Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandins (PG) A1, B1, E2, F2 alpha and plasma renin activity (PRA) were measured by radioimmunoassay in 8 patients with unilateral artery stenosis, 7 hypertensive patients with unilateral renal atrophy without stenosis ans 20 controls. The measurement of the PG and PRA in the hypertensive group was performed in the infra-renal inferior vena cava and in the two renal veins. PRA and PGA1 were significantly raised in the renovascular hypertensive patients but no significant change was observed in the group with unilateral renal atrophy. On the other hand, the PGE2 and PGF2 alpha were raised in both groups, especially in the renal veins on the stenosed or atrophic side. There was a positive significant correlation between PRA and PGA1 and PGB, but none with PGE2 or PGF2 alpha. This study suggests that the increase in PGA1 and PGE2 represents a secondary hypertensive mechanism which is diuretic and natiuretic. The increase of PGF2 alpha represents a direct mechanism of hypertension. Simultaneous measurement of the vasopressor (PRA and PGF2 alpha) and vasodepressor (PGA and PGE) systems may give a better diagnostic and prognostic approach to renovascular hypertension.
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PMID:[Prostaglandins in renovascular arterial hypertension]. 11 9

We examined the hypothesis that the vascular abnormalities of Bartter's syndrome are due to excess production of prostaglandin. Balance studies and vascular reactivity studies were performed before and after indomethacin (200 mg/day) in a patient with well-documented Bartter's syndrome. During indomethacin, potassium balance became positive, serum potassium rose from 2.1--3 mEq/1 in the absence of potassium supplementation, plasma renin activity decreased from 55--3.2 ng/day and peripheral plasma PGA-like activity fell from 1460 +/- 220 to 456 +/- 71 pg/ml. Before indomethacin, forearm vasoconstrictor responses to brachial arterial infusions of angiotensin II, norepinephrine and to neurogenic reflex stimulation elicited by lower body suction were greatly depressed compared to those of normal subjects. During indomethacin these responses were restored to normal. The dose of intravenous angiotensin II required to increase diastolic blood pressure 20 mm Hg decreased from 160--30 ng/kg/min. These data support the hypothesis that the vascular insensitivity to exogenous angiotensin II, norepinephrine and to neurogenic reflex stimulation observed in this patient with Bartter's syndrome is due to excess prostaglandin. Moreover, stimulation of the renin-angiotensin-aldosterone system in this syndrome appears to be a compensatory adaptation to excess prostaglandin production.
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PMID:Effects of indomethacin on the vascular abnormalities of Bartter's syndrome. 67 46

The role of PGA on the release of renin in the anesthetized dog has been studied. The infusion of prostaglandin for 60 minutes at a dose unable to cause pressor modifications (2 microgram/kg/min) was shown to increase the plasma renin activity (PRA); this effect was inhibited by propranolol and strengthened by aminophylline.
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PMID:Effect of prostaglandin A on renin secretion in the dog. 74 59

In addition to its well known prohypertensive role in various states of experimental and human hypertension, the kidney has also been shown to exert an antihypertensive "endocrine" function. According to this hypothesis, certain forms of experimental and human hypertension might not solely be the result of an excess in the activity of such renal pressor systems as the renin-angiotensin system and the sympathetic nervous system, but might also result from an absolute or relative deficiency of intra-renal vasodilator antihypertensive factors which might allow pressor systems to act unopposed to produce peripheral arteriolar vasoconstriction and sustained hypertension. At least four factors have been characterized in the kidney of various animal species and man which might be responsible for such an antihypertensive function. These are (1) the renomedullary prostaglandins (PGs), (2) the renomedullary antihypertensive neutral lipid, (3) antirenin phospholipid and (4) the renal kinins. This review is restricted to an examination of the possibility that the vasodepressor renomedullary prostaglandins (PGA and/or PGE) may, at least in part, mediate the so-called antihypertensive function of the kidney and participate in the regulation of renal blood flow and natriuresis by physiologic antagonism of various renal vasoconstrictor stimuli such as the renal renin-angiotensin and the sympathetic nervous systems.
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PMID:Renal prostaglandins and the regulation of blood pressure and sodium and water homeostasis. 79 89

