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)

Liddle's syndrome was diagnosed in a 23-yr-old Chinese girl with hypertension and hypokalemia by the presence of suppressed renin and negligible plasma and urinary aldosterone secretion. Adrenal corticosteroids, including aldosterone, were suppressed by dexamethasone and stimulated by ACTH. While spironolactone was ineffective, triamterene (2,4,7-triamino-6-phenyl-pteridine) treatment corrected the hypertension and hypokalemia and restored PRA to normal provided that sodium intake was not excessive. During long term treatment with triamterene, blood pressure was extremely sensitive to salt intake, increasing promptly with high intake and decreasing with low salt intake. As a result of the chronic hypervolemia and sodium retention consequent upon the patient's persistent high salt intake and increased renal tubular sodium reabsorption, plasma renin and aldosterone remained low. Erythrocyte sodium concentration and membrane permeability were increased. Triamterene with salt restriction was able to lower the intracellular sodium concentration but did not correct the increased sodium permeability. This suggests that there is an abnormality of sodium transport in Liddle's syndrome which affects the erythrocytes as well as the renal tubular cells.
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PMID:The effect of triamterene and sodium intake on renin, aldosterone, and erythrocyte sodium transport in Liddle's syndrome. 626 54

A 24-yr-old woman with hypertension, hypokalemic alkalosis, low plasma renin and hypoaldosteronism was studied. Plasma aldosterone, renin and potassium returned to normal and blood pressure fell after sodium restriction or the administration of triamterene. Thiazide therapy also normalized her blood pressure while dexamethasone, spironolactone and furosemide did not improve her symptoms. Plasma aldosterone levels were low and responded poorly to a short term ACTH injection, but responded well to the maximal adrenal stimulation by ACTH-Z. Plasma levels of cortisol, corticosterone and deoxycorticosterone were within the normal range. Adrenal scintigram with 131I-adosterol and abdominal computed axial tomography did not reveal the presence of a sizeable adrenal tumor. In addition, the urinary kallikrein excretion was low after sodium restriction and showed no response to saline infusion. These findings suggest that the excessive secretion of unusual mineralocorticoids may not exist in this case. From these observations and the results of the therapeutic responses to the diuretic agents, we conclude that the primary cause of the disorder of this patient seems to be a renal defect in the distal tubule in handling sodium and potassium which is similar to that in Liddle's syndrome.
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PMID:Hypertension, hypokalemia and hypoaldosteronism with suppressed renin: a clinical study of a patient with Liddle's syndrome. 627 44

Rats given water to drink only during a brief daily period respond to water presentation with a rapid decline in plasma corticosterone concentration. To determine whether this response is consequent to a decrease in plasma ACTH concentration or whether it reflects a sudden reduction in adrenal responsiveness to ACTH, we allowed rats access to water for 2 h/day at lights on and measured plasma ACTH and adrenal and plasma corticosterone concentrations at 3- or 5-min intervals after the onset of drinking. Adrenal and plasma corticosterone concentrations decreased significantly within 2-3 min after water presentation in the absence of concomitant changes in plasma ACTH concentration. The effect was apparent by 5 days after initiating the restricted drinking schedule and became stronger with time up to 21 days. Further characterization of the response showed that the in vitro corticosterone secretion of adrenals removed at intervals after water presentation followed the same pattern as the in vivo concentration. When empty water bottles were presented, plasma ACTH and corticosterone concentrations increased. Neither adrenal medullary function nor plasma renin concentration was found to be associated with the decline in adrenal responsiveness to ACTH after drinking. Hemisection of the spinal cord of unilaterally adrenalectomized rats attenuated the corticosterone response regardless of whether the hemisection was contralateral or ipsilateral to the remaining adrenal. These data suggest that the decreases in plasma and adrenal corticosterone concentration occurring after drinking in water-restricted rats are not dependent on changes in plasma ACTH concentrations, but may be related to changes in adrenal blood flow, steroid metabolism and distribution, or neural input to the adrenal cortex.
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PMID:Rapid decreases in adrenal and plasma corticosterone concentrations after drinking are not mediated by changes in plasma adrenocorticotropin concentration. 628 Sep 67

Glomeruli contain receptors for many hormones. Binding of angiotensin II (ANG II) or antidiuretic hormone (ADH) to glomerular mesangial cells elicits a contractile response. Other hormones induce synthesis of cyclic nucleotides (cAMP, cGMP). Glomeruli also synthesize several prostaglandins, renin, and ANG II. Micropuncture studies in Munich-Wistar rats have examined the effects of vasoactive drugs and hormones on the filtration process. Several vasodilators increase renal plasma flow in the dog and rat, but GFR remains relatively unchanged due to an offsetting fall in the ultrafiltration coefficient (Kf). Vasoconstrictor substances such as ANG II and norepinephrine cause declines in renal plasma flow and Kf, but GFR remains constant due to an increase in the transcapillary hydraulic pressure gradient. Antidiuretic peptides and parathyroid hormone also reduce Kf. Glomerular mesangial cells may regulate Kf by contracting and reducing glomerular capillary surface area. ANG II and ADH directly stimulate mesangial cell contraction in vitro. Other hormones appear to cause contraction by inducing local ANG II synthesis. These hormonal pathways are implicated in the pathogenesis of altered glomerular function in diverse forms of renal injury.
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PMID:Hormonal modulation of glomerular function. 629 13

