Lack of evidence for a hepatic osmoreceptor mechanism in conscious dogs

Schneider, E. G.; Davis, JO; Robb, CA; Baumber, JS; Johnson, J. A.; Wright, Fay

doi:10.1152/ajplegacy.1970.218.1.42

Cited by 40 publications

(18 citation statements)

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“…Note added in proof Since the submission of this report, Schneider, Davis, Robb, Baumber, Johnson & Wright (1970) found no evidence for an osmoreceptor mechanism (Haberich, 1968) in the liver of the dog. A low perfusion rate into the hepatic portal vein did not induce a diuretic or natriuretic response, but a faster rate of perfusion rate did.…”

Section: Resultsmentioning

confidence: 93%

The influence of hepatic portal circulation on urine flow

Liang¹

1971

The Journal of Physiology

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SUMMARY1. A study of the effect of changes in the hepatic portal venous pressure (HPVP) on the rate of urine flow in dogs has been made. Normally this pressure varies between 3-7 and 14-9 cm H20. It can be raised or lowered by varying the method of manipulation of the visceral organs.2. When the HPVP was raised within 15 cm H20 above the premanipulation level it caused an increase in urine flow to 2-3 times the normal levels within 2-5 sec. If the HPVP was raised to more than 15 cm H20 above the pre-manipulation levels it resulted in a period of antidiuresis. The urine flow returned rapidly to normal level immediately after the pressure was released.3. The kidney volume increased when an induced diuresis occurred and decreased when an antidiuresis occurred.4. The urine chloride concentration decreased during diuresis, but total chloride excretion increased. Total chloride excretion was reduced when an antidiuresis occurred.5. Topical application of local anaesthetics at the hilus of the kidney and on the renal nervous plexus abolished the response. This and other evidence indicate that this effect on urine flow is a result of nervous reflex activity, probably involving the sympathetic but not the vagus.6. The receptive area lies in the mesentery between the mesenteric capillaries and the main portal vein.

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Section: Resultsmentioning

confidence: 93%

The influence of hepatic portal circulation on urine flow

Liang¹

1971

The Journal of Physiology

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“…Despite some reports to the contrary (Potkay & Gilmore, 1970;Schneider, Davis, Robb, Baumber, Johnson & Wright, 1970) electrophysiological (Niijima, 1969a;Andrews & Orbach, 1973Adachi, Niijima & Jacobs, 1976) and behavioural (Daly, Roe & Horrocks, 1967;Strandhoy & Williamson, 1970;Lin & Blake, 1971;Passo, Thornborough & Rothballer, 1973) studies provide good evidence for neural receptors located in the liver which are sensitive to increased sodium concentration in the blood of the hepatic portal vein. There is conflicting evidence with respect to gluco-sensitive receptors (Niijima, 1939b; Andrews & Orbach, 1973; Russek, 1970;Stephens & Baldwin, 1974) and osmoreceptors (Schneider et al 1970; Niijima, 1969a;Andrews & Orbach, 1974;Adachi et al 1976;Passo et al 1973;PHY 274 130 W. D. BLAKE AND K. K. LIN Haberich, 1968).…”

Section: Introductionmentioning

confidence: 98%

“…There is conflicting evidence with respect to gluco-sensitive receptors (Niijima, 1939b; Andrews & Orbach, 1973; Russek, 1970;Stephens & Baldwin, 1974) and osmoreceptors (Schneider et al 1970; Niijima, 1969a;Andrews & Orbach, 1974;Adachi et al 1976;Passo et al 1973;PHY 274 130 W. D. BLAKE AND K. K. LIN Haberich, 1968). The present report deals with the sodium and glucose receptors involved in the control of NaCl solution drinking and with some of these characteristics which are consistent with dependence on an electrogenic Na pump.…”

Section: Introductionmentioning

confidence: 99%

Hepatic portal vein infusion of glucose and sodium solutions on the control of saline drinking in the rat.

Blake¹,

Lin²

1978

The Journal of Physiology

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6. Results are consistent with the presence of afferent nerve terminals in hepatic portal vessels which are sensitive to change in NaCl or glucose concentration and which, in response thereto, alter drinking behaviour. The effects of NaCl and glucose on the discharge rate of the nerve terminals may be interpreted in terms of changing activity or electrogenicity of a Na pump but changes in membrane conductance or Na influx cannot be ruled out.

