Adrenergic and cholinergic nerves of bovine, guinea pig and hamster salivary glands

1973 ◽  
Vol 138 (3) ◽  
pp. 407-420 ◽  
Author(s):  
Per Alm ◽  
Gunnar D. Bloom ◽  
Bengt Carls��
1986 ◽  
Vol 61 (3) ◽  
pp. 1025-1030 ◽  
Author(s):  
J. G. Martin ◽  
B. Collier

We measured acetylcholine (ACh) release from canine isolated tracheal smooth muscle (TSM) and bronchial spirals using a radioenzymic assay technique. Tissue was incubated in physiological salt solution containing physostigmine (3.10(-5) M), atropine (10(-7) M), and choline (5.10(-6) M), and bath fluid was collected every 15 min for assay. There was a resting release of ACh of 209 +/- 44 pmol/g tissue (mean +/- SE) from 53 to 77 specimens of TSM. Electrical field stimulation (ES) increased ACh release, which was blocked by tetrodotoxin (10(-6) g/ml), confirming the neural origin of ACh. The ACh output during ES (2-ms pulses) at 10 Hz increased linearly from 188 +/- 50 pmol/g tissue (mean +/- SE) for a 1-min volley, to 323 +/- 57 for three volleys, and 544 +/- 128 for five volleys. The ACh output/pulse was constant during ES at 20, 15, 10, and 5 Hz, but it was significantly higher at 2 than at 5 Hz (P less than 0.005). Incubation of TSM with norepinephrine (NE, 10(-5) M) did not affect ACh output either at 2 or 10 Hz. Likewise, ACh output from bronchial spirals during ES and 2 Hz was unaffected by NE. In contrast, NE treatment of isolated guinea pig ileum reduced the ACh released by ES at 2 Hz to 40 +/- 7% (P less than 0.001) of the control ACh output. It is concluded that evoked release of ACh (output/pulse) from cholinergic nerves in canine airway is frequency dependent, as in guinea pig ileum, but that, unlike guinea pig ileum, NE does not modulate its release.


1963 ◽  
Vol 41 (2) ◽  
pp. 519-524 ◽  
Author(s):  
B. C. R. Strömblad ◽  
Peter E. Dresel

Vasodilatation induced by stimulation of the parasympathetic nerve supply to the submaxillary and the parotid glands has long been known to be resistant to the blocking effect of atropine. We have found that dichloroisoproterenol does not block this vasodilatation, that d-tubocurarine blocks it by interfering with ganglionic transmission, and that a hemicholinium, HC-3, blocks it gradually under conditions in which interference with ganglionic transmission is excluded. It is concluded that the mechanism of vasodilatation includes the action of cholinergic nerves.


1980 ◽  
Vol 58 (1) ◽  
pp. 88-92 ◽  
Author(s):  
M. L. Paul ◽  
M. A. Cook

The nonadrenergic, noncholinergic inhibitory (NAI) response of guinea pig fundic strip to electrical field stimulation was examined in the presence of botulinum toxin and tetrodotoxin. Tetrodotoxin completely abolished the NAI response while botulinum toxin did not alter it. It is concluded that the mediator of NAI responses is unlikely to be released with acetylcholine from cholinergic nerves or that such release would have to occur by a mechanism resistant to botulinum toxin.


1958 ◽  
Vol 6 (2) ◽  
pp. 145
Author(s):  
R Tucker

The occurrence, site, and morphology of lipomatic changes in the salivary glands of the pig, sheep, cattle, horse, dog, goat, rhesus monkey, guinea pig, bandicoot, rabbit, and the echidna were investigated, special attention being given to the glands of the echidna. The areal, tubular, acinar, marginal, central, interlobular, peritubular, paratrabecular, and capsular accumulations were described. It was concluded that lipomatic changes in the salivary glands are of two distinctly different types, one being the formation of fatty cells from the cells of the connective tissue and the other being the partial or complete transformation of the glandular cells into fatty cells.


Sign in / Sign up

Export Citation Format

Share Document