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Biomedical subjects

G Tobin

Publications and source records attributed to G Tobin.

At least 37 records · Page 2Linked to original sources
PubMed1997

Acute ischemic preconditioning of skeletal muscle prior to flap elevation augments muscle-flap survival.

Ischemic preconditioning of the myocardium with repeated brief periods of ischemia and reperfusion prior to prolonged ischemia significantly reduces subsequent myocardial infarction. Following ischemic preconditioning, two "windows of opportunity" (early and late) exist, during which time prolonged ischemia can occur with reduced infarction size. The early window occurs at approximately 4 hours and the late window at 24 hours following ischemic preconditioning of the myocardium. We investigated if ischemic preconditioning of skeletal muscle prior to flap creation improved subsequent flap survival and perfusion immediately or 24 hours following ischemic preconditioning. Currently, no data exist on the utilization of ischemic preconditioning in this fashion. The animal model used was the latissimus dorsi muscle of adult male Sprague-Dawley rats. Animals were assigned to three groups, and the right or left latissimus dorsi muscle was chosen randomly in each animal. Group 1 (n = 12) was the control group, in which the entire latissimus dorsi muscle was elevated acutely without ischemic preconditioning. Group 2 (n = 8) investigated the effects of ischemic preconditioning in the early window. In this group, the latissimus dorsi muscle was elevated immediately following preconditioning. Group 3 (n = 8) investigated the effects of ischemic preconditioning in the late window, with elevation of the latissimus dorsi muscle 24 hours following ischemic preconditioning. The preconditioning regimen used in groups 2 and 3 was two 30-minute episodes of normothermic global ischemia with intervening 10-minute episodes of reperfusion. Latissimus dorsi muscle ischemia was created by occlusion of the thoracodorsal artery and vein and the intercostal perforators, after isolation of the muscle on these vessels. Muscle perfusion was assessed by a laser-Doppler perfusion imager. One week after flap elevation, muscle necrosis was quantified in all groups by means of computer-assisted digital planimetry. Our results show that ischemic preconditioning resulted in a significant reduction (p < 0.05) in muscle-flap necrosis immediately and 24 hours following ischemic preconditioning. Perfusion changes after flap elevation were similar among the three groups. Ischemic preconditioning of skeletal muscle prior to flap creation significantly reduces subsequent muscle-flap necrosis caused by the ischemia of flap creation immediately and 24 hours following ischemic preconditioning. Further elaboration of the mechanisms of ischemic preconditioning may allow pharmacologic preconditioning to be used in the augmentation of skeletal muscle-flap survival in the clinical setting.

Animals↗
PubMed1997

Nitric oxide in the control of submandibular gland function in the anaesthetized ferret.

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.

Animals↗
PubMed1996

Loss of the adrenoceptor-mediated secretory drive on the rat parotid gland during eating and the effect on parasympathetic substance P and VIP.

Phentolamine and propranolol (2 mg/kg i.p. of each) were administered to rats to be fed hard chow over a period of 80 min and to their fasting controls. The pharmacological elimination of the adrenoceptor mediated secretory drive on the parotid gland cells during feeding did not affect the gland content of the peptides substance P and vasoactive intestinal peptide localized to parasympathetic nerve fibres of the gland and thought to transmit secretory impulses. This is in contrast to the previously demonstrated effect of elimination of the parasympathetic acetylcholine-evoked secretion following administration of atropine, which resulted in reduced gland contents of these peptides.

Animals↗
PubMed1996

Neuropeptide Y in salivary glands of the rat: origin, release and secretory effects.

