Calcium, absorption hypertension

Kim et ah (1999) and Jung et ah (2005b) reported that fish peptides can accelerate calcium absorption. Under many conditions, dietary calcium becomes unavailable for absorption due to the formation of insoluble compounds inside the dietary tract, and inadequate dietary calcium is associated with a number of common and chronic diseases including osteoporosis, osteoarthritis, cardiovascular disease (hypertension and stroke), diabetes, obesity, and cancer (Anderson and Gamer,... 

Yuan, Y.V. and Kitts, D.D. 1991. Confirmation of calcium absorption and femoral utilization in spontaneously hypertensive rats fed casein phosphopeptide supplemented diets. Nutr. Res. 11, 1257-1272. 

It has long been known that vitamin D improves calcium absorption in the intestines. A deficiency in vitamin D causes rickets—a disease characterized by deformed bones and stunted growth. Recent research suggests that a deficiency in vitamin D may increase the risk of cardiovascular disease, hypertension, and diabetes. 

NaHCOs and CaCOs can neutralize HCl rapidly, depending on particle size and crystal structure, and effectively. NaHCOs acts rapidly but absorption of unneutralized NaHCOs produces risks for alkalosis and sodium retention which may lead to edema, hypertension or heart failure. Also neutralized antacids may cause alkalosis by permitting the absorption of endogenous NaHCOs. Ca + may stimulate the secretion of gastrin and HCl and calcium-containing antacids have been associated with rebound acid hypersecretion. 

Besides local toxicity, discussed above, there are numerous other modes of potential adverse interactions involving excipients (19,20). Many of these pose little threat provided the amounts of excipients are constrained to certain levels. Excessive amounts, however, can cause problems, particularly for patients who are intolerant of even modest levels. Commonly used phosphate buffers may cause calcium loss with formation of insoluble calcium phosphates when such buffers are administered in over-ambitious amounts (21). Calcium phosphate precipitation has been noted particularly in nutritional parenteral admixtures for neonates because of the high nutrient requirements. Similarly, renal toxicity has been associated with depletion of zinc and other trace metals caused by large parenteral doses of ethylenediaminete-traacetic acid (EDTA) (22). Excessive absorption of glycine solutions, when used as irrigants during transurethral resections, can cause hyponatremia, hypertension, and confusion (23). The use of preservatives has been associated with cardiac effects in a few patients (24). Premature neonates were found to be at risk for receiving toxic amounts of benzoic acid or benzyl alcohol in bacteriostatic solutions used to flush intravenous catheters (25). 

Renal effects of hypercalcemia include reduced glomerular filtration rate (GFR), polyuria, nephrocalcinosis, and renal stone disease. Hypercalcemia causes renal vasoconstriction which may contribute to decreased GFR. The hypercalcemia-induced polyuria results from 1) an impairment of active transport of NaCl in the loop of Henle, distal tubule and collecting duct and 2) an inhibition of vasopressin-facilitated absorption of water in the distal nephron. As a direct result of the polyuria, many side effects including polydipsia, thirst, nocturia and dehydration are common. Precipitation of calcium salts within the kidney leads to chronic inflammatory reactions (nephrocalcinosis), fibrosis, renal impairment, nephrolithiasis and urolithiasis. Further renal damage may occur indirectly from hypertension. 

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