Response of isolated coronary artery segments to serotonin in the presence of a flavinoid, indomethacin and acetylsalicylate

The aim of this work is to study the mechanism by which 4-metilesculetin (4-Me) cause the relaxation or inhibit the serotonin induced contraction in the smooth muscle. The effect of 4-Me, alone or associated with ascorbic-acid, on basal tone and serotonin induced contraction of isolated coronary strips have been studied. Experiments have been carried out in the presence of indomethacin (IN), specific inhibitor of prostaglandin synthetase. IN-decreased, but did not abolished, the 4-Me induced relaxation and reduced or suppressed the depressive effect of 4-Me on the serotonin dependent contraction. Therefore, it seems reasonable to conclude that the 4-Me influence could be mediated by prostaglandins release in the smooth muscle.     

Influence of bioflavonoid (4-methylesculetin) on the reaction of isolated calf hepatic artery to serotonin

The effect of 4-metilesculetin on strips of calf hepatic arteries was investigated. 4-metilesculetin antagonizes the contraction induced by 5-HT probably through activation of the synthesis of vasodilator prostaglandins.     

Influence of hydrocortisone on the response to noradrenaline of segments of isolated coronary arteries in the presence of a beta-adrenergic blocking agent

The effect of hydrocortisone on the noradrenaline-induces contraction, after propranolol, was studied in vitro. Contraction of response to noradrenaline were increased by hydrocortisone. We suggest that the hydrocortisone influence depends on inhibition of catecol-O-metiltransferase (COMT).     

Influence of desoxycorticosterone on the reaction of isolated segments of coronary arteries to noradrenaline in the presence of pyrogallol

The effect of the desoxycorticosterone on the noradrenaline-induced relaxation of coronary arteries waw studied in vitro, after a known inhibitor of COMT, pyrogallol. Relaxation induced by noradrenaline was enhanced by desoxycorticosterone. Relaxation in response to noradrenaline was increased by desoxycorticosterone. Pyrogallol potentiated the responses of coronary strips to noradrenaline and also reduced or abolished the enhancing effects of desoxycorticosterone. It is concluded that desoxycorticosterone enhances the reponse of coronary smooth muscle to noradrenaline by inhibiting and enzymatic pathway for the inactivation of catecolamines.     

Influence of pyridoxal-5'-phosphate on responses of isolated coronary arteries to noradrenaline, in the presence of pyrogallol

The effect of PLP on the noradrenaline-induced relaxation of coronary arteries was studied in vitro, after known inhibitor of COMT, Pyrogallol. Relaxation of response to noradrenaline were increased by PLP. Pyrogallol potentiated responses of coronary strips to noradrenaline and also reduced or abolished the enhancing effects of PLP. It is concluded that PLP enhances the response of coronary smooth muscle to noradrenaline by inhibiting a enzymatic pathway for the inactivation of catecolamines.     

The role of peripheral cholinergic and adrenergic receptor systems in the action of histamine on the isolated coronary arteries

The action of peripheral cholinergic and adrenergic receptor systems on the histamine coronary vasospastic effects are investigated in the experiments on the isolated ring-shaped strips of coronary arteries of pigs with the aid of specific agonists and antagonists. It has been demonstrated that neuromediator systems play a significant role in the regulation of contractile activity of the coronary spasm pathogenesis. When medicines are prescribed to patients with ischemic heart disease it is necessary to take into account the character of the preparations interaction which affect the peripheral neuromediator processes such as histaminergic, cholinergic, adrenergic and others.     

Influence of dexamethasone on the responses of isolated coronary arteries to adrenaline

The effect of Dexamethasone on the adrenaline-induced relaxation was studied in vitro. Relaxation of response to adrenaline increased by Dexamethasone. We suggest that the Dexamethasone influence depends on inhibition of Catecol-O-methyl transferase (COMT).     

Effect of histamine receptor antagonists and indomethacin on implantation in the rabbit

Anti-inflammatory drugs were given to pregnant rabbits during the 24-h period prior to the increase in the uterine vascular permeability which occurs on Day 7. Their effect on the vascular response was monitored by quantifying the concentration of extravascular Evans blue dye. The increase in vascular permeability normally seen on Day 7 was inhibited by either indomethacin or a combination of H1-(mepyramine) and H2-(cimetidine) receptor antagonists. When given alone, neither cimetidine nor mepyramine was as effective as the combination in reducing vascular permeability. Prostaglandins and histamine may be acting together since simultaneous administration of lower doses of indomethacin and the antihistamines reduced vascular permeability below that observed following administration of either class of anti-inflammatory drugs alone. In a second experiment, anti-inflammatory drugs were administered during the peri-implantation period (Days 6-8) and their effect on the weights of maternal and fetal tissues, and on fetal viability were evaluated on Day 14 of pregnancy. Indomethacin had a more deleterious effect on both parameters than did the combination of histamine receptor antagonists. Results from these experiments suggest that both prostaglandins and histamine may participate in the uterine vascular response, whereas the overall process of implantation appears to be more dependent upon the synthesis of prostaglandins than the action of histamine.     

