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Query: HUMANGGP:034761 (insulin)
 211,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of insulin-induced hypoglycemia on the blood levels of catecholamines and renin activity has been studied in five patients with moderate hypertension before and after treatment for 3 - 8 months with penbutolol (PEN) 20 - 30 mg twice daily. Penbutolol caused no change in fasting blood glucose level. Insulin o.1 IU per kg body weight i.v. reduced blood glucose concentration by approximately 50 per cent after 30 - 45 min, both before and during treatment with penbutolol. Hypoglycemia prior to medication was accompanied by a marked increase in the production of adrenaline and a minor increase of noradrenaline in all five patients. During treatment the response of adrenaline to hypoglycemia was reduced in four patients and the data was inconclusive in one. Basal renin activity was rather low in three patients, within the normal range in one and relatively high in one. Before penbutolol the hypoglycemia-induced increase in catecholamine production caused no change in plasma renin activity in the three patients with low basal levels, whereas a marked increase was observed in the other two. During medication plasma renin activity remained unchanged on induction of hypoglycemia regardless of the catecholamine response. Despite the marked increase in plasma adrenaline following insulin-induced hypoglycemia, no statistically significant increase in pulse rate was recorded.
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PMID:Long term treatment of moderate hypertension with penbutolol (Hoe 893d). II. Effect on the response of plasma catecholamines and plasma renin activity to insulin-induced hypoglycemia. 0 1

Essential hypertension (EH) can be subdivided according to the sympathetic and renin activity into two contrasting forms: (1) borderline beta-hyperadrenergic renin hyperresponsive and (2) stable beta-hypoadrenergic renin hyporesponsive EH. These two forms probably represent two expreme poles in the spectrum of EH in which sympathetic and renin hyper- or hyporeactivity cannot be accounted for by catecholamine determinations solely. beta-Adrenergic responsiveness monitored by plasma cyclic AMP determinations revealed plasma cyclic AMP, renin and circulatory hyperresponsiveness to isoproterenol in borderline hyperadrenergic EH while the opposite, cyclic AMP and renin hyporesponsiveness to insulin-induced hypoglycemia have been described in low renin stable EH. The kidney is in the center of the adrenergic abnormality in the two forms of EH with the borderline one excreting into the urine catecholamines not accounted for by their glomerular filtration. Catecholamines solely, however, do not account for the differences in both forms of EH which can probably be attributed to their different beta-adrenergic responsiveness.
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PMID:Catecholamines, cyclic AMP and renin in two contrasting forms of essential hypertension. 1 3

The beta1- and beta2-components in antidiuresis and sodium retention induced by beta-adrenergic agonists were analysed in ethanol-anesthetized, water-diuretic rats. Intravenous infusions of isoprenaline, salbutamol and carbuterol did not affect insulin clearance but increased plasma renin concentration to the same same extent. Propranolol completely blocked the decreases in urine volume (V) and urinary sodium excretion (UNaV) induced by isoprenaline; practolol (beta1-blocker) inhibited only the decrease in UNaV and butaxamine (beta2-blocker) inhibited only the decrease in V. The ratios of doses of beta-agonists which decreased UNaV and by 50% (ED50 UNaV decrease/ED50 V decrease) were 0.34, 0.68, 1.56 and 2.36 for isoprenaline, tretoquinol, salbutamol and carbuterol, respectively. This increasing order of the ratios coincided with the order reported for the preponderance of the beta2- over beta1-component of these agonists. These results indicate that the decrease in UNaV induced by beta-agonists is related to beta1 stimulation, while the decrease in V is related to beta2 stimulation.
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PMID:Antidiuresis induced by beta1- and beta2-adrenergic agonists in ethanol-anesthetized rats. 2 97

