vasoactive-intestinal-peptide and Muscular-Atrophy

Of the two known vasoactive intestinal peptide receptors (VPAC1R and VPAC2R), the VPAC2R is expressed in skeletal muscle. To evaluate the function of the VPAC2R in the physiological control of skeletal muscle mass, we utilized the VPAC1R selective agonist [K15,R16,L27]VIP(1-7) GRF(8-27)-NH2 and the VPAC2R selective agonist Ro-25-1553 to treat mice and rats undergoing either nerve damage-, corticosteroid-, or disuse-induced skeletal muscle atrophy. These analyses demonstrated that activation of VPAC2R, but not VPAC1R, reduced the loss of skeletal muscle mass and force during conditions of skeletal muscle atrophy resulting from corticosteroid administration, denervation, casting-induced disuse, increased skeletal muscle mass, and force of nonatrophying muscles. These studies indicate that VPAC2R agonists may have utility for the treatment of skeletal muscle-wasting diseases.

Topics: Adaptation, Physiological; Animals; Mice; Muscle Contraction; Muscle, Skeletal; Muscular Atrophy; Organ Size; Peptides, Cyclic; Receptors, Vasoactive Intestinal Peptide; Receptors, Vasoactive Intestinal Peptide, Type II; Vasoactive Intestinal Peptide

In 10 patients with amyotrophic lateral sclerosis (ALS), the CSF content of the neuropeptides vasoactive intestinal polypeptide (VIP) and cholecystokinin (CCK) as well as neural cell adhesion molecule (NCAM) was investigated. Compared with normal controls, no deviations were found in CCK or NCAM, while the values of VIP were significantly lower in ALS patients. This finding may reflect a loss of motor neurons.

Topics: Adult; Aged; Amyotrophic Lateral Sclerosis; Antigens, Surface; Bulbar Palsy, Progressive; Cell Adhesion Molecules; Cholecystokinin; Female; Humans; Male; Middle Aged; Muscular Atrophy; Vasoactive Intestinal Peptide