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)

he intermediate and latter stages of canine endotoxin shock are characterized by a progressive decrease in cardiac output, increase in total peripheral resistance, and hypoglycemia. We have hypothesized that the renin-angiotensin system and glucagon may mediate the loss of cardiovascular and glucose homeostasis. E. Coli endotoxin shock (1 mg/kg; 055:B5) was induced in three groups of dogs and systemic hemodynamics, angiotensin I activity, and glucagon were monitored for 5 hr; endotoxin shock (n = 13); endotoxin shock + prior immunization with J5 mutant of E coli 0111 (n = 5); Endotoxin + captopril (20 micrograms/kg/hr; n = 9); and sham-operated time-matched controls (n = 8). Thirty minutes postshock, angiotensin I and glucagon began to increase. Angiotensin I activity reached a peak at 60 min postendotoxin (90 +/- 25 vs 5 +/- ng/ml/hr; p less than 0.001) and plateaued. Increased glucagon levels plateaued at 3.5 hr postshock (1500 +/- 200 vs 155 +/- 77 pg/ml; p less than 0.001). Cardiac output began to progressively decrease, total peripheral resistance began to increase, and persistent hypoglycemia developed at 3 hr postshock. Captopril inhibited the increase in total peripheral resistance and had no effect on the decrease in cardiac output or the hypoglycemia. The initial glucagon response was attenuated but there was no difference at 5 hr (950 +/- 150 vs 1200 +/- 200 pg/ml). Prior immunization significantly preserved cardiac output, total peripheral resistance, plasma glucose levels, glucagon levels, and angiotensin I activity. It is concluded that 1) the renin-angiotensin system is a physiologic and not a pathophysiologic compensatory mechanism during the course of endotoxin shock and that inhibition of this system is deleterious; 2) glucagon may serve as an important mediator of both the myocardial dysfunction and glucose dyshomeostasis of endotoxin shock; and 3) immunological inhibition of the initial phase of endotoxin shock significantly preserves cardiovascular and glucose homeostasis and adds support to the concept that the initial vascular phase of endotoxin shock plays a primary role in determining the severity of the endotoxin/septic shock syndrome.
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PMID:Role of angiotensin I and glucagon in canine endotoxin shock: effect of converting enzyme inhibitor and prior immunization. 632 34

Mediators and the effect of captopril on amino acid-induced hyperfiltration were studied. Acute intravenous L-arginine (arginine) infusion tests were performed twice, without captopril administration in 6 normal subjects (group I), before and after pretreatment with captopril in 10 normal subjects (group II) and 10 IgA nephropathy patients with slight renal dysfunction (group III). It was found that in all groups with and without captopril, arginine infusion led to a significant decrease in renal vascular resistance, and significant increases in renal plasma flow and plasma glucagon level. GFR was significantly increased in response to arginine only in normals without captopril pretreatment. Captopril pretreatment attenuated the rise in GFR following arginine infusion in normal subjects. Plasma renin activity and urinary cGMP were significantly increased in response to arginine only in normals without captopril pretreatment. No significant increase in urinary PGE2 was observed after arginine infusion in any groups. It was concluded that cGMP and glucagon are possible mediators for arginine-induced hyperfiltration and inhibition of renin-angiotensin system attenuates the arginine-induced rise in GFR.
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PMID:Amino acid-induced hyperfiltration--mediators and effect of captopril. 792 65