Changes in glucagon, growth hormone (GH), cortisol, renin and aldosterone accompanying the metabolic disturbances and dehydration of severe diabetic ketoacidosis were studied over a 24 h period in eight patients treated with a constant intravenous insulin infusion. Mean steady state plasma-free insulin levels achieved were 28.6--49 mu/1 in patients receiving 2 u/h but a satisfactory rate of fall of glucose was not always obtained until the infusion dose was increased to 4 u/h or more. The total insulin dose administered was positively correlated with the level of plasma glucagon and cortisol on admission. During insulin infusion, both glucagon and cortisol fell but the rate of fall was not related to dose or plasma level of free insulin achieved. In six of eight patients studied increments in plasma GH above admission levels were observed during insulin treatment. Admission values of both plasma renin activity and plasma aldosterone were raised. The renin levels were highest in newly diagnosed diabetics, and two patients with long-established diabetes showed only small increments despite profound dehydration. Plasma renin activity, but not plasma aldosterone correlated with the fluid and sodium retention over the initial 24 h treatment period, but not with potassium requirements. The urinary excretion rates of the small molecular weight proteins GH and insulin, were considerably elevated over the treatment and convalescent periods.
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PMID:Hormonal responses during treatment of acute diabetic ketoacidosis with constant insulin infusions. 10 71

A new oral contraceptive (Org 2969) formulated of .05 mg of ethinyl estradiol and .1 mg or .125 mg of a new progestagen, 17 alpha-ethinyl-18-methyl-11-methyl-ene-4-estren-17 beta-ol, was studied to determine its effects in human volunteers on plasma renin activity (PRA), growth hormone (GH), and immunoreactive insulin (IRI). 7 healthy subjects were studied during an ovulatory menstrual cycle and during the 1st and 3rd cycles of oral contraception. 1 of 7 subjects showed ovulation after the 1st cycle of contraceptives; the remainder were anovulatory, and all subjects were anovulatory by the 3rd cycle of contraception. PRA on the 22nd day of the control cycle was significantly (P .01) higher than the mean PRA on days 2-5 of control. Mean PRA at the beginning of the 1st treatment cycle was not significantly higher than control cycles. By day 22 of treatment, however, it was significantly (P .001) higher than day 22 of control cycle. A significant PRA Increase after the 1st treatment cycle (P .05) was noted along with a continued significance in the 3rd cycle (P .05). At the end of the treatment cycle, GH was significantly higher (P .05) than at the end of the control cycle. The rise of GH over the 1st treatment cycle compared with control cycle was insignificant, but after the 3rd treatment cycle, GH was significantly higher than the control cycle values (P .05). There were no differences in GH throughout the control cycle. IRI did not differ within the control cycle. By the 2nd-4th day of the 1st treatment cycle, mean IRI was significantly higher than comparable control cycle values (P .01). The rise in IRI during treatment was also significant (P .05). No correlations were found among the individual GH and IRI values, and no significances for same sampling periods were found. Levels of the 3 parameters were unaffected by dosage of the new progestin.
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PMID:Effect of oral contraceptive containing a new progestin (ORG 2969) on plasma renin activity, growth hormone and immunoreactive insulin. 16 58

Insulin-induced hypoglycemia previously has been shown to provoke a beta-adrenergic response that normally results in an increase in plasma renin activity (PRA). In our study, hypoglycemia induced definite increases in PRA in a group of five patients with normal renin essential hypertension but failed to do so in a group of six patients with low renin essential hypertension. In both groups, plasma cyclic adenosine 3',5'-monophosphate (cyclic AMP; cAMP) increased more than 2-fold during hypoglycemia, but the response in the low renin group was significantly less than that previously observed in normal subjects under the same conditions. Plasma cortisol increased to an equal extent in both groups of hypertensive patients during hypoglycemia. Infusion of the phosphodiesterase inhibitor, theophylline, resulted in definite increases of PRA in patients with normal renin hypertension but not in patients with low renin hypertension. Because changes in the level of plasma cAMP during hypoglycemia have been thought to reflect adrenal catecholamine release, our finding of a blunted increase in plasma cAMP during hypoglycemia in patients with low renin hypertension may suggest that there is a generalized alteration in adrenergic responsiveness in this condition.
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PMID:Contrasting effects of hypoglycemia on plasma renin activity and cyclic adenosine 3',5'-monophosphate (cyclic AMP) in low renin and normal renin essential hypertension. 17 76

