relationship between nitric oxide [No] and gastric secretion

The role of NO in the regulation of gastric acid secretion was examined in the anaesthetized adult male albino rats. Continuous i.v. infusion of the NO donor, sodium nitroprusside [SNP, 12mg/kg/h] significantly inhibited both basal and stimulated gastric acid secretion which was mediated neuronally by gastric distension [20 cm H2O or i.v. bolus administration of 2-deosxy -D- glucose [150 mg/kg], as well as gastric acid responses induced by i.v infusion of submaximal doses of pentagastrin [8 micro g/kg/h]. By contrast, gastric acid responses to i.v. infusion of submaximal doses of histamine [1 mg/kg/h] were not influenced by the NO donor. Pretreatment with N[G] - nitro-L-arginine methylester[L-NAME, 10mg/kg, i.v.] did not affect basal acid secretion, but significantly potentiated the increase in acid secretion induced by 2-deoxy-D- glucose which was almost completely antagonized by coadministration of L-arginine [500 mg/kg, i.p.] and slightly augmented the acid secretory response to pentagastrin. Moreover, it was found that pentagastrin infusion caused an increase in luminal release of histamine and this response was significantly suppressed by i.v infusion of the NO donor.Intraperitoneal [i.p] administration of cimetidine [60 mg/kg], a histamine H2-receptor antagonist, significantly inhibited the increase in acid secretion in response to 2-deoxy-D-glucose [150 mg/kg, i.v.], pentagastrin [8 micro g/kg/h, i.v] and histamine [I mg/kg/h, i.v.] infusion. In conclusion, the present study suggests that NO has an inhibitory action on gastric acid secretion that may be through suppression of histamine release from enterochromaffin like [ECL] cells

role of magnesium and calcium ions in atrial natriuretic peptide secretion

For the purpose of examining the role of calcium and magnesium ions in the secretory process of atrial natriuretic peptide [ANP], we studied the effects of hypercalcemia, digitalis "Lanoxine", calcium ion channel blocker "verapamil", hypermagnesemia, potassium ion channel blocker "Glibenclamid", and potassium ion channel opener "cromakalim" on plasma concentration of immunoreactive ANP [ir ANP]. Pentobarbital-anesthetized dogs [n-36] were divided into-6-equal groups [6 each] and treated separately with calcium chloride infusion [0.136 mmol/Kg/min-10 min]. Lanoxine injection [30 micro g/Kg], verapamil injection [300 micro g/Kg], magnesium sulfate infusion [0.168 mmol/Kg/min-10 min] after an initial bolus dose of 1.5 mmol/Kg, glibenclamid injection [0.3 mg/Kg], and cromakalim injection [10 micro g/Kg]. Plasma ir ANP concentrations, mean arterial pressure [MAP], heart rate [HR] and serum calcium and magnesium concentrations were measured. With calcium chloride and magnesium sulfate infusions, serum calcium and magnesium levels and plasma ir ANP concentrations were significantly increased. Also, lanoxine and K[+] -channel blocker "glibenclamid" caused a significant increase in plasma ir ANP concentration while verapamil and the K[+]-channel opener "cromakalim" resulted in a significant decrease. Neither calcium chloride nor lanoxine produced a significant effect on heart rate, but both significantly increased MAP. In contrast, magnesium sulfate and verapamil produced a significant decrease in MAP and HR while glibenclamid and cromakalim were associated with insignificant changes in both HR and MAP. These results suggest that calcium ions may play a key role in the secretory process of ANP and indicate that magnesium ions may also influence ANP secretion by acting via modulation of K[+] -channels