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Calcium Deficiency as the Prime Cause of Hypertension in Pregnancy: A Hypothesis
Author(s) -
Patterson William B.
Publication year - 1984
Publication title -
asia‐oceania journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 0389-2328
DOI - 10.1111/j.1447-0756.1984.tb00716.x
Subject(s) - endocrinology , medicine , calcium , aldosterone , adrenal cortex , angiotensin ii , vascular smooth muscle , renin–angiotensin system , blood pressure , smooth muscle
High calcium intake usually prevents pregnancy hypertension. Malnutrition and physiological stress block adrenal steroidogenesis leading to continuous ACTH secretion. Emotional stress may do the same. Cortical exhaustion causes cyclic AMP (cAMP) to increase several 1000‐fold. Normally cAMP is inactivated by phosphodiesterase which requires calcium‐activated calmodulin to function. With calcium deficiency cAMP will not be degraded and may reach distant organs. In the adrenal it produces excess cholesterol and aldosterone resulting in hypercholesteremia, endarteritis and salt retention. In the juxtaglomerular cells cAMP produces excess renin‐angiotensin causing spastic vasculitis and hypertension. Placental vascular occlusion and villus degeneration result in progesterone deficiency. After midterm Cortisol is substituted for progesterone producing further exhaustion and, finally, necrosis of the cortex. Then cAMP, aldosterone and angiotensin recede to nonpregnant levels. Sodium retention and calcium deficiency result in hypocalcemia in extracellular fluids which increases the action potential of nerve and muscle cells. This leads to an influx of calcium which in vascular muscle causes spasms, arteriosclerosis and hypertension while in skeletal muscle it produces twitching and convulsions.