There is evidence that calcium (Ca) physiology is altered in essential hypertension. Intracellular Ca ions have direct effect on peripheral vascular tone, and hypertensive have increased intracellular free Ca that decreases to normal levels with anti- hypertensive treatment. Serum Ca levels have also been negatively associated with 24-hour urine sodium (Na) and positively associated with potassium (K) excretion. Blaustein (1977) suggested that intracellular Ca increase in hypertension is due to altered Na-Ca exchange across the cellular membrane of smooth muscles. altered Na transport in red blood cells (RBC) of hypertensives is seen by some researchers as a useful tool for detecting predisposition to, and differentiating essential from secondary hypertension. However, attempts to associate dietary Na and RBC Na transport have been disappointing. Similarly, potassium (KC1) supplementation has been associated with blood pressure (BP) lowering while KC1 deficiency is associated with RBC Na excrusion. However, there is no evidence that KC1 supplementation changes RBC Na transport, and, to date, KC1 deficiency experiments have not reliably increased BP. If abnormal cation transport is infact a marker and a precursor of hypertension it is important to identify potentially modifiable environmental or life style variables that might possible be useful for preventive purposes. Three experiments, using SHR and WKY rats, are proposed to investigate if (a) dietary Ca affects RBC Na transport, (b) Ca and Na interact to influence RBC Na transport, (c) Ca and K interact to influence RBC Na transport. In Exp. 1 the rats will be placed on diets of high, normal or low Ca. In Exp. II, they will be placed on combination diets of high and low Ca and Na. In Exp. III they will be placed on combination diets of high and low Ca and K. The rats will be maintained on the diets for 8 weeks following which blood will be collected via heart puncture for RBC Na flux analyses. Eight weekly tail cuff BP measures will be collected to be compared with the Na flux data.
| Barber, D L; Ganz, M B; Bongiorno, P B et al. (1992) Mutant constructs of the beta-adrenergic receptor that are uncoupled from adenylyl cyclase retain functional activation of Na-H exchange. Mol Pharmacol 41:1056-60 |
| Barber, D L; Cacace, A M; Raucci, D T et al. (1991) Fatty acids stereospecifically stimulate neurotensin release and increase [Ca2+]i in enteric endocrine cells. Am J Physiol 261:G497-503 |
| Ganz, M B; Pachter, J A; Barber, D L (1990) Multiple receptors coupled to adenylate cyclase regulate Na-H exchange independent of cAMP. J Biol Chem 265:8989-92 |
| Barber, D L; McGuire, M E; Ganz, M B (1989) Beta-adrenergic and somatostatin receptors regulate Na-H exchange independent of cAMP. J Biol Chem 264:21038-42 |