In the parotid gland, double immunostaining showed the perivascular and most of the periductal neuropeptide Y (NPY)-immunoreactive nerve fibres to contain dopamine beta-hydroxylase, while the majority of periacinar NPY-fibres contained vasoactive intestinal peptide. Sympathectomy caused a marked depletion of perivascular and periductal NPY-fibres, leaving periacinar NPY-fibres less affected. Following combined sympathectomy and parasympathectomy, only a few NPY-fibres persisted. The parasympathetic auriculotemporal nerve contributed most (75%) and the cervical sympathetic nerve least (15%) to the parotid gland content of NPY as judged by radioimmunoassay. The sensory neurotoxin capsaicin was without effect on the occurrence and gland content of NPY. Upon long-lasting electrical stimulation of the auriculo-temporal nerve at a high frequency, the gland content of NPY was reduced (by 55%), a depletion thought to indicate release of the peptide from parasympathetic nerve terminals. In vitro, tissues of parotid, submandibular and sublingual glands released concentration-dependently protein (and as to the parotid gland amylase also) in response to NPY; the protein response was largest from sublingual tissue (per unit weight). A concentration-dependent in vitro release of potassium from tissues of parotid and submandibular glands in response to NPY occurred and here, submandibular gland tissue was the most sensitive. Comparisons between the action of some secretagogues (at 10(-6) M) showed NPY to be less effective than vasoactive intestinal peptide and adrenaline, but as effective as bethanechol and substance P, in releasing protein (and amylase) in parotid and submandibular gland tissues; in sublingual gland tissue NPY was less effective than vasoactive intestinal peptide, in the range of adrenaline and more effective than bethanechol and substance P. As to potassium release (at agonist concentration of 10(-6) M) from tissues of parotid and submandibular glands NPY was less effective than substance P and vasoactive intestinal peptide. The fluid response to NPY upon i.v. administration was scanty from parotid and submandibular glands. NPY is likely to play a complementary role in mediating parasympathetic secretory responses in salivary glands of the rat. It seems preferentially involved in the control of protein secretion.

Amylases↗
PubMed1996

Electrophoretic analysis of rat parotid salivary protein composition: investigation of the parasympathetic atropine-resistant secretion.

Rats pretreated with atropine and adrenoceptor antagonists show secretion of saliva upon electrical stimulation of the parasympathetic nerve of the parotid gland. The protein composition of this secretion has been analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and compared with the protein profiles obtained with secretions evoked by parasympathetic stimulation (in the absence of atropine) or infusion of bethanechol with or without vasoactive intestinal peptide (VIP, a probable transmitter conveying parasympathetic secretory impulses). The SDS-PAGE patterns were highly reproducible for an individual rat although minor differences were detected between different rats. The method requires only microlitre volumes of unconcentrated rat saliva and thus is ideal for monitoring sequential aliquots collected from the same rat. The SDS-PAGE patterns indicated (i) little change in the protein profile during prolonged stimulation, (ii) a similar profile with parasympathetic stimulation or infusion of bethanechol, and (iii) a quantitative, rather than qualitative, response to administration of atropine (during parasympathetic stimulation) or VIP (during bethanechol infusion). Thus, the salivary protein composition associated with non-adrenergic, non-cholinergic (NANC) secretion appears similar to that evoked in response to parasympathetic nerve stimulation in the absence of muscarinic receptor blockade.

Animals↗
PubMed1996

The role of circulating catecholamines in the depletion of parotid acinar granules in conscious rats in the cold.

