Gene/Protein
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Drug
Enzyme
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Gene/Protein
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Target Concepts:
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Query: UMLS:C0406810 (
NAME
)
13,345
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Immunocytochemistry and in situ hybridization revealed abundant
secretin
expressing cells on duodenal villi with a gradual decrease throughout the small intestines of the rat. They were absent in pancreas, stomach and colon.
Secretin
caused relaxation of rat intestinal longitudinal muscle in vitro. Studies on colon revealed that the
secretin
-evoked response was unaffected by apamin, tetrodotoxin, L-
NAME
, VIP or PACAP pretreatment;
secretin
itself caused desensitization. Addition of VIP or PACAP when the
secretin
-evoked relaxation was maximal evoked a further relaxation suggesting the presence of distinct receptors.
Secretin
causes relaxation via activation of
secretin
receptors located on the smooth muscle and not via any of the related VIP/PACAP receptors.
...
PMID:Expression and motor effects of secretin in small and large intestine of the rat. 1109 Sep 23
The permeability in the intact and diabetic rat coronary circulation after administration of
secretin
(3.0 micromol/kg i.v.), an inhibitor of NOS (nitric oxide synthase), and L-
NAME
(N(G)-nitro-L-arginine-methyl ester hydrochloride) (1 mg/kg i.v.), and both substances given together, were studied. To measure protein extravasation Evans blue dye was used as a marker of vascular permeability. The vascular permeability of the left ventricle did not differ in intact and diabetic rats. In the diabetes state increased permeability of atria was observed. Administration of
secretin
did not influence the coronary vascular permeability in either the intact or the diabetic rats. L-
NAME
increased the atria permeability and did not change left ventricle permeability. In diabetes, injection of L-
NAME
caused a decrease in the permeability in both the atria and left ventricle. In intact rats
secretin
diminished the L-
NAME
effect in the atria. In diabetic rats co-administration of secretin+L-
NAME
increased the permeability of the atria and left ventricle, but L-
NAME
administered alone decreased them.
Secretin
modified the effect of L-
NAME
on coronary permeability in intact and diabetic rats.
...
PMID:Influence of secretin and L-NAME on vascular permeability in the coronary circulation of intact and diabetic rats. 1111 Oct 15
The present study aimed to determine the influence of nitric oxide (NO) on the action of
secretin
in the cardiovascular system in intact rats. The studies involved the in vivo measurements of the systolic (SBP) and diastolic (DBP) blood pressure. The measurements were conducted when NO was absent, which was attained by the use of NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-
NAME
), and when NO was in excess which was obtained by the administration of L-arginine (L-arg), the substrate for NO synthase or exogenous donor of NO, sodium nitroprusside (SNP).
Secretin
given at the following three doses: 0.75, 1.5 and 3.0 micromoles/kg iv increased SBP and DBP. L-
NAME
inhibited the slight hypertensive effect of
secretin
. L-arg abolished the hypertensive effect of the peptide given at the smallest dose, did not change the effect of
secretin
administered at the medium dose (which did not raise the pressure) and preserved the action of the highest
secretin
dose. SNP abolished the hypertensive effect of all doses of the peptide. In conclusion, the study has shown that both the lack and excess of NO change the in vivo effect of
secretin
in intact rats.
...
PMID:Influence of nitric oxide on the cardiovascular action of secretin in intact rats. Part A. Does nitric oxide influence the effect of secretin on arterial blood pressure? 1133 29
The present study was designed to examine the effect of absence or excess of NO on
secretin
-mediated responses in the isolated heart. This problem was investigated using the modified Langendorff's method.
