The ionic balances and transferences of the sheep's parotid gland during maximal stimulation

Coats, D. A.; Denton, D. A.; Wright, R. D.

doi:10.1113/jphysiol.1958.sp006089

Cited by 13 publications

(15 citation statements)

References 12 publications

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“…An estimate of 50 ml./min for blood flow through the gland was used for calculating the infusion rate. Flow rates of this order were reported by Coats, Denton and Wright [1958]. If blood flows were as low as 25-30 ml./min then the highest infusion rate would result in plasma PTH levels of about 30 ng/ml.…”

Section: Disclussionmentioning

confidence: 82%

“…An increase in blood flow rate through the parotid gland following vasodilation by PTH may conceivably lead to increased secretion of substances such as phosphate and potassium, for which the concentration is higher in saliva than plasma. The mineral secretion data of Coats et al [1958], however, do not give substance to this possibility. Moreover, the data in Study (ii) show that PTH enhances the phosphorus concentrating ability by the gland even at zero or near zero flow rates of saliva.…”

Section: Disclussionmentioning

confidence: 94%

“…In support of this suggestion is the rapidity of the decline in phosphorus secretion following cessation of PTH infusion, which indicates little or no residual effect of the hormone. The observed changes in the salivary potassium and sodium concentrations which occurred in both the whole animal and isolated gland studies may also have arisen from a membrane effect of the hormone [see Rasmussen et al, 1968] but could also be ascribed to perturbations associated with re-establishing a new equilibrium of ion secretions by the gland [Coats et al, 1958] in order to maintain electroneutrality and isosmolality.…”

Section: Disclussionmentioning

confidence: 99%

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The Influence of Parathyroid Hormone on the Secretion of Phosphate by the Parotid Salivary Gland of Sheep

Fürst

1974

Exp Physiol

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The effect of parathyroid hormone on phosphate secretion by the parotid salivary gland in sheep has been examined in three separate studies: the first, with 3 sheep, used freeflow salivary collection under anaesthesia and intravenous infusion of hormone; the second involved 4 sheep in which 'stop-flow' techniques were applied to one parotid gland; the third was carried out using 6 sheep in which the blood vessels to one parotid gland were isolated and hormone infused at graded rates directly into the arterial supply to the gland.Parathyroid hormone infusion caused an increase in parotid salivary phosphate concentration and secretion rate in all experiments. The response was rapid (within 2-4 min) and also declined rapidly following cessation of infusion. During hormone administration the ratio of salivary to plasma phosphate concentrations for stopped-flow samples was significantly higher than for controls (22-0 ± 2-1 (S.E.M.) Vs 16-0 ± 2.2).Hormone infusion into the blood supply of the isolated parotid gland at rates estimated to give rise to plasma parathyroid hormone levels of about 5, 10 or 20 ng/ml. caused salivary phosphate concentration to rise by 11-6, 19-6 and 25-7 m-mole/litre respectively.The increment, whether expressed as a percentage or on an absolute basis, was directly related to the dose rate.Parathyroid hormone infusion also altered the secretion of sodium, potassium and bicarbonate, but not of calcium or magnesium. These changes, and those of phosphate, are discussed in relation to the mode of action of parathyroid hormone.Reabsorption of phosphate by the renal tubules and absorption of phosphate from the gut are known to be affected by parathyroid hormone (PTH) [see Arnaud, Tenenhouse and Rasmussen, 1967]. The transport of phosphate by the renal tubules is inhibited by PTH in a direct and rapid manner [Pullman, Lavender, Aho and Rasmussen, 1960; Sallis, Hoperoft and Opit, 1967] but the exact mechanism for this action is not yet known. In contrast to the renal effect is the evidence for an enhancing effect of PTH upon gastro-intestinal phosphate transport [Cramer, 1963;Lifshitz, Harrison and Harrison, 1969] but, as in the case of renal transport, the mechanisms are not defined.Since the parotid salivary glands in ruminants actively secrete considerable quantities of phosphorus [McDougall, 1948;Kay, 1966] and since the secretion of phosphorus to the gut appears to play a major role in the regulation of phosphorus homeostasis in ruminants [Compere, 1966; Tomas, 1974] it seems plausible that PTH may exert an action on this secretion. Mayer, Ramberg and Kronfeld [1968] suggested this possibility to explain, in part, the effect of PTH on phosphorus excretion in cows.

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Section: Disclussionmentioning

confidence: 82%

Section: Disclussionmentioning

confidence: 94%

Section: Disclussionmentioning

confidence: 99%

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The Influence of Parathyroid Hormone on the Secretion of Phosphate by the Parotid Salivary Gland of Sheep

Fürst

1974

Exp Physiol

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“…), and phosphate, 72 + 37 #smol/min, were maximal during the first 10 s of maximal stimulation and then declined so that the losses approached zero after 2-4 min of stimulation. The total K+ deficits were 32-117,mol (Coats et al 1958).…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies showed that prolonged stimulation of the secretomotor cholinergic nerve supply of the sheep's parotid gland caused an initial discharge of K+ and phosphate from the gland and decreased the glandular content of K+ (Coats & Wright, 1957;Coats, Denton & Wright, 1958;Blair-West, Coghlan, Denton, Nelson, Wright & Yamauchi, 1969). The initial rates of glandular loss of K+, 85 ± 30,umol/min (mean + S.D.…”

Section: Introductionmentioning

confidence: 99%

The effects of K+ channel blockers on ovine parotid secretion depend on the mode of stimulation

Blair-West²

1990

Experimental Physiology

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SUMMARYThe vascularly isolated parotid glands of sheep were submaximally stimulated for 4 min by nerve stimulation, or by infusion of acetylcholine (ACh) or bethanechol directly into the artery supplying the gland. The three modes of stimulation caused almost equal increases in the rate of salivary flow, initial losses of K+ and phosphate from the gland and total glandular deficits of K+ and phosphate. Concurrent arterial infusion of the K+ channel blocker tetraethy!ammonium (TEA), at 1V5-33 mm in blood, almost abolished these responses to bethanechol but did not alter the responses to nerve stimulation or ACh. The responses to bethanechol were restored by increasing the concentration fourfold. Concurrent arterial infusion of 4-aminopyridine (4-AP), at 0 1-2-3 mm in blood, partially inhibited the increase in salivary flow due to bethanechol but not the response to nerve stimulation or ACh. The specificity and competitive nature of the action of TEA and 4-AP on responses to direct muscarinic stimulation by bethanechol are consistent with blockade of K+ channels in secretory end-piece cells. The failure of TEA and 4-AP to inhibit responses to nerve stimulation and ACh may be due to the blocking agents potentiating the release of neurotransmitter ACh. It is also possible that nerve stimulation and ACh may cause the release of a co-transmitter which bethanechol does not.

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A novel carbonic anhydrase from the ovine parotid gland

1979

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The ionic balances and transferences of the sheep's parotid gland during maximal stimulation

Cited by 13 publications

References 12 publications

The Influence of Parathyroid Hormone on the Secretion of Phosphate by the Parotid Salivary Gland of Sheep

The Influence of Parathyroid Hormone on the Secretion of Phosphate by the Parotid Salivary Gland of Sheep

The effects of K+ channel blockers on ovine parotid secretion depend on the mode of stimulation

A novel carbonic anhydrase from the ovine parotid gland

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