The possibility that circulating catecholamines might affect parotid gland function during feeding (over a period of 80 min) and cold stress (2-4 degree C) was investigated in rats that had been fasted for 30 h. In the first set of experiments, in which the glands had been sympathectomized by removing both superior cervical ganglia 10-12 days previously, there was a substantial reduction in the density of acinar secretory granules (42% compared with non-fed animals in the cold) and in the total glandular amylase activity (54%). However, similar, or even greater, losses were recorded in rats subjected to additional bilateral adrenal medullectomy and pretreatment with atropine and alpha- and beta-adrenoceptor blockers. The losses were therefore attributed to activation of parasympathetic non-adrenergic, non-cholinergic mechanisms. In a second set of experiments, employing only morphometric assessment, the parasympathetic auriculotemporal nerve was cut on one side in addition to bilateral sympathectomy and, as a further precaution, the animal was atropinized. It was then found that there was a loss of 17% of granules in the parasympathectomized plus sympathectomized gland, but not the contralateral gland, of non-fed cold-exposed rats compared with non-fed animals kept at room temperature. When rats were fed as well as exposed to cold the number of granules in parasympathectomized plus sympathectomized glands fell by 46% compared with similar non-fed animals in the cold and by 55% compared with those at room temperature. After adrenal medullectomy, cold exposure alone had no effect on the granular density of parasympathectomized plus sympathectomized glands but, when combined with feeding, granular loss amounted to 30%. Pretreatment with a combination of alpha- and beta-adrenoceptor blocking agents abolished this effect. Thus circulating catecholamines liberated not only from the adrenal medulla but also from other sources (extraglandular adrenergic nerve terminals and extra-adrenal chromaffin tissue) are able to induce losses in the number of acinar granules in the parasympathectomized plus sympathectomized glands. However, a high degree of sensitization of the parotid acinar cells may be required to allow the response to become manifest.

Animals↗
PubMed1996

Depletion of vasoactive intestinal peptide and substance P in parotid glands of atropinized rats during reflex secretion.

Rats previously starved for 30 h were offered hard chow over a period of 80 min, and the effect of eating on the parotid gland content of vasoactive intestinal peptide (VIP), substance P and neuropeptide Y (NPY) was examined. In rats pretreated with I.P. atropine and alpha- and beta-adrenoceptor blocking agents, the total amounts of VIP and substance P were reduced after feeding by 23 and 42%, respectively; in contrast the NPY content was not significantly affected. Similarly, in animals given atropine alone the VIP content was reduced by 25% and substance P by 40% after feeding. In the absence of autonomic receptor blockade, there was no loss of parotid neuropeptide content in response to feeding. Neither an intact sympathetic innervation nor a capsaicin-sensitive sensory innervation was a prerequisite for depletion of parotid neuropeptides in the presence of atropine and adrenoceptor blockers. The observed decrease in neuropeptide content is thought to reflect an imbalance between peptide release from nerve terminals and their replenishment by axonal transport, this imbalance resulting from the unusually high demands on the parasympathetic non-adrenergic, non-cholinergic (NANC) mechanism. Under normal conditions salivary peptidergic mechanisms are spared as seen in the absence of autonomic receptor blockade.

Adrenergic Antagonists↗
PubMed1996

Nitric oxide and release of the peptide VIP from parasympathetic terminals in the submandibular gland of the anaesthetized cat.

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.

Animals↗
PubMed1996

Non-adrenergic, non-cholinergic influences on parotid acinar degranulation in response to stimulation of the parasympathetic innervation in the anaesthetized rat.

In pentobarbitione-anaesthetized rats the parasympathetic auriculotemporal nerve of the parotid gland was continuously stimulated at supramaximal voltage and at maximal frequency (40 Hz) for salivary secretion. The animals were pretreated with phentolamine and propranolol (2 mg kg-1 i.p. of each) and, in some groups, additionally with atropine (2 mg kg-1 i.p.). Morphometric assessment at the light microscopic level (x 100) showed that the numerical density of parotid acinar secretory granules (per 100 microns2 acinar epithelial cytoplasm) was reduced by 30 and 39% after 40 and 80 min, respectively, of stimulation in non-atropinized animals and by 30 and 27% in atropinized animals. The numerical density of acinar granules was not influenced by pretreatment with the protein synthesis inhibitor cycloheximide. The results suggest that most of the parasympathetic nerve-induced degranulation in the absence of muscarinic receptor blockade can be attributed to the action of non-adrenergic, non-cholinergic mechanisms.

Animals↗
PubMed1995

In vivo and in vitro effects of muscarinic receptor antagonists on contractions and release of [3H]acetylcholine in the rabbit urinary bladder.