The effect of angiotensin II on peripheral levels of immunoreactive prostaglandin A2 (IR-PGA) was determined in 17 normal male volunteers. IR-PGA rose from 338 +/-65 (SE) pg/ml to 635+/-142 in response to pressor infusions of angiotensin II (p less than 0.05 on paired analysis). This increase was not observed when indomethacin, 75 mg p.o., was given to 8 patients two hours prior to a repeat infusion. Five patients of the original group were placed on a low sodium diet (10-20 mEg). The response to angiotensin was now exaggerated (278+/-52 pg/ml to 916+/-284). These five patients were kept on a low sodium intake and given indomethacin 50 mg p.o. g 6 hourly for 4 days. There was no significant rise with angiotensin infusion (106+/-31 pg/ml to 120+/-70). Pressor infusions of angiotensin II raise peripheral levels of IR-PGA, and this response is exaggerated by a low sodium diet and blocked by either acute or chronic indomethacin administration. This data supports the concept that vasodilatory prostaglandins may be released by endogenous angiotensin and thus provide a dynamic antagonism to the renin angiotensin system in man.
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PMID:The effect of angiotensin II and indomethacin on immunoreactive prostaglandin "A" levels in man. 94 20

Prostaglandins PGE-1 or PGA-1 (0.5 to 1 mug per min) were infused into the stenosed renal artery of anesthetized hypertensive dogs. Increased urine volume, sodium and potassium excretion, and p-aminohippurate clearance were found during the prostaglandin infusion period in the infused kidney as compared to the control periods before infusion. Creatinine clearance was increased during infusion of PGE-1. The noninfused, nonischemic kidney showed no effect at the time of infusion with PGE-1 but in the case of PGA-1, the p-aminohippurate and creatinine clearances and urine diuresis were decreased. As a result, the mean aortic blood pressure decreased. Both prostaglandins increased the renal vein renin in the infused kidney. PGA-1 did affect renin release of the noninfused kidney, but PGE-1, which is rapidly inactivated by the lung, did not have this effect. Renin release seems to be influenced by electrolyte diuresis operating through the macula densa mechanism. However, the lowering of blood pressure seen in this study cannot exclude the involvement of the stretch receptors (the juxtaglomerular cells) for renin release. The increased renin release after prostaglandin administration seems to be a protective renal mechanism against the drug-induced hypotension. It seems to be induced by the direct sodium and water diuretic effects of prostaglandins.
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PMID:Direct effect of prostaglandins in renal function and renin release in the presence of renal ischemia in the dog. 111 61

Cortisol, insulin, somatotropin, thyreotropin, thyroxine, triiodothyronine, testosterone, aldosterone, c-AMP, c-GMP, prostaglandins (PGF1-x, PGF2-x, PGA + E), and renin concentrations in serum or plasma of the venous blood of the third international crew of the scientific orbital complex of "Soyuz 29 - Salyut 6 - Soyuz 31" were determined following the 7-day space flight. The increased activity of the renin-angiotensin-aldosterone system before the flight as well as variations in the pressor/depressor prostaglandin ratios indicate an increased strain during the pre-flight period. During the first stage of the post-flight period some parameters were changed due to the landing process and the returning to earth gravity. The associated physical load and the onset of reactions for enhancement of the orthostatic tolerance resulted in an increase of cyclic nucleotid and thyroxine concentrations. The relatively higher levels of the pressor PGs of group F in comparison with the prostaglandins A + E could be evaluated as a compensatory reaction for enhancement of the orthostatic tolerance. The cortisol and STH concentrations increased with growing motor activity. The variations seen after the 7-day space flight were essentially within the reference areas. It may be assumed that the readaptation was not yet totally accomplished by the 8th day after landing.
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PMID:[Results of endocrinolgic studies of the 3rd international crew of the scientific orbital station complex; Soyuz 29 - Salyut 6 - Soyuz 31 (joint space flight enterprise of the USSR - GDR). 2. Hormones and biologically active substances in blood]. 675