Secretin
administered at two higher doses increased the cardiac contraction amplitude (p < 0.05), but did not change the heart rate and coronary outflow. NO was depleted from experimental system by perfusion of the isolated heart with NO synthase inhibitor L-
NAME
(NG-nitro-L-arginine methyl ester) at 10 microM. It caused a significant decrease in coronary outflow (p < 0.01) and the tendency to bradycardia (p > 0.05) with no change in cardiac contraction amplitude. L-
NAME
abolished the positive inotropic effect of the medium
secretin
dose and preserved the inotropic effect of the highest dose of the peptide. It reversed the tendency to decrease coronary outflow induced by
secretin
(and L-
NAME
) given separately. To study the effect of NO excess, we applied the substrate for NO synthesis, amino acid L-arginine (L-arg) (100 microM) or exogenous donor of NO--sodium nitroprusside (SNP) (100 microM). Both substances did not affect the isolated heart function. L-arg did not change the effect of
secretin
, however it abolished non significant decrease in coronary outflow evoked by the highest dose of
secretin
. SNP preserved the positive inotropic action of the peptide and expressively reversed the negative values of coronary outflow observed after its co-administration with the highest dose of
secretin
. These results indicate that both the absence and excess of NO change the cardiac effect of
secretin
in the same direction.
...
PMID:Influence of nitric oxide on the cardiovascular action of secretin in intact rats. Part B. Does nitric oxide influence the effect of secretin on isolated heart function? 1133 30
The modulation by condition of the lack or the excess of nitric oxide (NO) on cardiovascular action of
secretin
in diabetic rats was investigated. In vitro the isolated heart function and in vivo, the systolic (SBP), diastolic (DSP) blood pressure and heart rate (HR) were measured.
Secretin
evoked inotropic positive effect and increased coronary outflow (CO), in vivo did not increase systemic pressure and the highest dose of the peptide increased the heart rate. NO synthase inhibitor, N(G) nitro-L-arginine methyl ester (L-
NAME
) deeply increased the systemic pressure and in vitro decreased coronary outflow. L-arginine and sodium nitroprusside (SNP) did not influence the isolated heart function and in vivo decreased the systemic pressure. L-
NAME
preserved the inotropic positive effect of
secretin
and the increase of the coronary outflow. In vivo co-administration of L-NAME+secretin evoked hypotensive effect and abolished the increase of the heart rate after the highest dose of the peptide. L-arginine abolished inotropic positive effect of the peptide and the increase of coronary outflow. In vivo co-administration of these substances caused hypotension and attenuated the increase of the heart rate after the highest dose of
secretin
. Co-injection of SNP and
secretin
preserved the inotropic effect of
secretin
and abolished the increase of the coronary outflow. In vivo infusion of SNP+secretin evoked hypotension and similarly to L-arginine, SNP abolished tachycardia induced by the highest dose of
secretin
. Both the lack and the excess of nitric oxide changed the cardiovascular action of
secretin
in diabetic rats.
...
PMID:Diabetes-induced changes of nitric oxide influence on the cardiovascular action of secretin. 1195 70
C-type natriuretic peptide (CNP) is the major natriuretic peptide in the brain and its mRNA has been reported in the central nervous system, which supports local synthesis and its role as a neuromodulator. The aim of the present work was to study the effect of centrally applied CNP on pancreatic secretion. Rats were fitted with a lateral cerebroventricular cannula one-week before secretion studies. The central administration of CNP dose-dependently enhanced pancreatic fluid and protein output. CNP response was diminished by atropine and hexamethonium, but it was abolished by vagotomy. Neither adrenergic antagonists nor the administration of (D-p-Cl-Phe(6),Leu(17))-vasoactive intestinal peptide (VIP antagonist) or N(omega) Nitro-L arginine methyl ester (L-
NAME
) (nitric oxide synthase inhibitor) affected CNP response. The effect induced by CNP was mimicked by 8-Br-cGMP but not by c-ANP-(4-23) amide (selective agonist of the natriuretic peptide receptor C). Furthermore, CNP interacted with cholecystokinin (CCK) and
secretin
in the brain to modify pancreatic secretion. Present findings show that centrally applied CNP enhanced pancreatic secretion through a vagal pathway and suggest that CNP response is mediated by the activation of natriuretic peptide guanylyl cyclase coupled receptors in the brain.
...
PMID:C-type natriuretic peptide applied to the brain enhances exocrine pancreatic secretion through a vagal pathway. 1626 10
