Fluid and electrolyte secretion from the isolated, perfused submandibular and sublingual glands of the rat

Compton, Jeffrey S.; Martinez, J. Ricardo; Martinez, A. M.; Young, J. A.

doi:10.1016/0003-9969(81)90017-0

Cited by 50 publications

(30 citation statements)

References 13 publications

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“…Therefore, in this study, we designed a submandibular gland perfusion system to investigate the action of GABA on salivary secretion. Some groups have employed an isolated submandibular gland perfusion system (17,18). In contrast, our goal was to construct an in situ perfusion system so that physiological functions such as innervation would not be compromised.…”

Section: Rat Submandibular Gland Perfusion Methods For Clarifying Inhimentioning

confidence: 99%

Rat Submandibular Gland Perfusion Method for Clarifying Inhibitory Regulation of GABAA Receptor

Okubo

Kawaguchi

2013

J Pharmacol Sci

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Abstract. GABA is an inhibitory transmitter found in rat salivary gland. However, the inhibitory potential of GABA on salivary secretion is unclear. Using an in vivo cannulation method, intraperitoneal administration of GABA was ineffective in the absence of gabaculine, a GABA transaminase inhibitor, on pilocarpine-induced salivary secretion, suggesting that GABA was rendered metabolically inactive before reaching the salivary gland. We hypothesized that the action of a drug on the salivary glands could be measured directly using a submandibular gland perfusion system. The submandibular gland artery, veins, and duct were cannulated in situ so that physiological functions such as innervation would not be compromised. Hank's balanced salt solution (pH 7.4) was perfused at a rate of 0.5 ml/min together with 1 M carbachol (CCh) over a 5-min period every 30 min. Amount of secreted saliva showed no change to the recurrent addition of CCh to the perfusate. GABA or muscimol dose-dependently inhibited CCh-induced salivary secretion. This effect was blocked by bicuculline, a GABA A -receptor (GABA A -R) antagonist, and enhanced by clonazepam, a central-type benzodiazepine-receptor agonist. These results suggest that salivary secretion is suppressed by GABA A -R in rat salivary gland and that the perfusion method used was effective in clarifying inhibitory regulation of GABA A -R.

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Section: Rat Submandibular Gland Perfusion Methods For Clarifying Inhimentioning

confidence: 99%

Rat Submandibular Gland Perfusion Method for Clarifying Inhibitory Regulation of GABAA Receptor

Okubo

Kawaguchi

2013

J Pharmacol Sci

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“…The rats were anaesthetized by intraperitoneal injection of pentobarbitone sodium (Nembutal, 60-70 mg kg l). The submandibular gland was isolated for perfusion as described elsewhere (Compton, Martinez, Martinez & Young, 1981). A polyethylene cannula was inserted into the artery of the gland, which was perfused at a rate of 4.3 ml min--with a peristaltic pump (7553-70; Cole-Palmer, Niles, IL, USA).…”

Section: Gland Isolation and Perfusionmentioning

confidence: 99%

Osmotic flow transients during acetylcholine stimulation in the perfused rat submandibular gland

Nakahari¹,

Mc²,

Yoshida³

et al. 1997

Experimental Physiology

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SUMMARYOsmotic stress was applied to the perfused rat submandibular gland during steady-state fluid secretion. Alterations of perfusate osmolarity, by addition or withdrawal of sucrose or NaCi, caused transient changes in secretory rate during continuous stimulation with I /LM acetylcholine (ACh). Hyposmotic perfusates transiently increased, and hyperosmotic perfusates transiently reduced, the secretory rate. The transients were attributed to changes in osmotic flow resulting from changes in the instantaneous transepithelial osmotic gradient. The time course of the change in interstitial osmolarity was determined by using a Cl-electrode to record the changes in interstitial Cl-concentration following a step change in perfusate Cl-concentration. From the calculated changes in interstitial osmolarity and the resulting changes in secretory rate, the osmotic

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“…From an examination of their list, it is apparent that the salivary secretary mechanism is different in character since salivary secretion is not markedly dependent on the concentration of extracellular Na+ (Compton, Martinez, Martinez & Young, 1981;M. Hunter, unpublished) or Cl- (Case & Hunter, 1981).…”

Section: Effect Of Inhibitors Of Carbonic Anhydrasementioning

confidence: 99%

The role of buffer anions and protons in secretion by the rabbit mandibular salivary gland.

Case¹,

Conigrave²,

Favaloro³

et al. 1982

The Journal of Physiology

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SUMMARY1. The role of extracellular HCO3-and H+ in the formation of primary saliva and its subsequent modification by the glandular ducts has been investigated in the isolated perfused mandibular salivary gland of the rabbit.2. Variation of extracellular HCO3-concentration between 12-5 and 50-0 mmol/l was without effect on salivary flow rate or on Na+ and K+ excretion, even though salivary HCO3-(and Cl-) content altered with changes in the extracellular concentration of the two anions.3. Complete replacement ofperfusate HCO3-by Cl-reduced fluid secretion by 34 % and almost abolished ductal Na+ absorption. However, when extracellular pH was controlled by replacing HCO3-with the hydrophilic HEPES buffer, fluid secretion but not ductal Na+ absorption was restored to normal.4. Complete replacement ofexogenous HCO3-with acetate increased fluid secretion by 110 % and also stimulated ductal Na+ absorption. This effect did not appear to be related to changes in cell pH and remains unexplained. Acetate entered the saliva in concentrations comparable to those seen for HCO3 in control experiments. 5. Salivary secretion showed an almost linear dependence on extracellular pH, rising from 14 % of control (pH 7 4) levels at pH 6-2 to 130 % at pH 7-8. Ductal Na+ absorption showed a similar pH dependence.6. Carbonic anhydrase inhibitors did not affect fluid secretion rates (except when supramaximal doses of ACh were used to evoke secretion) but they did cause a large reduction in salivary HCO3-output. In glands perfused with acetate rather than HCO3 , carbonic anhydrase inhibitors had no effect on excretion of fluid, acetate or metabolically derived HCO3. Duct perfusion studies suggested that the effect of the inhibitors on HC03-output was at the site of primary secretion rather than at the ductal site of HCO3-transport.

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Fluid and electrolyte secretion from the isolated, perfused submandibular and sublingual glands of the rat

Cited by 50 publications

References 13 publications

Rat Submandibular Gland Perfusion Method for Clarifying Inhibitory Regulation of GABAA Receptor

Rat Submandibular Gland Perfusion Method for Clarifying Inhibitory Regulation of GABAA Receptor

Osmotic flow transients during acetylcholine stimulation in the perfused rat submandibular gland

The role of buffer anions and protons in secretion by the rabbit mandibular salivary gland.

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