1.
Edwards, A V, et al.
(author)
Nitric oxide and release of the peptide VIP from parasympathetic terminals in the submandibular gland of the anaesthetized cat.
1996
In: Experimental physiology. - 0958-0670. ; 81:3, s. 349-59
Journal article (peer-reviewed) abstract
The role of nitric oxide (NO) in mediating various submandibular responses to stimulation of the parasympathetic innervation has been investigated in anaesthetized cats, in which N omega-nitro-L-arginine methyl ester (L-NAME; 30 mg kg-1 I.A.) was used to block the synthesis of NO. L-NAME significantly reduced the vasodilator response and the flow of saliva, together with the output of salivary protein that occurred during stimulation of the chorda lingual nerve (20 Hz for 1 s at 10 s intervals), without significantly reducing the output of vasoactive intestinal peptide (VIP) from the gland. The results show that NO is implicated not only in the release of VIP, as established previously, but also in mediating its actions following release in the submandibular gland of the cat.
2.
Tobin, Gunnar, 1954, et al.
(author)
Nitric oxide in the control of submandibular gland function in the anaesthetized ferret.
1997
In: Experimental physiology. - 0958-0670. ; 82:5, s. 825-36
Journal article (peer-reviewed) abstract
Stimulation of parasympathetic innervation of the submandibular gland (2 or 20 Hz continuously or 20 Hz for 1 s at 10 s intervals), in the ferret, produced secretion of fluid and protein and a fall in vascular resistance. The responses following the administration of N omega-nitro-L-arginine methyl ester (L-NAME; 2 mmol kg-1 i.a.) to block the synthesis of nitric oxide (NO) were reduced, and the persisting responses were abolished (at 2 Hz continuously and 20 Hz intermittently) or further reduced (at 20 Hz continuously) by the additional administration of atropine. The output of vasoactive intestinal peptide (VIP) from the gland was not affected. Neither the secretory nor the vascular response to intra-arterial infusions of acetylcholine (1.25 nmol kg-1) was affected by L-NAME, whereas the vascular responses to both VIP (10 pmol kg-1) and pituitary adenylate cyclase-activating peptide (1-38) (PACAP) (0.5 pmol kg-1) were reduced thereby. Neither peptide evoked a fluid secretion per se. However, when infused during parasympathetic stimulation of saliva secretion, VIP increased both flow rate and the output of protein. These effects of VIP were abolished by L-NAME. The experiments were performed in the presence of sodium nitroprusside at doses (4-8 nmol min-1 kg-1 i.v.) aimed to counterbalance the systemic effects of L-NAME. The results show that, in the ferret, parasympathetic nerve activity increases submandibular blood flow, and elicits the flow of saliva and output of protein by mechanisms that involve in situ generation of NO, upon which the effects of VIP and PACAP but not acetylcholine are largely dependent.
