Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An isolated rat liver perfusion system was used to study the effects of insulin and glucagon on renin substrate production. Normal livers synthesized renin substrate at a rate of 28.3 +/- 3.8 (S.E.M.) ng angiotensin I equiv./g liver each h (n = 8). The addition of insulin (more than 0.1 i.u.) to the perfusion significantly enhanced the production of renin substrate which was about twofold higher than normal control values (P less than 0.001). However, glucagon (20 micrograms) did not affect the synthesis of renin substrate. These results indicated that insulin promoted the synthesis of renin substrate by the isolated rat liver.
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PMID:Effects of insulin and glucagon on production of renin substrate by the isolated rat liver. 699 3

1. In eight hypertensive diabetic subjects receiving hydrochlorothiazide, glucose homeostasis as measured by the changes in plasma glucose, insulin and glucagon after an oral glucose load was not significantly affected by 8 weeks of therapy with metoprolol. 2. The combination of metoprolol plus hydrochlorothiazide significantly lowered blood pressure in all subjects. 3. Plasma renin activity was suppressed by therapy with metoprolol.
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PMID:Metoprolol in diabetes mellitus: effect on glucose homeostasis. 700 35

To investigate the pathogenic role of the sympathetic nervous system and the renin-angiotensin system in essential hypertension, we evaluated plasma catecholamine and PRA levels after glucagon stimulation and during one hour in upright posture after i.v. injection of furosemide. In nine normal and high renin essential hypertensive (NHRH) subjects, i.v. injection of 1000 micrograms of glucagon caused rapid and significant increases in plasma epinephrine(E) concentration. Both the 5 min. level after glucagon injection (314 +/- 30 pg/ml, mean +/- S.E., p less than 0.05) and peak value (358 +/- 87 pg/ml, p less than 0.05) were significantly higher than the basal level(170 +/- 25 pg/ml). Plasma norepinephrine(NE) concentration of the peak value(1065 +/- 231 pg/ml) was significantly higher than the basal(357 +/- 50 pg/ml, p less than 0.02). PRA levels increased in 4 out of 9 patients. In seven patients with low renin essential hypertension(LRH), there was an impaired PRA response to glucagon, E also failed to increase at any time after glucagon injection, but peak value of NE(1212 +/- 274 pg/ml) was significantly higher than the basal level(391 +/- 77 pg/ml, p less than 0.01). NE level of NHRH during one hour in upright posture after i.v. injection of 40 mg of furosemide were higher than LRH. Particularly at 10 min. level, the NE level of NHRH(895 +/- 115 pg/ml) was significantly higher than LRH(523 +/- 91 pg/ml, p less than 0.05). These results suggest that the sympathetic-adrenomedullary function in LRH is diminished, and the renin secreting ability of JG cells is also diminished in LRH. The glucagon stimulation test is useful to assess renin secreting ability of JG cells.
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PMID:[Response of plasma catecholamine and PRA to i.v. injection of glucagon in upright posture after furosemide injection in essential hypertension (author's transl)]. 702 7

Isoproterenol infusion increases renin release at low but not at control blood pressure. To examine whether this effect is dependent on arteriolar dilation and is specific for agonists of beta-adrenoceptors, responses to intrarenal infusion of isoproterenol (0.2 micrograms.kg body wt-1.min-1), glucagon (0.1 micrograms.kg body wt-1.min-1), and dopamine (1 micrograms.kg body wt-1.min-1) were compared at control and low or high ureteral pressure, which also dilates the renal arterioles. During renal arterial constriction, renin release was equal at two perfusion pressures below the range of autoregulation and was 76 +/- 24 micrograms/min higher during isoproterenol than during propranolol administration. Intravenous infusion of isoproterenol gave qualitatively similar results. Intrarenal infusion of glucagon and dopamine increased renin release by 13 +/- 3 and 22 +/- 12 micrograms/min, respectively; enhancement of renin release was also present after propranolol administration. During ureteral occlusion, intrarenal infusion of isoproterenol, dopamine, and glucagon increased renin release from 30-40 micrograms/min by 78 +/- 11, 13 +/- 3, and 31 +/- 10 micrograms/min, respectively. At control blood and ureteral pressure, the effects on renin release of infusing isoproterenol, dopamine, or glucagon were small or absent. Thus, isoproterenol, dopamine, amd glucagon enhance renin release when the arterioles are dilated by renal arterial constriction or ureteral occlusion.
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PMID:Conditions for enhancement of renin release by isoproterenol, dopamine, and glucagon. 703 49