Influence of desoxycorticosterone on the response of calf coronary artery strips to adrenaline

The effect of desoxycorticosterone on the adrenaline-induced relaxation of coronary arteries was studied "in vitro". It resulted that the effect of adrenaline was enhanced by desoxycorticosterone. It is concluded that desoxycorticosterone potentiates the effects of adrenaline by inhibiting its inactivation by Catechol-O-methyltransferase.     

Effect of indomethacin on the adrenal renin response to nephrectomy in the rat

The role of prostaglandins in the control of adrenal renin in vivo was evaluated in nephrectomized rats. Nephrectomy increased adrenal renin from 13.2 +/- 1.37 ng angiotensin I/mg protein/hr to 166.5 +/- 17.3 ng angiotensin I/mg protein/hr. Indomethacin treatment significantly suppressed the adrenal renin response to nephrectomy. (47.8 +/- 5.22 ng angiotensin I/mg protein/hr). Adrenal aldosterone was also suppressed by indomethacin. Adrenal prostaglandin E2 increased after nephrectomy and decreased after indomethacin. Plasma corticosterone and serum potassium did not change after indomethacin. These data indicate that inhibition of prostaglandin synthesis by indomethacin partially blocks the adrenal renin response to nephrectomy, suggesting that prostaglandins may play a role in the adrenal response to nephrectomy.     

Effect of indomethacin on the adrenal renin response to nephrectomy in the rat

The role of prostaglandins in the control of adrenal renin in vivo was evaluated in nephrectomized rats. Nephrectomy increased adrenal renin from 13.2 ± 1.37 ng angiotensin I/mg protein/hr to 166.5 ± 17.3 ng angiotensin I/mg protein/hr. Indomethacin treatment significantly suppressed the adrenal renin response to nephrectomy. (47.8 ± 5.22 ng angiotensin I/mg protein/hr). Adrenal aldosterone was also suppressed by indomethacin. Adrenal prostaglandin E₂ increased after nephrectomy and decreased after indomethacin.Plasma corticosterone and serum potassium did not change after indomethacin. These data indicate that inhibition of prostaglandin synthesis by indomethacin partially blocks the adrenal renin response to nephrectomy, suggesting that prostaglandins may play a role in the adrenal response to nephrectomy.     

Effect of presence of a dominant follicle on the superovulatory response in buffalo (Bubalus bubalis)

Ten buffalo were superovulated by administration of 8 doses of FSH in a descending schedule spread over 4 d (5.5/5.5, 4.5/4.5, 3.5/3.5 and 2.5/2.5 mL, i.m.; total dose of 64 AU in 32 mL) beginning on Day 10 of an unstimulated estrous cycle, and 30 and 20 mg Lutalyse was given alongwith the 5th and 6th injections of FSH, respectively, to induce luteolysis. The number of corpora lutea (CL) was determined on 6 d post estrus. The ovaries were examined daily by ultrasonography from Day -5 to Day 5 (Day 0 = day of start of superovulation). The animals were retrospectively classified into 2 groups depending upon the presence (n = 4) or absence of a dominant follicle (n = 6). The mean diameter of the largest follicle (F1) increased from 8.25 +/- 0.48 mm on Day -5 to 10.75 +/- 0.25 mm on Day 0 in the dominant group, whereas in the nondominant group the F1 follicle exhibited a progressive decrease from 9.00 +/- 0.45 mm to 7.00 +/- 0.65 mm during the same period, the difference in profiles between the 2 groups was significant (P = 0.042). The profile of the diameter of the second largest follicle (F2) and the difference in diameters between largest and second largest follicles (F1-F2) were not significantly different between the 2 groups. The profile of mean number of large (> or = 10 mm diameter), but not small (2 to 5 mm diameter) or medium (6 to 9 mm diameter) follicles differed significantly (P = 0.001) between the 2 groups from Day -5 to Day 5 (P = 0.030). The number of CL was not significantly different between nondominant (4.00 +/- 0.97) and dominant groups (3.25 +/- 1.31). The number of CL was positively correlated (P < 0.01) with the number of medium follicles and the total number of follicles on the day of initiation of superovulation, but not with follicles of any size category or total number of follicles on any previous day. The results of this study indicate that following the use of morphological criteria based on the size of the largest follicle alone, the superovulation response is not affected by the presence of a dominant follicle at the initiation of superovulation in buffalo.     

Influence of 6-methylprednisolone on responses of isolated coronary arteries to adrenaline

The effect of 6-Methylprednisolone on the adrenaline-induced relaxation was studied in vitro. Relaxation of response to adrenaline increased by 6-Methylprednisolone. We suggest that the 6-Methylprednisolone influence influence depends on inhibition of Catecol-O-methyl transferase (COMT).