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D Stojić

Publications and source records attributed to D Stojić.

13 recordsLinked to original sources
PubMed2005

The effects of acute and chronic lithium treatment on rat submandibular salivation.

OBJECTIVE: Acute and chronic actions of lithium on salivation induced by agonists associated with receptor-linked hydrolysis of membrane inositol phospholipids (carbachol and phenylephrine) and by agonist linked to activation of adenylate cyclase (isoproterenol) were investigated. MATERIAL AND METHODS: In anaesthetized rats, submandibular salivation induced by intravenous injection of carbachol, phenylephrine and isoproterenol, was measured and expressed as volume of fluid (microl) elicited per 100 mg wet weight of each gland per minute. The experiments were repeated after acute and chronic treatment of lithium (7 mg kg(-1)). The results were analysed with unpaired t-test. RESULTS: Chronic, but not acute lithium treatment significantly decreases carbachol- and phenylephrine-induced salivation while isoproterenol-induced salivation was not changed neither after acute nor after chronic administration of lithium. CONCLUSION: The results suggest that hyposalivation during chronic lithium therapy could be mediated by alterations in the phosphatidylinositol cycle and a consequent lack of inositol after agonist stimulation.

Acute Disease↗
PubMed2004

The relaxant effect of vasoactive intestinal polypeptide in the isolated canine uterine artery: the role of endothelium.

The purpose of this study was to examine the effect of vasoactive intestinal polypeptide (VIP) on the uterine artery obtained from non-pregnant dogs. VIP (3 x 10(-9)-3 x 10(-7) M) induced concentration-dependent relaxation in canine uterine arteries with intact endothelium, pre-contracted with 10(-5) M phenylephrine (pEC(50) = 7.52 +/- 0.02, maximal response was 82.19 +/- 2.15%, n = 36). The administration of the cyclooxygenase inhibitor indomethacin (10(-5) M) or 4-aminopyridine (4-AP), a blocker of potassium channels (10(-5) M), did not modify the relaxation induced by VIP. Contrary to this, N(G)-nitro-L-arginine (L-NOARG) (10(-5) M) inhibited relaxation is evoked by VIP. Indomethacin applied with L-NOARG did not provoke further inhibition of VIP-induced relaxation. In the presence of both L-NOARG and L-NOARG + indomethacin, 4-AP led to the further inhibition of VIP-induced relaxation of canine uterine artery. It is concluded that VIP induces endothelium-dependent relaxation of uterine arteries of non-pregnant dogs, which can be entirely explained by the production of nitric oxide (NO) from the endothelial cells. We proposed that when NO synthesis is inhibited, VIP induces further relaxation, independent of the edothelium-derived relaxing factors, probably through activation of K(+) channels.

4-Aminopyridine↗
PubMed2003

Endothelium-dependent relaxation of canine uterine artery in response to acetylcholine: the possible involvement of alternative pathways.

The effect of acetylcholine on the isolated, pre-contracted, uterine artery of non-pregnant dog was investigated. Acetylcholine-induced concentration-dependent relaxation of isolated canine uterine artery with endothelium (pEC50 = 6.48 +/-0.01, n = 37) and was without effect on arterial segments denuded of endothelium. Indomethacin, 4-aminopyridine (10-5 m) and pre-contraction with K+-rich Krebs-Ringer bicarbonate solution had no effect on acetylcholine-induced relaxation. NG-nitro-l-arginine (l-NOARG) (10-5 m) inhibited relaxation evoked by acetylcholine. Indomethacin applied with l-NOARG led to further inhibition of acetylcholine-induced relaxation. In the presence of both l-NOARG and indomethacin, 4-aminopiridine did not provoke further inhibition of acetylcholine-induced relaxation of canine uterine artery. It is concluded that the acetylcholine-induced relaxation of canine uterine artery is probably mediated by endothelial production of nitric oxide (NO). However, if NO-synthase is inhibited, acetylcholine-induced vasorelaxation may be, in part, mediated through activation of cyclooxygenase pathway.

Acetylcholine↗
PubMed1998

Carbachol-induced oxygen consumption in slices from developing rat submandibular and parotid glands.

