cyclic-gmp and Intestinal-Diseases

In several bacterial diseases, the clinical, laboratory, and histologic findings result from the elaboration by the organism of a toxic product that binds to and may enter the host cell to alter its metabolism. In some cases, the intracellular mediators of toxin action are the cyclic nucleotides, cyclic adenosine 5'-monophosphate (cAMP) and cyclic guanosine 5'-monophosphate (cGMP), the ubiquitous second messengers through which numerous hormones, neurotransmitters, and drugs exert their effects. Certain toxins act by enhancing the activity of cellular enzymes that synthesize cAMP or cGMP; and others, by themselves catalyzing cAMP synthesis after entering the cell. Studies of the mechanism of action of these toxins have helped in deciphering the enzymatic components within animal cells that are responsible for cyclic nucleotide synthesis, degradation, and function as well as in understanding the pathogenesis of the diseases in which they are involved.

Topics: Adenosine Diphosphate Ribose; Adenylyl Cyclases; Animals; Bacillus anthracis; Bacterial Toxins; Bordetella pertussis; Cell Membrane; Cholera Toxin; Cyclic GMP; Enterotoxins; Enzyme Activation; Escherichia coli; Escherichia coli Infections; Escherichia coli Proteins; Guanylate Cyclase; Humans; Intestinal Diseases; Intestinal Mucosa; Nucleotides, Cyclic; Organ Specificity; Virulence Factors, Bordetella

Intractable gastrointestinal (GI) diseases often develop during infancy. Our group previously reported that natriuretic peptide receptor B (NPR-B)-deficient Npr2

Topics: Animals; Cyclic GMP; Female; Gastrointestinal Tract; Intestinal Diseases; Intestines; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Microcirculation; Receptors, Atrial Natriuretic Factor; Signal Transduction

Administration of L-nil, a selective inhibitor of inducible nitric oxide synthase (iNOS), improves ileus in an animal model of resuscitation induced intestinal edema. The purpose of this study was to elucidate the iNOS/nitric oxide (NO) signal transduction pathway in intestinal edema.. Male Sprague Dawley rats were divided into two groups; CONTROL and RESUS+VH (edema, 80 cc/kg normal saline (resuscitation) with mesenteric venous hypertension). iNOS mRNA and protein, iNOS activity, NO tissue levels, soluble guanylyl cyclase (sGC) expression, and cyclic guanosine monophosphate (cGMP) levels were measured. As a functional endpoint, we evaluated intestinal contractile strength and frequency in L-nil treated animals.. Edema was associated with increased iNOS mRNA and protein expression without subsequent increases in iNOS activity or tissue NO levels. There was no significant change in sGC expression or increase in cGMP induced by edema. Administration of L-nil did not decrease edema development or preserve contractile strength, but increased contractile frequency.. Hydrostatic intestinal edema is not associated with increased iNOS activity or tissue NO levels. Administration of L-nil in edema increases intestinal contractile frequency. This may represent a potential mechanism for the amelioration of ileus seen with the administration of L-nil.

Topics: Animals; Cyclic GMP; Edema; Gastrointestinal Motility; Guanylate Cyclase; Hydrostatic Pressure; Immunohistochemistry; Intestinal Diseases; Lysine; Male; Nitric Oxide; Nitric Oxide Synthase Type II; Rats; Rats, Sprague-Dawley; RNA, Messenger; Signal Transduction

Topics: Calcium; Cell Membrane Permeability; Cyclic AMP; Cyclic GMP; Food Hypersensitivity; Humans; Intestinal Diseases; Intestinal Mucosa; Intestine, Small; Ion Channels

Topics: Acute Disease; Adolescent; Child; Child, Preschool; Cyclic AMP; Cyclic GMP; Humans; Infant; Intestinal Diseases