Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mesenteric hemodynamic response to circulatory shock is characteristic and profound; this vasoconstrictive response disproportionately affects both the mesenteric organs and the organism as a whole. Vasoconstriction of post-capillary mesenteric venules and veins, mediated largely by the alpha-adrenergic receptors of the sympathetic nervous system, can effect an "autotransfusion" of up to 30% of the total circulating blood volume, supporting cardiac filling pressures ("preload"), and thereby sustaining cardiac output at virtually no cost in nutrient flow to the mesenteric organs. Under conditions of decreased cardiac output caused by cardiogenic or hypovolemic shock, selective vasoconstriction of the afferent mesenteric arterioles serves to sustain total systemic vascular resistance ("afterload"), thereby maintaining systemic arterial pressure and sustaining the perfusion of non-mesenteric organs at the expense of mesenteric organ perfusion (Cannon's "flight or fight" response). This markedly disproportionate response of the mesenteric resistance vessels is largely independent of the sympathetic nervous system and variably related to vasopressin, but mediated primarily by the renin-angiotensin axis. The extreme of this response can lead to gastric stress erosions, nonocclusive mesenteric ischemia, ischemic colitis, ischemic hepatitis, ischemic cholecystitis, and/or ischemic pancreatitis. Septic shock can produce decreased or increased mesenteric perfusion, but is characterized by an increased oxygen consumption that exceeds the capacity of mesenteric oxygen delivery, resulting in net ischemia and consequent tissue injury. Mesenteric organ injury from ischemia/reperfusion due to any form of shock can lead to a triggering of systemic inflammatory response syndrome, and ultimately to multiple organ dysfunction syndrome. The mesenteric vasculature is therefore a major target and a primary determinant of the systemic response to circulatory shock.
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PMID:The mesenteric hemodynamic response to circulatory shock: an overview. 1133 91

Changes in serum protein levels are produced by oral contraceptives. They reflect hepatic synthesis of proteins. Changes range from a 40% decrease in orosomucoid to an 180% increase in ceruloplasmin. Alterations in the concentration of some globulin proteins lead to altered serum levels of some hormones and trace metals. Plasma levels of cortisol and thyroxine are most affected. An estrogen-induced increase in thyroxine-binding globulin causes a transient reduction in free thyroxine (T4). This results in a compensatory increase in thyroid-stimulating hormone. The net effect is an unchanged concentration of T4 and the patient may be reported as euthyr id. Increases in renin substrate with rise in renin activity, angiotensin 2, and aldosterone, may be related to the development of hypertension in some women. Oral contraceptives may cause significant increases in some lipids. Elevations in cholesterol and nonesterified fatty acids are less changed. The drug-induced changes can complicate a definite diagnosis of hyperlipidemia. The glucose tolerance curve in users of oral contraceptives may simulate the diabetic type. Hepatic function tests may suggest hepatic damage. There is a higher incidence of cholecystitis and gallstones in women using oral contraceptives. Blood coagulation tests may be modified. Drug interference from oral contraceptive use must be considered in interpreting laboratory reports.
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PMID:Drug interference with laboratory tests: oral contraceptives. 1226 Jan 55