In contrast to the submandibular gland, the developing rat parotid gland shows refractoriness to cholinergic secretagogues until 2 wks of age. To assess the underlining mechanism of this refractoriness, I investigated changes in oxygen consumption as a function of animal age in slices from rat submandibular and parotid glands, measuring both basal and carbachol-stimulated levels. The oxygen consumption was determined by a direct manometric method in the Warburg apparatus. Carbachol-induced oxygen uptake in submandibular gland slices was observed by 1 day of age and reached the adult level of stimulation by 3 wks of age. In the parotid gland, carbachol failed to stimulate oxygen uptake in the early post-natal period, and the first response was detected at 2 wks of age, reaching the adult level at 4 wks of age. Para-fluorohexahydro-sila-diphenidol (pFHHSiD), a selective M3 antagonist, inhibited carbachol-induced oxygen uptake in both glands, while pirenzepine, a selective M1 antagonist, had no effect, suggesting that the M3 muscarinic receptors are involved in this process. The respiratory effect of carbachol, in both glands, was inhibitable by ouabain and, to a lesser extent, by furosemide, indicating that carbachol-enhanced oxygen uptake is due to Na,K-ATPase and that the furosemide-sensitive co-transport of Na+ entry is underdeveloped in immature cells. The ouabain-sensitive Na,K-ATPase activity in the parotid gland increased from birth until 28 days of age. At the time of parotid gland refractoriness to carbachol, Ca2+ ionophore A23187 caused an increase of oxygen uptake only in the presence of extracellular Ca2+. In the presence of carbachol, the effect of ionophore was significantly higher than that of ionophore alone. These results raise the possibility that the refractoriness of the parotid gland to carbachol is due to the inability of carbachol to increase Ca2+ uptake rather than to the lack of distal limb, which resides on the pathway from receptor stimulation to Na,K-ATPase activation.

Age Factors↗
PubMed1990

Differentiation of alpha adrenoceptors mediating increase of oxygen consumption in rat submandibular salivary gland slices.

Clonidine, noradrenaline and adrenaline (in the presence of propranolol), but not phenylephrine and methoxamine, stimulated an increase in the oxygen consumption of these slices that was blocked by yohimbine but not by prazosin. The stimulation was inhibited by ouabain and required the presence of Ca2+ in the incubation medium. The calcium ionophore A 23187 stimulated oxygen consumption in the tissue slices and enhanced the respiratory effect of clonidine. Atropine and (D-Pro2, D-Trp7.9)-substance P failed to block the respiratory response to clonidine in concentrations that inhibited the respiratory effects of carbachol and substance P, respectively. Release of acetylcholine from the unstimulated gland slices was reduced by clonidine or Ca2+ omission. Yohimbine prevented the clonidine effect and stimulated acetylcholine resting release. Nifedipine did not affect either the release of acetylcholine or the clonidine-induced reduction of acetylcholine release but blocked the oxygen uptake due to clonidine or to release acetylcholine.

Acetylcholine↗
PubMed1987

Oxygen consumption mediated by M2 muscarinic receptors in rat salivary glands.

Carbachol and oxotremorine stimulated the consumption of oxygen in rat parotid, submandibular, and sublingual gland slices in a dose-dependent manner. Their actions were abolished by atropine and nifedipine but not by trihexyphenidyl. The findings suggest that carbachol and oxotremorine enhanced oxygen consumption in the major salivary gland slices by the activation of the calcium-dependent muscarinic M2 receptors.

Animals↗
PubMed1984

The effects of epinephrine, norepinephrine, and carbachol on oxygen consumption in rat sublingual gland slices.

Epinephrine and carbachol, but not norepinephrine, significantly stimulated oxygen consumption in rat sublingual gland slices. The response to epinephrine was blocked by phentolamine and yohimbine, while propranolol and prazosin did not affect it. The response to carbachol was blocked by atropine. Also, oxygen consumption induced by both epinephrine and carbachol was inhibited by verapamil. These findings suggest that epinephrine enhanced oxygen consumption in sublingual gland slices by activation of alpha 2-adrenergic receptors, while carbachol activated muscarinic receptors; activation of both receptors mediated the respiratory response by facilitating the entry of extracellular Ca.

Animals↗
PubMedDate not supplied

The inhibitory effect of guanabenz on submandibulary salivation induced by chorda tympani stimulation in anaesthetized cat.

The actions of guanabenz, an alpha 2-adrenoceptor agonist, on submandibulary salivation were examined in the anaesthetized cat. Guanabenz reduces submandibulary salivation evoked by electrical stimulation of the chorda tympani in dose and frequency dependent manner. This effect was antagonized by yohimbine but not by prazosin. Guanabenz increased salivation elicited by intraarterial injection of carbachol. This potentiated effect was suppressed by yohimbine, but not by prazosin. On noradrenaline induced salivation guanabenz has no effect, while prazosin virtually abolished it, indicating involvement of alpha 1-adrenoceptors. It appears that guanabenz reduces peripheral parasympathetically evoked submandibulary salivation influencing the presynaptic control of transmitter release alpha 2-adrenoceptors. Postsynaptic alpha 2-adrenoceptors are not involved in the inhibition of salivation by this agent.

Anesthesia↗