The functional effects of muscarinic receptor antagonists were examined in vivo and in vitro on the rabbit urinary bladder. Inhibitory effects on carbachol-evoked contractions of detrusor strips were pronounced for 4-diphenylacetoxy-N-methylpiperidine (4-DAMP; -logIC50: 8.64), p-fluoro-hexahydro-sila-diphenidol (pFHHSiD; 7.84) and atropine (8.27), while they were less pronounced for pirenzepine (6.62) and methoctramine (5.36). 4-DAMP and methoctramine increased 3H overflow from [3H]choline-labelled strips in response to electrical stimulation, contrary to pirenzepine, which decreased the overflow. Concomitant contractions were markedly reduced by 4-DAMP and by pirenzepine, but not by methoctramine. The -logIC50 estimations for atropine-sensitive electrically evoked contractions revealed methoctramine (4.85) to be less potent on nerve-evoked contractions than on carbachol-evoked contractions, in contrast to pirenzepine (7.15) and 4-DAMP (9.15). The effects of the antagonists in anaesthetized rabbits resembled those in vitro. Thus, muscarinic receptors in the rabbit urinary bladder are heterogeneous; prejunctional facilitatory (M1) and inhibitory (M2) for acetylcholine release, and postjunctional muscarinic M3 receptors mediating contractile responses.

Acetylcholine↗
PubMed1995

The Biosure Study: influence of composition of diet and food consumption on longevity, degenerative diseases and neoplasia in Wistar rats studied for up to 30 months post weaning.

The 1200-rat Biosure Study had six interrelated aims: (1) To see whether dietary restriction (80% ad lib.) reduces the age-standardized incidence of fatal or potentially fatal neoplasia before the age of 30 months. (2) To see whether the beneficial effects of diet restriction can be achieved by (a) limiting the daily period of access to food to 6 hr, or by (b) limiting the energy value of the diet. (3) To see whether reduced calorie intake between weaning and age 4 months influences survival and/or incidence of non-neoplastic and neoplastic diseases. (4) To compare effects of food consumption, energy intake and protein intake on survival and disease. (5) To study the relationships between body weight at different ages with eventual survival and disease incidence. (6) To provide a database for studying relationships between various in-life measurements and eventual survival and disease incidence in individual animals. Twelve groups of SKF Wistar rats consisting of 50 animals of each sex were fed according to different dietary regimens from when they were weaned at the age of 3 wk until they died, or had to be killed because they were sick, or until the experiment was terminated at 30 months. For five of the 12 dietary regimens, satellite groups consisting of 30 animals per sex were maintained in parallel and used to supply information on the effect of diet on circulating hormone levels during the course of the study. During the 13 wk post weaning a Standard Breeder diet (SB) was provided either ad lib. (four groups), 80% ad lib. (three groups), or with access to food limited to 6 hr per day (one group). During this same period two other groups were fed a Low Nutrient Breeder diet (LB) ad lib. A further group was fed a Low Nutrient Maintenance (high fibre) diet (LM) ad lib. Finally, one group was fed the high protein Porton Rat diet (PR) ad lib.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1995

Presence and effects of pituitary adenylate cyclase activating peptide in the submandibular gland of the ferret.

Pituitary adenylate cyclase activating peptide (PACAP), a recently described vasoactive intestinal peptide-like neuropeptide, was found to be present in neurons in the submandibular gland of the ferret, where PACAP-immunoreactive nerve fibers were distributed around blood vessels, acini and ducts. Most of the PACAP-immunoreactive fibres were distinct from those storing vasoactive intestinal peptide. PACAP occurs in tissues as PACAP1-38 and PACAP1-27. PACAP1-38 and PACAP1-27 but not PACAP16-38 displayed biological activity with about the same potency. They exerted vasodilator effects on the submandibular vasculature, which resulted in a greater fall in vascular resistance than an equimolar dose of vasoactive intestinal peptide. The vasodilator response was independent of muscarinic receptor activation. Neither vasoactive intestinal peptide nor PACAP alone evoked any flow of saliva. However, both vasoactive intestinal peptide and PACAP enhanced the fluid response to acetylcholine, and the flow of saliva as well as the output of protein in response to parasympathetic nerve stimulation, vasoactive intestinal peptide being more potent than PACAP. In vitro, protein was released from submandibular gland tissue in response to both vasoactive intestinal peptide and PACAP, vasoactive intestinal peptide being more potent than PACAP. PACAP (and vasoactive intestinal peptide) exerted its in vitro effect following adrenoceptor and muscarinic blockade and following degeneration of sympathetic nerves. Sympathetic denervation combined with parasympathetic preganglionic denervation resulted in supersensitivity to both vasoactive intestinal peptide and PACAP. The fact that PACAP and vasoactive intestinal peptide occur in different nerve fibre populations suggests different roles for the two peptides in the submandibular gland.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