Cardiovascular drugs have varying effects on hemodynamic, metabolic, and hormonal responses to exercise. To evaluate the effects of the novel angiotensin-converting enzyme (ACE) inhibitor, perindopril on these exercise-related responses, we studied 9 healthy volunteers in a double-blind, randomized, placebo-controlled trial. After a week of perindopril 4 mg orally daily or placebo therapy, volunteers performed a treadmill effort test; the sequence was repeated after a 1-week washout period. Perindopril caused a significant reduction in mean resting systolic and diastolic blood pressure (SBP, DBP) without increasing resting heart rate (HR); 15-min post-exercise SBP was also significantly reduced. There were no significant differences between the perindopril and placebo effort tests with respect to metabolic indexes studied (serum K+, plasma glucose, plasma free fatty acids) or plasma hormonal concentrations measured (ACTH and cortisol, norepinephrine (NE) and epinephrine (EPI), glucagon and insulin, growth hormone and prolactin, renin activity). In the perindopril arm of the study, however, there were modest but significant increases in mean serum K+ before exercise to immediately after exercise (0.4 +/- 0.1 mM, p < 0.01) and mean plasma glucose from before exercise to 5 min (0.6 +/- 0.2 mM, p < 0.01) and 15 min (0.5 +/- 0.2 mM, p < 0.05) after exercise. These data show that perindopril does not impair the hormonal changes associated with exercise in healthy subjects but induces a more consistent increase in blood K+ and glucose concentrations.
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PMID:Perindopril and physiologic responses to exercise. 752 76

The pressor, renal and endocrine effect of the physiological precursor of endothelial derived nitric oxide, L-arginine was compared, with a substrate inactive on nitric oxide, hypertonic D-glucose, in hypertensive patients. Ten mild-moderate essential hypertensives were assigned to either L-arginine (n = 5) or D-glucose (n = 5). Substances were infused over 25 min at equiosmolal rates preceded and followed by saline infusion for 25 min. Blood pressure and heart rate were monitored at 3-min intervals, while hormonal and humoral variables, inulin and paraaminohippurate clearance and electrolyte excretion were measured at the end of each period under conditions of maximal diuresis. L-arginine and D-glucose increased serum osmolality comparably and caused similar haemodilution to that with control saline. During L-arginine infusion, systolic and diastolic blood pressure decreased by 16.6% and 11%, respectively, and recovered in the postinfusion period. Heart rate, plasma renin activity, and plasma noradrenaline did not change significantly. The percent blood pressure decrement induced by L-arginine was significantly greater than that by D-glucose. Glomerular filtration rate was stable and renal plasma flow was increased by both substances. However, natriuresis, kaliuresis and chloruresis were markedly stimulated only by L-arginine, which also promoted the development of systemic acidosis, possibly as a consequence of hydrochloridric acid generated during its metabolism. Circulating insulin, atrial natriuretic peptide, growth hormone and glucagon levels were increased and plasma aldosterone was unchanged during infusion of L-arginine. Insulin was stimulated and the other hormones inhibited during infusion of D-glucose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pressor, renal and endocrine effects of L-arginine in essential hypertensives. 758 41

In this study we compared the pressor, renal and endocrine effects of the physiological precursor of endothelial derived nitric oxide, L-arginine, with D-glucose, a substrate inactive on nitric oxide. Ten subjects with mild to moderate primary hypertension underwent infusion with either L-arginine (5 patients) or D-glucose (5 patients). The substances were infused over 25 min at equiosmolar rates, preceded and followed by a 25-min saline infusion. Blood pressure (BP) and heart rate were monitored at 3-min intervals; hormonal and humoral variables, inulin and para-aminohippurate clearance, and electrolyte excretion were measured at the end of each period at maximum diuresis. L-arginine and D-glucose brought about comparable increases in serum osmolality and similar hemodilution as compared with control saline. During L-arginine infusion, systolic and diastolic BP dropped by 16.6% and 11% respectively and recovered during the post-infusion period. Heart rate, plasma renin activity, and plasma norepinephrine did not change significantly. The percent BP decrease induced by L-arginine was significantly greater than that caused by D-glucose. Glomerular filtration rate remained stable, and renal plasma flow increased with both substances. However, only L-arginine stimulated markedly natriuresis, kaliuresis, and chloruresis. It also seemed to induce systemic acidosis, possibly as a consequence of hydrochloric acid generated during its metabolism. Circulating insulin, atrial natriuretic peptide, growth hormone, and glucagon levels increased, and plasma aldosterone remained unchanged during L-arginine infusion. During D-glucose infusion, insulin was stimulated and the other hormones were inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pressor, renal and endocrine effects of systemic infusion of L-arginine in hypertensive patients]. 761 49