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“…The use of this simultaneous infusion technique confined the osmotic perturbations to the liver and its vasculature (and to a segment of the vena cava) and thereby precluded the activation of putative osmoreceptors located in the brain (Blass & Epstein, 1971;Peck & Novin, 1971;Verney, 1947; but also see Bie, 1980) or elsewhere in the viscera (Goldstein & Halperin, 1977;Inchina & Finkinshtein, 1964). However, although the data from several investigations have provided additional support for the finding that hepatic mechanisms influence fluid balance (Daly et al, 1967;Lydtin, 1969;Passo et al, 1973), other studies have produced conflicting results (Glasby & Ramsay, 1974;Kapteina, Motz, Schwartz-Porsche, & Gauer, 1978;Lindahl, Lund, Boas, & Schmidt, 1974;Potkay & Gilmore, 1970;Schneider, Davis, Robb, Baumber, Johnson, & Wright, 1970).…”

Section: Discussionmentioning

confidence: 99%

Visceral control of drinking in rats

Martin

Novin

1982

Psychobiology

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Hepatic-portal infusion of .77 M NaCI (.5% aWl resulted in a shorter latency to drink than did jugular infusion for both sham-operated rats and rats subjected to abdominal vagotomy. However, .5-h water intake was not differentially. affected by the route of hypertonic saline infusion in either group. Hepatic-portal infusion of an isotonic saline load resulted in greater water intake than did jugular infusion for both vagotomized and control rats, and the latency was shorter in vagotomized rats, but not in control animals, after hepatic-portal infusion than after a jugular infusion. Hypertonic saline was a more potent dipsogenic stimulus than isotonic saline for both routes of infusion, and vagotomy reduced water consumption produced by osmotic challenge. The results provide some evidence for a hepatic drinking system by demonstrating a differential effect of hepatic-portal and systemic saline infusions. However, this effect persists after abdominal vagotomy and possibly 'is mediated wholly, or in part, by other visceral innervation. In addition, abdominal vagotomy reduced water intake, but not latency to drink, induced with osmotic challenge given via either vascular route, an effect that may possibly be due to alterations in gastrointestinal function or to loss of afferent input from hypothetical visceral osmo-or sodium-sensitive cells that modulate drinking.Recent experimental results have provided evidence that receptors located within the circulation of the liver detect perturbations in water and electrolyte balance and activate appropriate homeostatic mechanisms (Sawchenko & Friedman, 1979). Electrophysiological investigations have provided evidence for the existence of osmo-or sodium-sensitive cells in several species (Adachi, Niijima, & Jacobs, 1976;Andrews & Orbach, 1974;Niijima, 1969). In addition, a number of studies have demonstrated the greater efficacy of hepatic-portal infusions of saline loads than of systemic infusions in eliciting physiologicalcompensatoryresponses (Daly, Roe, & Horrocks, 1967;Haberich, Aziz, & Nowacki, 1965;Lydtin, 1969;Passo, Thornborough, & Rothballer, 1973). However, relatively few investigations have considered the behavioral consequences of the activation of hepatic sodium-or osmo-sensitive mechanisms. Lin and Blake (1971) hepatic-portal infusion of hypertonic saline decreased saline drinking, whereas infusion of hypertonic saline through the vena cava, as well as infusion of an equiosmotic sodium-free solution through either vein, failed to alter intake in a test of rats deprived of fluid for 24 h and then presented simultaneously with both water and saline. More recently, Blake and Lin (1978) demonstrated that, following right cervical vagotomy, hepatic-portal infusion of hypertonic saline no longer decreased saline drinking preference' although this denervation did not affect water or saline intake during control infusions or during a 24-h period of ad-lib food and water access.Thus, there has accrued evidence for a hepatic mechanism that is sensitive to fluctuations i...

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Lack of evidence for a hepatic osmoreceptor mechanism in conscious dogs

Cited by 40 publications

References 0 publications

The influence of hepatic portal circulation on urine flow

The influence of hepatic portal circulation on urine flow

Hepatic portal vein infusion of glucose and sodium solutions on the control of saline drinking in the rat.

Visceral control of drinking in rats

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