

doi:10.1152/ajpregu.1983.245.2.r259

Cited by 7 publications

(4 citation statements)

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“…Indirect support for this contention has been provided by studies which have demonstrated that a-adrenoceptor antagonists inhibited the angiotensin II-induced increase in active sodium transport in rat kidney cortical slices (Brunton, Parsons & Poat, 1978) and the angiotensin II-induced antinatriuresis in intact rats (Radhi, Chapman & Munday, 1982), implying that angiotensin II exerted its effect indirectly through the release of noradrenaline from sympathetic nerve endings. Two studies in the dog have also shown that captopril or angiotensin II receptor antagonists attenuated the renal nerve-mediated antinatriuresis during hypercapnic acidosis (Anderson, Henrich, Gross & Dillingham, 1982) or shock avoidance (Koepke & Obrist, 1983), in the absence of changes in renal haemodynamics. Together these data would establish that angiotensin II plays an important role in modulating neurotransmission at the level of the renal tubule comparable to that exhibited at neurovascular junctions within the sympathetic nervous system.…”

Section: Low-level Renal Nerve 8timulationmentioning

confidence: 97%

Interaction of the renin‐angiotensin system and the renal nerves in the regulation of rat kidney function.

Handa¹,

Johns²

1985

The Journal of Physiology

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SUMMARY1. Stimulation of the renal sympathetic nerves in pentobarbitone anaesthetized rats achieved a 13 % reduction in renal blood flow, did not change glomerular filtration rate, but reduced urine flow by 37 %, absolute sodium excretion by 37 %, and fractional sodium excretion by 34 %. Following inhibition of converting enzyme with captopril (0-38 mmol kg-' h-1), similar nerve stimulation reduced both renal blood flow and glomerular filtration rate by 16 %, and although urine flow and absolute sodium excretion fell by 32 and 31 %, respectively, the 18 % fall in fractional sodium excretion was significantly less than that observed in the absence of captopril.2. Renal nerve stimulation at low levels, which did not change either renal blood flow or glomerular filtration rate, reduced urine flow, and absolute and fractional sodium excretions by 25, 26 and 23 %, respectively.3. In animals receiving captopril at 0-38 mmol kg-' h-1, low-level nerve stimulation caused small increases in glomerular filtration rate of 7 % and urine flow of 12 %, but did not change either absolute or fractional sodium excretions. At one-fifth the dose of captopril (0-076 mmol kg-' h-'), low-level nerve stimulation did not change renal haemodynamics but decreased urine flow, and absolute and fractional sodium excretions by 10, 10 and 8 %, respectively. 4. These results showed that angiotensin II production was necessary for regulation of glomerular filtration rate in the face of modest neurally induced reductions in renal blood flow and was compatible with an intra-renal site of action of angiotensin II preferentially at the efferent arteriole. They also demonstrated that in the rat the action of the renal nerves to decrease sodium excretion was dependent on angiotensin II.

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Section: Low-level Renal Nerve 8timulationmentioning

confidence: 97%

Interaction of the renin‐angiotensin system and the renal nerves in the regulation of rat kidney function.

Handa¹,

Johns²

1985

The Journal of Physiology

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“…The results of the present study would also be compatible with the view that angiotensin II may interact synergistically with the renal nerves, during reflex activation, to decrease sodium excretion by facilitating adrenergic transmission at the neuro-tubular epithelial junction. Several studies in the dog support this contention, as it was shown that captopril or angiotensin II receptor antagonists attenuated the renal nerve-mediated antinatriuresis during hypercapnic acidosis (Anderson et al 1982) or shock avoidance (Koepke & Obrist, 1983), without changing renal haemodynamic responses. Together these studies strongly suggest that angiotensin II can facilitate neurotransmission at the neuro-tubular epithelial junction comparable to that exhibited at the neuro-vascular junctions of the sympathetic nervous system.…”

mentioning

confidence: 95%

The role of angiotensin II in the renal responses to somatic nerve stimulation in the rat.