An experimental model for long-term examinations of urethral and uterine pressures in conscious dogs: effect of a highly selective compound contracting urethral smooth muscles.

An experiment model was designed for studies of urethral and uterine pressures in a conscious animal, thereby avoiding the interference of anesthesia on these responses. Dogs were trained to stand in cradles for an experimental period of 3 hours, during which urethral and uterine pressures and ECG were recorded. Substances were administered either orally or intravenously. Intravenously given phenylpropanolamine (PPA; 0.3 mg./kg.) and a newly synthetized compound S113 (0.5 mg./kg. intravenously) increased the urethral pressure by about 30 and 100%, respectively. Oral administration of PPA (3.5 mg./kg.) and S113 (6 mg./kg.) increased it by about 60 and 85%, respectively. In contrast to PPA, S113 evoked no cardiac effects. Whereas PPA had pronounced effects on uterine contractility, S113 had only minor effects. Furthermore, the responses in the experiments were stable and reproducible. This dog model seems to be useful for long-term recordings of urethral and uterine pressures.

Administration, Oral↗
PubMed1995

Muscarinic receptor subtypes in the submandibular gland and the urinary bladder of the rabbit: in vivo and in vitro functional comparisons of receptor antagonists.

1. In pentobarbitone-anaesthetized rabbits, the inhibitory effects of muscarinic receptor antagonists with different selectivity profiles were examined on carbachol-evoked submandibular secretion and urinary bladder contractions, and on parasympathetically nerve-evoked secretion. On isolated submandibular gland fragments, the inhibitory effects of the antagonists were studied on carbachol-evoked release of potassium and on the overflow of tritium in response to electrical field stimulation. 2. In vivo, 4-DAMP equipotently inhibited simultaneously carbachol-evoked submandibular secretory and contractile responses of the urinary bladder, while pirenzepine was found to be four times as potent in inhibiting the secretory response compared with the contractile response. 3. The inhibition of carbachol-evoked salivation caused by atropine, 4-DAMP and pirenzepine was as great as their inhibition of parasympathetic nerve-evoked salivation. Methoctramine exerted less inhibitory effect on nerve-evoked salivation than on carbachol-evoked, thus seemingly causing greater presynaptic inhibition. 4. In vitro, pirenzepine was only 30 times less potent in inhibiting carbachol-evoked potassium release than 4-DAMP (pA2, 9.58 vs 8.10). Whereas atropine, 4-DAMP and pirenzepine abolished the overflow of tritium from isolated glands in response to electrical field stimulation, methoctramine increased it. 5. It is concluded that the muscarinic secretory response in the rabbit submandibular gland is exerted via both muscarinic M1 and M3 receptors, while the contractile response of the urinary bladder to muscarinic agonists is exerted via muscarinic M3 receptors. The release of acetylcholine from nerve terminals in the gland can be inhibited via M2 autoreceptors in rabbits.

Animals↗
PubMed1995

Fluid and protein secretion from ferret submandibular and parotid glands in response to sympathetic nerve stimulation or administration of sympathomimetics.

