Abstract

The major objectives of this research project are to determine the mechanisms responsible for volume regulation in dog regulation in dog erythrocytes. When dog erythrocytes are exposed to anastomotic media, the is an activation of either the Na/H antiporter or K-C1 cotransport systems to return the cell back to its normal volume. Studies in our laboratory have been designed to quantitate these pathways and determine the stoichimetry, inhibitors and activators of these transport systems. Recent studies have been design to determine the heterogeneity of cells have been assayed for their ion and water content as well as their specific density. Future studies will be designed to determine the transport properties of these cell fractions in order to explain the physiological mechanism responsible for these observations. It is anticipated that the results of these studies will allow us to determine the mechanisms responsible for cell volume regulation in vivo.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Minority Biomedical Research Support - MBRS (S06)
Project #
5S06GM008091-26
Application #
6239994
Study Section
Project Start
1997-06-01
Project End
1998-07-31
Budget Start
1996-10-01
Budget End
1997-09-30
Support Year
26
Fiscal Year
1997
Total Cost
Indirect Cost

  Institution

Name
Tuskegee University
Department
Type
DUNS #
128214178
City
Tuskegee
State
AL
Country
United States
Zip Code
36088

  Publications

Mathews, Ensa; Braden, Tim D; Williams, Carol S et al. (2009) Mal-development of the penis and loss of fertility in male rats treated neonatally with female contraceptive 17alpha-ethinyl estradiol: a dose-response study and a comparative study with a known estrogenic teratogen diethylstilbestrol. Toxicol Sci 112:331-43
Goyal, H O; Braden, T D; Williams, C S et al. (2009) Estrogen-induced developmental disorders of the rat penis involve both estrogen receptor (ESR)- and androgen receptor (AR)-mediated pathways. Biol Reprod 81:507-16
Cooper, Marvis S; Reeve Jr, Joseph R; Abdalla, Mohamed O et al. (2008) Cholecystokinin-33 is more effective than cholecystokinin-8 in inhibiting food intake and in stimulating the myenteric plexus and dorsal vagal complex. Brain Res 1205:27-35
Raboin, Shannon J; Reeve Jr, Joseph R; Cooper, Marvis S et al. (2008) Activation of submucosal but not myenteric plexus of the gastrointestinal tract accompanies reduction of food intake by camostat. Regul Pept 150:73-80
Cooper, Marvis S; Reeve Jr, Joseph R; Raboin, Shannon J et al. (2008) Cholecystokinin-58 and cholecystokinin-8 produce similar but not identical activations of myenteric plexus and dorsal vagal complex. Regul Pept 148:88-94
Goyal, H O; Braden, T D; Williams, C S et al. (2007) Role of estrogen in induction of penile dysmorphogenesis: a review. Reproduction 134:199-208
Goyal, H O; Braden, T D; Cooke, P S et al. (2007) Estrogen receptor alpha mediates estrogen-inducible abnormalities in the developing penis. Reproduction 133:1057-67
Sullivan, Cherese N; Raboin, Shannon J; Gulley, Stephen et al. (2007) Endogenous cholecystokinin reduces food intake and increases Fos-like immunoreactivity in the dorsal vagal complex but not in the myenteric plexus by CCK1 receptor in the adult rat. Am J Physiol Regul Integr Comp Physiol 292:R1071-80
Raboin, Shannon J; Gulley, Stephen; Henley, Sheryce C et al. (2006) Atropine methyl nitrate increases myenteric but not dorsal vagal complex Fos-like immunoreactivity in the rat. Physiol Behav 88:448-52
Raboin, Shannon J; Gulley, Stephen; Henley, Sheryce C et al. (2006) Effect of sympathectomy and demedullation on increased myenteric and dorsal vagal complex Fos-like immunoreactivity by cholecystokinin-8. Regul Pept 134:141-8

Showing the most recent 10 out of 29 publications