Handa¹,

Johns²

1987

The Journal of Physiology

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SUMMARY1. Electrical stimulation of the brachial nerves at 3 Hz (15 V, 0-2 ms), in sodium pentobarbitone-anaesthetized rats whose renal arterial pressure was held constant, elicited a 26 % increase in systemic blood pressure, a 15 % rise in heart rate, an 11 % reduction in renal blood flow, did not alter glomerular filtration rate and significantly reduced absolute and fractional sodium excretions and urine flow by 44, 49 and 31%, respectively.2. In a separate group of rats, brachial nerve stimulation at 3 Hz increased plasma renin activity approximately 2-fold, while in animals in which the brachial nerves were not stimulated plasma renin activity did not change.3. Following inhibition of the renin-angiotensin system with captopril or sar-1-ile-8-angiotensin II, brachial nerve stimulation resulted in similar increases in systemic blood pressure and heart rate as in the animals with an intact renin-angiotensin system but, in captopril-infused rats, did not change renal haemodynamics or urine flow while absolute and fractional sodium excretions were reduced by 20 and 25 %, respectively. In sar-l-ile-8-angiotensin II-infused animals, similar nerve stimulation decreased renal blood flow by 12%, glomerular filtration rate by 7% and absolute and fractional sodium excretions and urine flow by 25, 18 and 18%, respectively. These decreases in sodium and water output were significantly smaller than those observed in animals with an intact renin-angiotensin system. 4. Stimulation of the brachial nerves increased post-ganglionic efferent renal nerve activity by 20 % and the magnitude of this response was unaffected following inhibition of the renin-angiotensin system. 5. The results show that low rates of brachial nerve stimulation in the rat can increase efferent renal nerve activity and result in an antinatriuresis and antidiuresis which is dependent on the presence of angiotensin II, and appears to be due to an action of angiotensin II at the level of the kidney.

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“…In our study, dogs did not face an acute stress, but a chronic anxiety problem: it is possible that under this condition the hematological system does not react with a ''stress leukogram,'' but with less clear variations. Individual differences (Lawler et al, 1975;Koepke and Obrist, 1983) may further increase variability in stress responses and make interpretation even more difficult (Beerda et al, 1997). No difference was found in mean heart rate in Anxious and Nonanxious dogs over time.…”

Section: Discussionmentioning

confidence: 98%

Efficacy of a diet containing caseinate hydrolysate on signs of stress in dogs

Palestrini

Minero

Cannas

et al. 2010

Journal of Veterinary Behavior

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The purpose of this randomized, double-blind, placebo-controlled trial was to evaluate the efficacy of a diet containing caseinate hydrolysate (CH) on signs of stress in 2 groups of dogs (defined as Anxious and Nonanxious), using physiological (serum cortisol and lysozyme, N:L ratios and heart rate) and behavioral parameters.From an initial group of 40 female Beagle dogs, ranging in age from 10 months to 4 years (mean 5 1.47 years; SD 5 0.53) belonging to a dog colony, 32 were selected for this study according to their level of anxiety. A group of 16 Anxious dogs and a group of 16 Nonanxious dogs were identified.A baseline period, aimed to obtain reference values of investigated parameters, preceded the experimental phase. Both groups (Anxious and Nonanxious) were divided into a treatment group, which received the diet containing CH, and a control group which received a placebo diet (PD). Anxious CH and PD groups were balanced for anxiety level. Each dog was evaluated 3 times a day at 4 weeks intervals (T1-T2-T3). Each evaluation lasted 2 days and involved a Reactivity Evaluation Form, a blood sampling, heart rate recording, and a 10-minute behavioral video recording. Results from Reactivity Evaluation Form scores showed that although at T1 Anxious dogs had significantly higher scores (Mann-Whitney test, P , 0.001) compared with Nonanxious dogs, no difference was found between Anxious dogs fed with CH diet and Nonanxious fed with PD or CH diet at T3. Behavioral observations evidenced some signs of improvement in Anxious dog fed with CH diet. Cortisol level significantly decreased in Anxious dogs fed with CH diet (Friedman test, P , 0.05). Individual differences in physiological measures of stress responses may have contributed to the large variability, making interpretation of these measures difficult. These results suggest that CH may be used as a functional ingredient alleviating stress in dogs.

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Angiotensin II in the renal excretory response to behavioral stress in conscious dogs

Cited by 7 publications

References 0 publications

Interaction of the renin‐angiotensin system and the renal nerves in the regulation of rat kidney function.

Interaction of the renin‐angiotensin system and the renal nerves in the regulation of rat kidney function.

The role of angiotensin II in the renal responses to somatic nerve stimulation in the rat.

Efficacy of a diet containing caseinate hydrolysate on signs of stress in dogs

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