Electrical stimulation of the sympathetic innervation evoked secretion of submandibular and parotid saliva. By changing the mode of stimulation from a continuous to an intermittent one the fluid response increased and glandular blood flow improved. The volumes from the submandibular glands were larger than those from the parotid glands and further, the protein concentration of submandibular saliva was higher than that of parotid saliva. Adrenaline, isoprenaline and phenylephrine evoked larger fluid responses from submandibular than from parotid glands. However, the fluid response was small compared to the parasympathetic one. Substance P-evoked saliva was used as carrier for protein released by sympathetic nerve stimulation or administration of adrenaline and isoprenaline. In vitro tissues of submandibular and parotid glands responded to adrenaline with a dose-dependent release of protein. Taken together, the analytical pharmacology performed in vivo and in vitro, and including the antagonists phentolamine, dihydroergotamine, propranolol and metoprolol, showed that in submandibular glands, alpha(alpha 1)adrenoceptors were predominantly involved in fluid secretion and beta(beta 1)-adrenoceptors predominantly involved in protein secretion. In parotid glands, fluid secretion seemed solely to depend on alpha(alpha 1)-adrenoceptors, while beta(beta 1)-adrenoceptors seemed almost solely involved in protein secretion.

Animals↗
PubMed1994

Parasympathetic non-adrenergic, non-cholinergic reflex secretion of parotid acinar granules in rats pretreated with atropine and adrenoceptor antagonists.

In parotid glands of fasted rats, feeding for 60-90 min reduced numerical density of acinar secretory granules by 52% and total activity of glandular amylase by 38%. In the presence of adrenoceptor antagonists (phentolamine and propranolol, 2 mg/kg, i.p., of each) the corresponding decrease was 31% and 32%, and in combination with atropine (1 mg/kg, i.p.) 32% as to both these indices. These non-adrenergic non-cholinergic (NANC) responses depended on an intact parasympathetic auriculo-temporal nerve since they did not occur following section of this nerve. In anaesthetized animals, electrical stimulation of the sympathetic innervation (50 Hz, 1 s every 10th second) for 60 min caused secretion of parotid saliva and decreases in number of acinar granules, by 65%, and in total amylase activity, by 49%; the adrenoceptor antagonists at the above-mentioned doses completely abolished the expected responses of the parotid gland and thus showing that these antagonists at the dose level chosen achieved an effective receptor blockade. In conclusion, parasympathetic NANC mechanisms are reflexly mobilized in response to eating, and these mechanisms are potentially responsible for the whole parasympathetic response and for the major part of that response in the absence of any antagonists. Under natural reflex conditions adrenergic, cholinergic and non-adrenergic, non-cholinergic mechanisms are most likely engaged to varying extents in order to generate the most purposeful response.

Adrenergic Antagonists↗
PubMed1994

Depletion of secretory granules from the feline parotid gland: action of NANC transmitters per se.

A parotid acinar degranulation of approximately 60 and 40% was observed in cats under pentobarbitone anaesthesia after a 90-min period of continuous stimulation of the parasympathetic auriculo-temporal nerve at 10 Hz in the absence and presence of atropine, respectively. Atropine completely abolished the large fluid response of the gland to the nerve stimulation. In the non-atropinized cats, bethanechol, infused into the carotid artery at a dose rate evoking a salivary flow similar to that in response to parasympathetic nerve stimulation, caused an acinar degranulation of approximately 25% and acinar vacuolation. Vasoactive intestinal peptide (VIP; 0.5 microgram kg-1 min-1 also infused into the carotid artery for 90 min) caused an acinar degranulation of the same magnitude as the parasympathomimetic drug but the peptide did not give rise to any fluid secretion or vacuole formation. The experiments were performed in the presence of alpha- and beta-adrenoceptor blockers. Thus, in parotid glands of the cat, producing no overt secretion of fluid, non-adrenergic, non-cholinergic (NANC) mechanisms may be at work causing exocytosis of the acinar granules. These mechanisms are also likely to contribute to the secretion of granules in response to parasympathetic nerve activity in the absence of blockade of the classical autonomic receptors.

Adrenergic alpha-Antagonists↗