Effects of stimulating the sympathetic innervation in bursts on submandibular vascular and secretory function in cats.

Abstract

SUMMARY1. The effects of continuous stimulation of the peripheral end of the ascending cervical sympathetic nerve were compared with those of intermittent stimulation, so arranged as to deliver the same total number of impulses, in cats under chloralose anaesthesia.2. Continuous stimulation caused a flow of saliva at 5-10 Hz, but not at 2 Hz. In contrast, the same total number of impulses delivered intermittently in bursts elicited a prompt secretion at a frequency as low as 20 Hz for 1 s at 10 s intervals (corresponding to 2 Hz continuously) and a significantly higher rate of secretion at 50 Hz in bursts than that obtained in response to 5 Hz continuously.3. Continuous stimulation also caused a rise in submandibular vascular resistance (s.v.r.), which persisted throughout the period of stimulation, and was followed immediately thereafter by an intense but transient fall in s.v.r. During stimulation in 1 s bursts, each burst was followed first by a brief rise in s.v.r. and shortly after by a fall. The balance between these two components varied widely between individual animals but often led to an overall fall in s.v.r. during stimulation i.e. complete reversal of the mean vascular effect. A further fall in s.v.r. was then recorded when the stimulus was discontinued.4. Propranolol (1-0 mg/kg) reduced but failed to abolish the secretary response. It also altered the balance between the two phases of the vascular response slightly in favour of a rise in s.v.r. during stimulation, without apparently affecting the size of the after-dilatation.5. Pre-treatment with dihydroergotamine (1-0 mg/kg) invariably blocked secretion and revealed a small vasodilator response during sympathetic stimulation with either pattern of stimulation; it also blocked the after-dilatation.6. Following combined pre-treatment with propranolol and dihydroergotamine, to produce total adrenergic blockade, there was a small residual vasoconstrictor component which amounted to an increase in mean s.v.r. of about 20% during stimulation at 10 Hz continuously. This may have been due to release ofneuropeptide Y (NPY).7. Small but significantly greater amounts of NPY were released into the effluent S. R. BLOOM, A. V. EDWARDS AND J. R. GARRETT blood during stimulation of the ascending cervical sympathetic nerve at 70 Hz in bursts than during continuous stimulation. No significant release of vasoactive intestinal peptide (VIP), somatostatin, bombesin, substance P or calcitonin generelated peptide (CGRP) was observed during stimulation at any frequency.8. It is concluded that, in addition to a vasodilator component due to ,-adrenoceptor activation, stimulation of the sympathetic innervation to the submandibular gland in the cat elicits a vasodilator response by some pathway that depends upon a-adrenoceptor activation. This is sufficiently potent to override aadrenergic vasoconstriction during certain patterns of stimulation and is mainly responsible for the transient dilatation which occurs on cessation of stimulation. These vasodilator effects may invol...

Nitric oxide‐related vasodilator responses to parasympathetic stimulation of the submandibular gland in the cat.

“…Furthermore, as single impulse and low frequency parasympathetic vasodilator responses are blocked by atropine (Emmelin et al 1968;Darke & Smaje, 1972), no effective release of NO, can be occurring from the nerves under these conditions to cause a direct effect on the smooth muscle cells. It should also be mentioned that the sympathetic c-adrenergic vasodilator response attributed to EDRF release (Edwards & Garrett, 1992) cannot be attributed to NOX release from nerve terminals, because it is blocked by total adrenergic postganglionic blockade (Bloom et al 1987).…”

“…The preparatory surgical techniques were as described previously (Bloom, Edwards & Garrett, 1987) acetylcholine or VTIP. in the presence and absence of dV"-nitro-L-arginine methyl ester HCI (Sigma; L-NAME).…”

Secretory interactions between the sympathetic and parasympathetic innervations of the submandibular gland in the anaesthetized cat

“…This time-honoured technique inevitably causes vasoconstriction (Bernard, 1858), due to the overriding effect of a-adrenoceptor activation (Bhoola, Morley, Schachter & Smaje, 1965), and the consequent restriction of the blood flow to the active gland may interfere with any other effects which sympathetic activity might elicit. When the sympathetic fibres are activated for short periods of time intermittently this problem is eliminated, at least in the cat, because a vasodilator component then predominates (Bloom, Edwards & Garrett, 1987) and salivary secretory responses are potentiated in both the cat and rat (Bloom et al 1987; Anderson, Garrett & Proctor, 1988). Furthermore, this is the natural pattern of sympathetic activity when recorded from individual nerve fibres, in the absence of anaesthesia (Wallin, 1981), albeit in other tissues, and can therefore be justified physiologically.…”

GI Tract

“…; n = 5). Preparatory surgery was carried out as described previously (Bloom et al 1987). The animals were pretreated with propranolol and phentolamine (2-0 mg kg-1 LV.…”