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Biomedical subjects

J W Putney

Publications and source records attributed to J W Putney.

At least 163 records · Page 9Linked to original sources
PubMed1980

Membrane potential changes in lacrimal gland acinar cells elicited by carbachol and epinephrine.

Intracellular microelectrode recordings of acinar cell membrane potentials were made from fragments of the rat lacrimal gland superfused in vitro. The average resting membrane potential was -45 mV. Carbachol and epinephrine produced virtually identical membrane potential changes consisting of an initial hyperpolarization (1 mV), lasting approximately 7 sec, followed by a depolarization of approximately 12 mV. The membrane potential generally returned to prestimulation levels after 2 min of exposure to agonist. The responses to carbachol and epinephrine were blocked by atropine and phentolamine, respectively. Superfusion with media lacking Ca or Cl reduced significantly both the resting membrane potential and the agonist-induced depolarization. The hyperpolarization was increased significantly in the absence of Ca and generally prolonged in the absence of Cl. Superfusion with 10 mM Co had no effect on either the resting membrane potential or the agonist-induced membrane potential changes. The hyperpolarization initiated by agonist was significantly enhanced during superfusion with low K, ouabain or amiloride while the depolarization was significantly reduced during superfusion with low K, amiloride or low Na. Resting membrane potentials during superfusion with low K, amiloride or low Na were not significantly different from control, whereas ouabain caused a small depolarization. It is concluded that muscarinic or alpha adrenergic receptor stimulation initiates a membrane potential change characterized by a hyperpolarization, due to an increased in membrane permeability to K, followed by a depolarization due to an increase in membrane permeability to Na.

Animals↗
PubMed1979

Relationship between calcium release and potassium release in rat parotid gland.

1. A study was made of the role of Ca release in mediating the sustained phase of K release (86 Rb release) in the rat parotid gland due to receptor activation. 2. Sr could substitute for Ca in supporting the sustained phase of the 86Rb release due to carbachol. Sr was less effective than Ca, while Ba was ineffective. 3. Sr could also restore responsiveness of the transient phase to agonists in media lacking Ca. Again, Sr was less effective than Ca, and Ba was without effect. 4. Carbachol stimulated release of 45Ca from parotid gland slices. The amount of Ca released (about 0.2 micromole/g) was much greater than the estimated Ca influx for the same period. 5. Release of 45Ca by carbachol prevented release due to a subsequent exposure to substance P. 6. Release of 45Ca due to substance P was significantly increased if muscarinic receptors were activated during tissue labelling. 7. These results support an earlier hypothesis whereby different agonists (such as carbachol and substance P) stimulate the release of Ca from a common pool and the release of this Ca mediates the transient phase of the K release response.

Animals↗
PubMed1979

Calcium and receptor regulation of radiosodium uptake by dispersed rat parotid acinar cells.

1. Dispersed rat parotid acinar cells were used to study the effects of secretagogues on 22Na uptake. 2. Carbachol stimulated 22Na uptake, and caused a net gain in total Na and a loss in total K. These effects were accentuated in the presence of 10(-3) M-ouabain. 3. Substance P, epinephrine and phenylephrine also stimulated 22Na uptake while isoproterenol and angiotensin II did not. 4. The 22Na uptake due to carbachol was inhibited by atropine, procaine or CoCl2; the response to Substance P was inhibited by CoCl2 only. 5. Extracellular Ca was required for stimulation of 22Na uptake by carbachol. Strontium but not Ba could substitute for Ca in supporting 22Na uptake. 6. Uptake of 22Na was stimulated by the divalent cationophore, A-23187, and Ca was required for this effect. 7. It is concluded that activation of Ca influx by muscarinic, alpha-adrenergic or peptide agonists triggers, among other effects, an increased membrane permeability to Na.

Adrenergic alpha-Agonists↗
PubMed1978

Control of calcium channels by membrane receptors in the rat parotid gland.