Literature on the biochemical effects of oral contraceptives (OCs) is reviewed. The effects of OCs on concentrations of mineral elements ( calcium, phosphorus, magnesium, iron, copper, and zinc), vitamins (ascor bic acid, folic acid, and Vitamins-B6, B12, and E), hormones, (gonadotro pins, progesterone, estrogens, androgens, corticosteroids, aldosterone, renin-angiotensin, insulin, growth hormone, thyroid hormones, catecholamines, and prolactin), amino acids and proteins (free amino acids, tryptophan, metalloproteins, hormone-binding proteins, miscellaneous serum proteins, and blood coagulation factors), carbohydra tes (glucose tolerance tests, glucose metablism and other carbohydrates) , lipids (total serum lipids, triglycerides, phospholipids, fatty acids, and cholesterol), and enzymes (aminotransfereases, alkaline phosphatase, and glutamyltransferase) are reviewed. Changes induced by combined, sequential, and low-dose OCs in 116 biochemical parameters are summarized in a table.
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PMID:Biochemical effects of oral contraceptives. 18 Jul 84

Insulin-induced hypoglycemia caused an increase in plasma aldosterone as well as in renin activity and cortisol. After the suppression of the renin-angiotensin system by the prior administration of propranolol, insulin-induced hypoglycemia still caused a significant increase in plasma aldosterone similar to the increase in plasma cortisol, though plasma renin activity was suppressed. Conversely, after the suppression of endogenous ACTH by the prior admininstration of dexamethasone, insulin-induced hypoglycemia failed to induce a rise in plasma aldosterone and plasma cortisol, through plasma renin activity increased. The increase of plasma aldosterone in response to exogenous ACTH was not different with or without the prior administration of dexamethasone. We conclude that ACTH is largely responsible for the increased aldosterone secretion after insulin-induced hypoglycemia.
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PMID:Aldosterone response to hypoglycemia: evidence of ACTH mediation. 18 91

The effect of diuretics on serum lipids and lipoproteins was evaluated in 23 patients with essential hypertension treated with chlorthalidone for six weeks. Compared to placebo conditions, diuretic therapy significantly increased serum beta (+8%, p less than 0.05) or low-density-lipoprotein (LP) cholesterol (+17%, p less than 0.025). Since alpha-LP or high-density-LP cholesterol was unchanged or tended to decrease slightly, there was also an increase in the beta/alpha-LP (+26%, p less than 0.025) or low/high-density-LP cholesterol (21%, p less than 0.025) ratio. Serum cholesterol (+4%), triglycerides (+3%), phospholipids and the Apo-LP A-I, A-II and B were not changed significantly. Blood pressure and plasma potassium were decreased (p less than 0.01), blood volume and serum insulin were not changed significantly, and serum glucose was increased mildly. Plasma renin, aldosterone and norepinephrine levels rose significantly (p less than 0.05), while circulating epinephrine was unaltered. Alterations in LP were not related to variations in blood pressure, blood volume, plasma electrolytes or serum glucose or insulin; and they did not correlate with chlorthalidone-induced increases in plasma renin, aldosterone or norepinephrine. Treatment with certain diuretics may have an adverse influence on lipoprotein metabolism.
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PMID:[The effect of diuretic therapy on serum lipoproteins: an undesirable effect?]. 21 71

We have examined insulin-induced hypoglycemia to determine whether prazosin inhibits the response to sympathetic stimulation, either centrally or at beta adrenergic receptors. Nine patients with essential hypertension were studied during administration of prazosin, hydralazine or placebo. Plasma renin activity increased significantly with hydralazine and was unchanged during prazosin administration. In response to insulin, blood glucose decreased equally with both drugs and placebo, and small increases in dopamine beta-hydroxylase occurred. Plasma renin activity and heart rate increased during hypoglycemia; the increases were greater in patients taking prazosin or hydralazine. The unimpaired responses of plasma dopamine beta-hydroxylase, renin activity and heart rate to insulin-induced hypoglycemia provide evidence that prazosin does not block either the sympathetic discharge elicited by central stimulation (hypoglycemia) or the responses mediated through beta adrenergic receptors.
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PMID:Unimpaired beta adrenergic responses during prazosin administration. 22 24


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