Experimental studies with laboratory animals have shown that behaviorally-induced hypoventilatory breathing potentiates the hypertensinogenic effects of high sodium intake. Current studies in this project focus on the interactions of pCO-2, sodium intake and blood pressure in humans. One experimental study investigates the correlation that exists between resting pCO-2 and (a) higher ambulatory blood pressure in the natural environment, and (b) the magnitude of pressor response during laboratory role playing of social conflict. A study in progress also investigates blood pressure sensitivity to high sodium intake as a function of resting pCO-2.
Anderson, David E; Parsons, Beverly A; McNeely, Jessica C et al. (2007) Salt sensitivity of blood pressure is accompanied by slow respiratory rate: results of a clinical feeding study. J Am Soc Hypertens 1:256-263 |
Scuteri, Angelo; Stuehlinger, Markus C; Cooke, John P et al. (2003) Nitric oxide inhibition as a mechanism for blood pressure increase during salt loading in normotensive postmenopausal women. J Hypertens 21:1339-46 |
Anderson, D E; Scuteri, A; Metter, E J et al. (2001) Association of high resting end tidal CO2 with carotid artery thickness in women, but not men. J Hypertens 19:459-63 |
Anderson, D E; Scuteri, A; Agalakova, N et al. (2001) Racial differences in resting end-tidal CO2 and circulating sodium pump inhibitor. Am J Hypertens 14:761-7 |
Anderson, D E; Parsons, D J; Scuteri, A (1999) End tidal CO2 is an independent determinant of systolic blood pressure in women. J Hypertens 17:1073-80 |