1. The mechanism of action of agonists that stimulate K release from the parotid gland was investigated by monitoring efflux of 86Rb from rat parotid slices. 2. As in previous studies, the 86Rb release was increased by agonists in a biphasic manner. An early, transient phase occurred that was independent of extracellular Ca. This was followed by a sustained (or slowly falling phase) that required extracellular Ca. 3. The agonists were investigated as to their additivity and to their sensitivity to inhibition by a number of putative Ca-antagonists. 4. When carbachol, epinephrine and Substance P were employed in supramaximal concentrations, no combination of agonists produced a summated 86Rb release response, despite the fact that the Ca concentration was submaximal. 5. The sustained phase of 86Rb release, which is dependent on extracellular Ca, was blocked by La, Ni, Co and neomycin; the transient phase was unaffected by these agents. 6. The local anaesthetics tetracaine and procaine inhibited both the transient and sustained phases of the responses to carbachol and phenylephrine; responses to Substance P and to the divalent cationophore, A23187, were largely refractory to this effect. 7. These results support the contention that, in the parotid, muscarinic, alpha-adrenergic and peptide receptors regulate the same Ca influx sites. 8. Also, these results suggest that La, Ni, Co and neomycin appear to antagonize the action of Ca by impeding inward movement of the cation through activated Ca influx sites. 9. Finally, the local anesthetics appear to inhibit, and therefore, serve to define, a transduction step between receptor occupation and channel activation. 10. In the case of the Substance P mechanism, it appears that the transduction mechanism must be qualitatively different to that for the muscarinic or alpha-adrenergic mechanisms.

Animals↗
PubMed1978

An alpha-adrenergic receptor mechanism controlling potassium permeability in the rat lacrimal gland acinar cell.

1. Rat lacrimal gland slices, incubated in a balanced, buffered salt solution, were found to be physiologically stable for up to 2 hr with respect to O2 consumption, extracellular space, and water and ion content. 2. The release of 86Rb serves as a good substitute for 42K in monitoring the movement of K through the cell membrane. 3. Adrenaline appears to increase membrane permeability to K as evidenced by an increase in the rate of 86Rb efflux. 4. This response to adrenaline was blocked by phentolamine but not by propranolol and was mimicked by phenylephrine but not by isoprenaline. 5. The magnitude of the 86Rb release indicates that it is being released, at least in part, from the lacrimal gland acinar cell. 6. It is concluded that the lacrimal gland acinar cell has an alpha-adrenergic receptor, activation of which leads to an increase in membrane permeability to K.

Animals↗
PubMed1978

The role of calcium in the receptor mediated control of potassium permeability in the rat lacrimal gland.

1. In the presence of extracellular Ca, adrenaline stimulated a large increase in the rate of K (86Rb) release from rat lacrimal slices, followed by a lower, more sustained rate. 2. In the absence of extracellular Ca, adrenaline elicited only a transient release of 86Rb. 3. The artificial introduction of Ca into the cytosol by the ionophore A-23187 could also initiate the release of 86Rb. 4. In a zero-Ca medium, if either adrenaline or carbachol produced a transient release of 86Rb, the tissue could not respond to the other agonist with a transient release unless Ca was momentarily reintroduced to the medium. 5. If Ca was present in a limiting concentration, the Ca-dependent rate of 86Rb release elicited from a lacrimal slice exposed simultaneously to carbachol and adrenaline was not significantly different from the release seen with carbachol alone. 6. It is concluded that the agonist-induced release of K from the lacrimal gland consists of both a Ca-independent phase which is initiated by the release of a limited pool of Ca, and a Ca-dependent phase which is mediated by the influx of extracellular Ca. 7. It is also concluded that both alpha-adrenergic and muscarinic receptor occupation activate a common, post-receptor mechanism which may be responsible for both phases of K release.

Animals↗
PubMed1978

Role of calcium in the fade of the potassium release response in the rat parotid gland.

