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• W1982193434 abstract "P RIMARY insulin resistance is ari abnormality of cellular insulin action which characterizes several common metabolic disorders such as obesity, diabetes mellitus, and endogenous hypertriglyceridemia. The finding of insulin resistance (or its compensatory counterpart, hyperinsulinemia) in association with essential hypertension I has aroused interest because it raises the possibility that insulin action may be involved in the regulation of hemodynamics and vascular growth. In general, the association between hyperinsulinemia and essential hypertension has the following characteristics: (I) it emerges from population surveys rather consistently but with variable strength; (2) it is potently interfered by obesity and body fat distribution3,4; (3) it is under the control of ethnic factors5,6; and (4) it remains consistent in longitudinal observations (in all three follow-up studies so far published).7-9 Interestingly, in contrast to the association between hyperinsulinemia and hypertension, the association between insulin resistance and essential hypertension (which has only been examined in case-control studies) has so far been completely consistent. 10 More recent studies have brought out other factors in the relationship between insulin action and blood pressure which may have special relevance to kidney damage: namely, microalbuminuria and a high rate of sodiumflithium countertransport activity in circulating cells. In particular, evidence has been produced to show that insulin resistance and high rates of sodium/ lithium countertransport activity have a strong tendency to cluster together in nondiabetic patients with essential hypertension. II 'Furthermore, more severe insulin resistance is found in noninsulin-dependent diabetic patients who are either normotensive but microalbuminuric or hypertensive but normoalbuminuric. 12 Thus, to the extent that micro albuminuria and/ or high blood pressure mark the actual presence or the risk for renal damage in both nondiabetic and diabetic individuals, there appears to be a link between insulin resistance and kidney disease. All these associations fall short of proving a cause-effect relationship between insulin resistance/hyperinsulinemia and blood pressure. A number of candidate mechanisms have been suggested,13 each of which has been explored, or is currently under investigation, in a variety of different models. On theoretical grounds, there is no reason to suppose that one mechanism (eg, stimulation by insulin of sympathetic nervous activity) should predominate (over, eg, the antinatriuretic action of insulin) in the putative pathway connecting insulin resistance and high blood pressure. It is amply possible that different mechanisms may coexist in the same subject (eg, if obese), or prevail in different subgroups of hypertensive subjects (eg, borderline versus established hypertension) or in different stages of the hypertensive disease (eg, early versus late hypertension). In the uncharted territory of hypotheses, two facts stand out as relevant guidelines. Firstly, hyperinsulinemia precedes the appearance ofhypertension in confirmed prehypertensives,7 and insulin resistance is present in high-risk groups (eg, normotensive offspring of hypertensive parents) at a time when their blood pressure levels are completely normal. 14 Thus, to the best of available information, the pathway leading from hyperinsulinemia/insulin resistance to hypertension is more plausible than the reverse pathway. Secondly, if one accepts Guyton's model for the regulation of blood pressure,15 in which the various factors governing arterial pressure homeostasis are ranked along a time scale as well as according to potency, then the renal-blood volume pressure control is the one candidate mechanism which may stabilize blood pressure at a" @default.
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• W1982193434 date "1993-05-01" @default.
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• W1982193434 title "Insulin Resistance and Hypertension: Connections With Sodium Metabolism" @default.
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• W1982193434 doi "https://doi.org/10.1016/s0272-6386(12)70253-6" @default.
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