Urinary immunoreactive PGA and PGE, plasma and urinary aldosterone, and plasma renin activity (PRA) were determined in eleven control subjects and four patients with diabetic hyporeninaemic hypoaldosteronism (HH) before and during 4 days of sodium chloride restriction and frusemide administration. Aldosterone and PRA increased steadily in control subjects, but not in patients with HH. Increases in urinary PGA and PGE were observed during volume depletion. The basal levels and increases observed were comparable in both groups. The apparently normal stimulation of PGA and PGE in subjects with diabetic HH suggests that this syndrome is not associated with abnormal prostaglandin metabolism, despite the fact that drug-induced abnormalities of the latter may precipitate or aggravate the clinical syndrome in susceptible individuals. The increase in PGA and PGE following frusemide treatment and salt depletion supports the possibility of a relationship between renal prostaglandin metabolism, frusemide-induced natriuresis and/or renin secretion. While the nature of this relationship remains obscure, the increases in PGA and PGE in the absence of increases in renin-angiotensin levels in subjects with HH suggests that these changes are not due to activation of the renin-angiotensin system.
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PMID:Urinary prostaglandins following frusemide treatment and salt depletion in normal subjects and subjects with diabetic hyporeninaemic hypoaldosteronism. 701 40

Autoimmune polyglandular syndrome (APs) type 2 is characterized by the presence of Addison's disease, in association with autoimmune thyroid disease and/or type 1 diabetes mellitus and is rare in children. A 12.5 yr old prepubertal boy presented with symptoms related to Addison's disease and a large goiter. He was euthyroid with positive thyroid antibodies, low cortisol, aldosterone and very high adrenocorticotropin (ActH) and renin levels. Growth hormone (GH) secretion and an MrI scan of the pituitary were normal. He was started on hydrocortisone, fludrocortisone and subsequently on L thyroxine. Eighteen months later, decreased growth rate was noted and GH deficiency was detected, apparently secondary to autoimmune hypophysitis. Interestingly, he did not develop any other pituitary hormone deficiencies. He was started on GH therapy and had a good treatment response in the next 3 years. the combination of adrenal and thyroid insufficiencies with autoimmune hypophysitis is a very rare manifestation of APs-type 2. GH deficiency as the only symptom of lymphocytic hypophysitis is extremely rare. In children with autoimmune polyendocrine disorders, careful monitoring of growth is needed. In the case of low growth rate, GH should be evaluated by dynamic tests and, if GH deficiency is detected, treatment with hGH must be initiated.
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PMID:Growth hormone deficiency in a patient with autoimmune polyendocrinopathy type 2. 1772 10

Autoimmune polyglandular syndrome type 2 (APS 2) is defined by the presence of Addison's disease (AD) associated with autoimmune thyroid disease and/or Type 1 diabetes mellitus (T1DM). It is a rare disease, affecting about 1.4-2 cases/100,000 inhabitants. Its less frequent clinical presentation is the combination of AD, Graves' disease, and T1DM. We present the case of a 42-year-old woman with a history of total thyroidectomy due to Graves' disease, type 2 diabetes mellitus, and hypertension, who sought the ED due to asthenia, dizziness, nausea, and vomiting. She reported having stopped antihypertensive therapy due to hypotension and presented a glycemic record with frequent hypoglycemia. On physical examination, she had cutaneous hyperpigmentation. She had no leukocytosis, anemia, hypoglycemia, hyponatremia or hyperkalemia, and a negative PCR. Serum cortisol <0.5 ug/dl (4,3-22,4), urine free cortisol 9 ug/24h (28-214), ACTH 1384 pg/mL (4,7-48,8), aldosterone and renin in erect position of 0 pg/ml (41-323) and 430.7 uUI/ml (4.4-46.1) respectively. Quantiferon TB was negative; computerized axial tomography of the adrenals showed no infiltrations, hemorrhage, or masses. The 21-hydroxylase antibody assay was positive. B12 vitamin was normal, anti-GAD antibodies were positive, anti-insulin, anti-IA2, and anti-transglutaminase antibodies were all negative. The patient started insulin therapy and treatment for AD with prednisolone and fludrocortisone with good clinical response. This case aims to alert to the need for high clinical suspicion in the diagnosis of AD. Since this is a rare autoimmune disease, it is important to screen for other autoimmune diseases in order to exclude APS.
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PMID:Autoimmune Polyglandular Syndrome type 2. 3199 21


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