1. The 86Rb release response in the parotid due to alpha-adrenergic (epinephrine), muscarinic (carbachol) or peptide (Substance P) receptor activation exhibited 'fade': a return of efflux to control levels despite the continuing presence of agonist. 2. The time course of fade of the response to all three agonists was independent of the concentration of the agonist. 3. After fade was fully developed to one agonist, the response to an agonist acting on a different receptor was either absent or greatly diminished. 4. Removal of carbachol from muscarinic receptors with atropine 10 min prior to Substance P partially restored the ability of Substance P to produce a response. 5. Fade of the response with all three agonists was greatly retarded by the omission of Ca. 6. release of alpha-amylase did not appear to fade following exposure to carbachol or Substance P. 7. It is concluded that the K+ release response may be inactivated with time due to diminution in responsiveness of the K+ channel to an increase in internal Ca2+.

Amylases↗
PubMed1978

Calcium and the control of potassium efflux in the sublingual gland.

The effects of cholinergic stimulation on K efflux from rat sublingual gland slices was investigated. The sublingual gland slices appeared stable on incubation as indicated by electrolyte content and ultrastructural analysis. Carbachol induced a biphasic increase in release of 86Rb (an index of K efflux); a transient phase lasting 2--4 min was followed by a sustained (or slowly falling) phase. Both phases of the response were blocked by atropine, but only the sustained phase was blocked by omission of Ca or by the addition of LaCl3. The divalent cationophore A-23187 produced a Ca-dependent release of 86Rb. Substance P stimulated a biphasic release of 86Rb, similar to that obtained with carbachol, but epinephrine did not. The response to substance P demonstrated a Ca dependence similar to that of carbachol. When a transient response to carbachol was elicited, no transient response to carbachol was elicited, no transient response to substance P could be obtained. This suggests that the receptors for these agonists may reside in the same cells. Also, the magnitude of the responses suggests that most of the affected cells are probably the mucous elements of the sublingual gland.

Animals↗
PubMed1978

Ionic milieu and control of K permeability in the parotid gland.

The roles of Mg, K, Na, and Cl ions in the biphasic K-permeability response (86Rb release) to receptor activation in the parotid gland were investigated. Both the transient and sustained phases of K release (86Rb release) were unaffected by alterations in Mg concentration. Elevating extracellular K enhanced 86Rb release presumably by decreasing the negativity of the membrane potential. Elevating extracellular K had no effect on the transient or sustained phases of 86Rb release due to carbachol and 1.0 mM Ca. Measurements of responses to carbachol with various substitutes for NaCl suggested that extracellular Cl and ionic strength are important for the K-permeability response. Experiments with LiCl suggested the operation of a Na-Ca exchange similar to that seen earlier in experiments with amylase release. When tetraethylammonium Cl was substituted for NaCl, the cation appeared to block K fluxes directly. Choline Cl, in partial substitution for NaCl, potentiated the sustained phase of response to substance P and, in complete substitution, produced both Ca-dependent and Ca-independent increases in 86Rb release. It was concluded that the 86Rb-release response in relatively (but not completely) insensitive to alteration in the ionic milieu. It was also concluded that Na regulates K permeability in part directly and in part by means of a Na-Ca exchange.

Animals↗
PubMed1978

Stimulus-secretion coupling in the rat lacrimal gland.

The role of calcium in stimulus-secretion coupling in the lacrimal gland was investigated. Rat exorbital lacrimal gland slices released peroxidase into the incubation medium after muscarinic or alpha-adrenergic receptor stimulation. In both cases, secretion appeared to involve exocytosis as revealed by electron microscopy. Secretion due to the muscarinic agonist carbachol was inhibited by Ca omission and by lanthanum. Secretion due to the alpha-adrenergic agonist phenylephrine was inhibited by Ca omission at 10(-5) M concentration but not at 10(-4) M concentration. The effects of 10(-4) M phenylephrine could be blocked by lanthanum or by reduction of extracellular Na. Both agonists stimulated 45Ca efflux, but phenylephrine was less efficacious. These results suggest that the agonists may cause exocytosis by stimulating influx of Ca or release of cellular Ca. Sodium may play a role in the Ca-release mechanism.

Animals↗