Membrane Stabilizing Effects of Calcium in Salt-induced Hypertensive Pregnancy | Abstract
Anatomy & Physiology: Current Research

Anatomy & Physiology: Current Research
Open Access

ISSN: 2161-0940


Membrane Stabilizing Effects of Calcium in Salt-induced Hypertensive Pregnancy

Aigbiremolen AA, Odigie OM, Iribhogbe IO and Aloamaka CP

Though Calcium is involved in the mechanisms of increase contractility, it has been shown that at high concentration, calcium ions may cause membrane stabilization in which case the smooth muscle responsiveness decreases. Theoretically, a decrease in membrane permeability to calcium ions caused by increased extracellular calcium concentration stabilizes membranes. Apparently, administration of high level of calcium ion may become useful either by way of preventing or diminishing pregnancy induced hypertension (preeclampsia). The goal of this study was to examine the effect of calcium ion on the sensitivity of blood vessels during pregnancy, especially in salt induced hypertensive pregnancy. The isolated aorta of Forty adult Sprague Dawley rats [four groups of ten rats each; with Group 1=non pregnant fed with normal rat chow, Group 2=normal rat chow + 5% CaCl2 prior to and during 6 weeks feeding on 1.6% NaCl, Group 3=normal rat chow + 8% NaCl for 6 weeks, and Group 4=pregnant rats (350-380) fed on normal rat chow] was cut into 2 mm ring segments and each segment was suspended between two L-shaped holders. The lower holder was fixed to the base of 20 ml organ baths containing physiological salt solution, while the upper holder was connected to isometric transducer coupled to Ugo Bassile recorder. The presence of functional endothelium was ascertained before the start of the experiment by the observation of at least, 42% relaxation to 10-7 M acetylcholine in blood vessels contracted with 10-7 M noradrenaline. Concentration response tests to phenylephrine, KCl, and CaCl2 were done and result compared. Results show that the maximum contraction to phenylephrine of rings from pregnant rats fed on calcium chloride diets were insignificantly different from those of rats fed only with sodium chloride diet. Their sensitivities were however significantly (p<0.05) different. This observation suggests that the effect of Ca2+ feeding may be limited to the sensitivity, rather than the maximum contraction. Prior calcium feeding along with simultaneous high salt (sodium chloride) intake appears to interfere with the enhancement of vascular contractility associated with high salt intake. Ca2+ would therefore be relevant in the prevention and treatment of salt-induced hypertension in pregnancy.