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in hemodialyzed patients. Two groups of hemodialyzed patients, each of which comprised 17 subjects, were examined. The first group was treated by EPO (EPO group) while the second one did not receive this hormone (No-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9, and 12 month points of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex- and age-matched healthy subjects. After EPO therapy, an increase of the hematocrit value from 21.8 +/- 0.9 to 32.6 +/- 0.9% was observed, which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the No-EPO group, a significant although less marked rise of the hematocrit value (21.4 +/- 0.4 to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change plasma levels of electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose, and alkaline phosphatase as well as plasma concentrations of calcium-related hormones (PTH, calcitonin, 1,25[OH]2D3), vasopressin, and triiodothyronine. EPO treatment induced a significant decrease in somatotropin, prolactin, follitropin, lutropin, ACTH, cortisol, plasma renin activity, aldosterone, noradrenaline, adrenaline, dopamine, glucagon, pancreatic polypeptide, and gastrin plasma levels and an increase in plasma insulin, estradiol, testosterone, atrial natriuretic peptide, thyrotropin, and thyroxine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Function of endocrine organs in hemodialyzed patients of long-term erythropoietin therapy. 762 22

The aims were to investigate 1) the effects of endothelin-1 (ET-1) during exercise and 2) the influence of exercise on arterial ET-1 levels. Six healthy subjects performed two exercises of 2 h duration at 50% of peak oxygen uptake preceded by intravenous infusion of physiological saline or ET-1 (4 pmol.kg-1.min-1). Blood specimens were taken from arterial and hepatic vein catheters. Arterial ET-1 rose 15-fold during the infusion. Splanchnic blood flow fell after ET-1 and remained lower than in control subjects during exercise (P < 0.001). Splanchnic glucose production was approximately 25% lower compared with control values during the whole exercise period (P < 0.01). Neither heart rate, arterial glucagon, insulin, catecholamines, renin, glucose, lactate, nor glycerol levels differed from control exercise values. The calculated gluconeogenesis from glycerol and lactate did not differ from the control values. ET-1 levels rose approximately twofold in the control exercise (P < 0.01) and in another group of seven subjects performing 1 h of exercise at 70% of peak oxygen uptake (P < 0.001). In conclusion, ET-1 levels increased during exercise without ET-1 administration. In addition, circulating ET-1 has a (direct or indirect) regulatory action on splanchnic blood flow and glucose metabolism during exercise (and possibly under pathophysiological conditions) in humans.
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PMID:Metabolic and vascular effects of circulating endothelin-1 during moderately heavy prolonged exercise. 766 32

The role of the hypothalamic suprachiasmatic nucleus (SCN) was examined in rats and obtained following results: (a) The time-dependent (light > dark) hyperglycemic response to intracranial injection of 2-deoxy-D-glucose (2DG) disappeared in rats with bilateral lesions of the SCN, in rats on weeks 4-6 after surgical blinding, and in congenitally blind (hereditary microphthalmic) rats; (b) The hyperglycemia induced by electrical stimulation of the SCN was not observed in weeks 4-8 after surgical blinding; (c) Change in the blood glucose concentration after insulin injection into the SCN was eliminated by SCN lesions; (d) Alterations in activity of autonomic efferents to peripheral organs on light exposure disappeared after SCN lesions; (e) SCN lesions decreased the blood glucagon level and increased the blood insulin level; (f) SCN lesions decreased protein intake, and glucagon increased it; (g) Increases in the plasma renin activity and vasopressin concentration after water-deprivation were suppressed in hereditary microphthalmic rats with abnormal SCN. These findings suggest that the SCN is involved in the mechanism of blood glucose and body fluid intake as well as that of circadian rhythm.
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PMID:Circadian rhythms and energy metabolism with special reference to the suprachiasmatic nucleus. 770 72


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