Chronic hyperinsulinemia and blood pressure. Interaction with catecholamines?

Abstract

Although hyperinsulinemia and increased adrenergic activity have been postulated to be important factors in obesity-associated hypertension, a cause and effect relation between insulin, catecholamines, and hypertension has not been established. The aim of this study was to determine whether chronic hyperinsulinemia, comparable with that found in obese hypertensive patients, causes hypertension in normal dogs, increases plasma catecholamines, or potentiates the blood pressure effects of norepinephrine. In six normal dogs, insulin infusion (1.0 milliunits/ kg/min) for 7 days, with euglycemia maintained, increased fasting insulin fourfold to sixfold. However, mean arterial pressure did not increase, averaging 99 ±2 mm Hg during the control period and 91 ±3 mm Hg during the 7 days of insulin infusion. Insulin did not alter plasma norepinephrine or epinephrine, which averaged 171±27 and 71±14 pg/ml, respectively, during the control period and 188 ±29 and 45 ±12 pg/ml during the 7 days of insulin infusion. In six dogs, norepinephrine was infused (0.2 /tig/kg/min) for 7 days to raise plasma norepinephrine to 2,940±103 pg/ml. Insulin infusion (1.0 milliunits/kg/min) for 7 days during simultaneous infusion of norepinephrine did not further increase mean arterial pressure, which averaged 101 ±3 during norepinephrine and 98 ±2 mm Hg during insulin plus norepinephrine infusion. Thus, chronic hyperinsulinemia did not increase mean arterial pressure or plasma catecholamines and did not potentiate the blood pressure actions of norepinephrine. These observations provide no evidence that chronic hyperinsulinemia or interactions between insulin and plasma catecholamines cause hypertension in normal dogs. (Hypertension 1990;15:519-527) A association between obesity and hypertension has been noted by numerous investigators, and reductions in caloric intake and body weight often lower blood pressure in obese hypertensive patients.1 -3 Several lines of indirect evidence suggest that insulin could be an important link between changes in caloric intake, activity of the sympathetic nervous system, and hypertension associated with obesity. 4 -5 Increased caloric intake because of carbohydrate ingestion elevates insulin levels and appears to activate the sympathetic nervous system, whereas caloric restriction suppresses insulin and sympathetic activity as assessed by variFrom the

The effect of insulin on the vascular reactivity of isolated resistance arteries taken from healthy volunteers

“…Therefore, an insulin-induced structural change in resistance vessels may be responsible for increased peripheral resistance or lead to increased sensitivity to vasoconstrictor agonists. However, neither chronic hyperinsulinaemia associated with insulinoma in man [51] nor prolonged intravenous administration of insulin to dogs for up to 28 days [52] have been shown to elevate blood pressure.…”

Obesity-related hypertension: possible pathophysiological mechanisms

“…2. Insulin resistance was also suggested to participate in the pathogenetic mechanisms of hypertension (Rahmouni et al 2003), but there is considerable evidence against its major role in obesity (Hall et al 1990, Rocchini et al 2004.…”

Antihypertensive effect of insulin via nitric oxide production in the Zucker diabetic fatty rat, an animal model for non-insulin-dependent diabetes mellitus

“…Insulin has vasodilative and hypotensive effects (3)(4)(5)(6)(7)(8)(9). It has been reported that hypertension was improved by insulin treatment in patients with DM (10)(11)(12).…”

“…It has been reported that hypertension was improved by insulin treatment in patients with DM (10)(11)(12). The antihypertensive effect of insulin was explained either by the secondary action of improved glucose metabolism after insulin treatment or by the direct action on peripheral arterial vessels (4,(10)(11)(12)(13)(14)(15)(16). Peripheral arterial resistance is a critical factor for the regulation of diastolic blood pressure, which is increased by atherosclerosis or vasoconstriction (17)(18)(19)(20).…”