Plasma renin activity and thirst following hypovolemia or caval ligation in rats

Leenen, F. H. H.; Stricker, EM

doi:10.1152/ajplegacy.1974.226.5.1238

Cited by 44 publications

(18 citation statements)

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“…Angiotensin II, when injected into sensitive areas of the brain (40,41) or when injected systemically, is a powerful stimulus for water intake, as is activation of the renin-angiotensin axis (42), providing a mechanistic explanation for the association of thirst with abnormalities of body fluid volume. Thirst is a common complaint for patients with congestive heart failure (43,44), frequently plagues dialysis patients, and likely contributes to the prevalence of hyponatremia in these populations.…”

Section: Thirstmentioning

confidence: 99%

Osmotic Homeostasis

Danziger

Zeidel

2015

Clinical Journal of the American Society of Nephrology

170

103

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Alterations in water homeostasis can disturb cell size and function. Although most cells can internally regulate cell volume in response to osmolar stress, neurons are particularly at risk given a combination of complex cell function and space restriction within the calvarium. Thus, regulating water balance is fundamental to survival. Through specialized neuronal "osmoreceptors" that sense changes in plasma osmolality, vasopressin release and thirst are titrated in order to achieve water balance. Fine-tuning of water absorption occurs along the collecting duct, and depends on unique structural modifications of renal tubular epithelium that confer a wide range of water permeability. In this article, we review the mechanisms that ensure water homeostasis as well as the fundamentals of disorders of water balance.

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Section: Thirstmentioning

confidence: 99%

Osmotic Homeostasis

Danziger

Zeidel

2015

Clinical Journal of the American Society of Nephrology

170

103

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“…These responses were maintained in adrenalectomized animals, but were reduced after nephrectomy. In view of the facts that renal renin secretion, and hence circulating angiotensin concentrations, are enhanced following extracellular fluid volume depletion (Leenen & Stricker, 1974) and that angiotensin, at physiological concentrations, stimulates intestinal fluid transport, it would seem likely that the responses of the intestine to extracellular volume manipulation are, at least to some degree, under the control ofthe renin-angiotensin system . Also associated with extracellular fluid volume depletion is a general increase in sympathetic nervous system activity (Folkow, 1955) which, on the basis of the effects of noradrenaline on intestinal function, would also be expected to alter the rate of intestinal transport.…”

Section: Measurement Of Intestinal Fluid Transportmentioning

confidence: 99%

Noradrenaline as a possible mediator of the actions of angiotensin on fluid transport by rat rejunum in vivo

Levens

Munday

Parsons

et al. 1979

The Journal of Physiology

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SUMMARY1. Net fluid absorption and transmural potential difference were measured in the rat jejunum in vivo.2. Increased rates of net fluid transport were observed following infusions of angiotensin or noradrenaline. There was a small, but significant, fall in transmural p.d. associated with noradrenaline but not with angiotensin infusions.3. The a-adrenergic antagonists phentolamine and dihydroergotamine abolished both the angiotensin and the noradrenaline stimulations of transport and the noradrenaline-induced fall in p.d., whereas the ,f-adrenergic antagonist propranolol did not significantly affect these responses.4. Phentolamine did not alter the rise in p.d. following administration of the cholinergic agonist pilocarpine.5. The protein synthesis inhibitor cycloheximide abolished both the angiotensin and the noradrenaline-induced stimulation of fluid transport.6. Neither angiotensin nor noradrenaline significantly altered jejunal cyclic AMP levels. 7. Bilateral nephrectomy had no apparent effect upon the increase in fluid transport following noradrenaline infusions.8. The noradrenaline-induced stimulation of transport was unaffected, and the fall in p.d. potentiated in rats pre-treated with reserpine, but a marked inhibition of transport was observed following angiotensin infusions.9. The results are consistent with the view that noradrenaline may mediate the actions of angiotensin upon intestinal fluid absorption in the rat.

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“…For example, when subcutaneous injections of polyethylene glycol (PEG) solution in rats were used to disrupt the Starling equilibrium and cause progressive deficits in plasma volume without affecting arterial blood pressure (25, 34), large quantities of water and NaCl solution were consumed in amounts appropriate to form an isotonic fluid mixture sufficient to repair the deficits (27,30,32). In addition, there was increased neurohypophysial secretion of vasopressin (VP) (9, 36), which has important pressor actions during hypovolemia (12), as well as activation of the renin-angiotensin-aldosterone system (18,35).In previous studies of hypovolemic thirst, rats given access to drinking water immediately after PEG treatment experienced osmotic dilution of systemic body fluids due to renal retention of ingested water. Osmotic dilution inhibited further water intake, despite continued plasma volume deficits (26), whereas consumption of concentrated NaCl solution was stimulated (32).…”

mentioning

confidence: 99%

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confidence: 99%

Presystemic influences on thirst, salt appetite, and vasopressin secretion in the hypovolemic rat

Smith¹,

Curtis²,

Smith³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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The present studies investigated the influence of presystemic signals on the control of thirst, salt appetite, and vasopressin (VP) secretion in rats during nonhypotensive hypovolemia. Rats were injected with 30% polyethylene glycol (PEG) solution, deprived of food and water overnight, and then allowed to drink water, 0.15 M NaCl, or 0.30 M NaCl. The PEG treatment, which produced 30-40% plasma volume deficits, elicited rapid intakes in an initial bout of drinking, but rats consumed much more 0.15 M NaCl than water or 0.30 M NaCl. In considering why drinking stopped sooner when water or concentrated saline was ingested, it seemed relevant that little or no change in systemic plasma Na(+) concentration was observed during the initial bouts and that the partial repair of hypovolemia was comparable, regardless of which fluid was consumed. In rats that drank 0.15 M NaCl, gastric emptying was fastest and the combined volume of ingested fluid in the stomach and small intestine was largest. These and other observations are consistent with the hypothesis that fluid ingestion by hypovolemic rats is inhibited by distension of the stomach and proximal small intestine and that movement of dilute or concentrated fluid into the small intestine provides another presystemic signal that inhibits thirst or salt appetite, respectively. On the other hand, an early effect of water or saline consumption on VP secretion in PEG-treated rats was not observed, in contrast to recent findings in dehydrated rats. Thus the controls of fluid ingestion and VP secretion are similar but not identical during hypovolemia.

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Plasma renin activity and thirst following hypovolemia or caval ligation in rats

Cited by 44 publications

References 0 publications

Osmotic Homeostasis

Osmotic Homeostasis

Noradrenaline as a possible mediator of the actions of angiotensin on fluid transport by rat rejunum in vivo

Presystemic influences on thirst, salt appetite, and vasopressin secretion in the hypovolemic rat

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