We report a case of primary aldosteronism in a 30-year-old woman without hypertension or any other characteristic symptoms. The condition was first suspected by hypokalemia (2.6 mEq/liter), which was incidentally found by routine checkup. There was evidence of suppressed plasma renin activity (PRA) and elevated plasma aldosterone levels. However, the blood pressure never reached a hypertensive level, and the circulating blood volume was within a normal range. A functioning right adrenal tumor was diagnosed by adrenal scintigraphy, computerized x-ray tomography, and adrenal venography. Adrenal venous catheterization suggested an aldosteronoma, which was confirmed by lateralized hypersecretion of aldosterone. After removal of the benign adenoma, the biochemical abnormalities were corrected, yet the blood pressure remained much the same. Hypertension is not necessarily a sign of primary aldosteronism.
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PMID:Asymptomatic normotensive primary aldosteronism. Case report. 633 52

Long-term beta-blockade is said to increase the number of beta-receptors. The effect of beta-blockers could therefore be reduced after long use. We tested this hypothesis in nine healthy subjects given 15 mg pindolol daily for 4 wk. Plasma concentrations (measured fluorometrically), isoproterenol dose-response relationship (to calculate the dose needed to increase heart rate by 25 bpm), renin, epinephrine, and norepinephrine were measured several times before and after the first and last dose. Kinetic parameters remained stable: total clearance (Cltot) = 45.2 and 42.9 l/hr, and Vdss = 205.8 and 198.6 l after the first and last dose. The concentration-effect relationship, plotted as the "dose ratio minus one" against the log of the plasma concentration was identical after 4 wk. Basal plasma renin activity was reduced slightly and the increase of stimulated plasma renin was blunted by pindolol even after 4 wk. The initial lowering of unstimulated renin by pindolol in the first 2 hr after dosing was not detectable after 4 wk. Epinephrine and norepinephrine levels in plasma were not changed initially nor after 4 wk. It is concluded that pindolol has a stable kinetic profile over time and that its beta-blockade does not induce tachyphylaxis.
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PMID:Constant kinetics and constant concentration-effect relationship during long-term beta-blockade with pindolol. 634 4

Several studies report a substantial rise in plasma catecholamines after caffeine. Epinephrine infusion induces a pressor response after nonselective beta-blockade. We studied the hemodynamic and humoral effects of drinking coffee after placebo and after both nonselective (propranolol) and beta 1-selective (metoprolol) blockade in 12 normotensive subjects. After placebo, coffee induced a rise in systolic and diastolic blood pressure and a fall in heart rate, whereas forearm blood flow did not change. Plasma catecholamines, especially epinephrine (+150%), rose and plasma renin activity, fell after drinking coffee. The effects of coffee on blood pressure, forearm blood flow, and all humoral parameters were not altered by pretreatment with propranolol or metoprolol. The fall in heart rate after coffee, however, seemed to be greater during propranolol. We conclude that the rise in plasma epinephrine after coffee was too small to reveal differences in reaction in propranolol- and metoprolol-pretreated subjects.
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PMID:Hemodynamic and humoral effects of coffee after beta 1-selective and nonselective beta-blockade. 634 98

We have examined the relationship between plasma renin activity and renal perfusion pressure by determining the stimulus-response curve of the renal baroreceptor in conscious, uninephrectomized dogs, and the modulation induced by catecholamines and varying salt intake. Renal perfusion pressure was controlled by step-wise inflation of a constricting cuff previously implanted around the renal artery. The stimulus-response curve of the renal baroreceptor may be divided into two ranges: a relatively flat portion close to normal pressure (100 mmHg), and a much steeper section below a "threshold" pressure of 75-80 mmHg. Epinephrine (I.V. or I.R.) produced a parallel shift of the curve to the right, i.e., a smaller drop in pressure was needed to reach "threshold." Changing the diet from normal salt intake (80 meq/day) to a low salt intake (10 meq/day) increased the gain of the stimulus-response curve. Thus, the same elevated PRA may be reached either by a shift of the curve to the right, or by increase in gain.
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PMID:Modulation of renal baroreceptor function by catecholamines and salt intake in the conscious dog. 636 69

The authors have studied on 50 patients hospitalized in the Adrenal Pathology unit of the Institute of Endocrinology, the etiopathogeny of arterial hypertension (AH) in hypercorticism and the therapeutic implications, arriving at the conclusion that in 20% of the cases AH was probably due to an increased activity of renin-angiotensin and in 47% to elevated levels of aldosterone. The authors hypothesize that AH in the remaining 30% of the hypercorticism cases in this study is due to other mineralocorticoids in excess and suggest that the treatment should be pathogenic and strictly individualized.
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PMID:Plasma renin activity (PRA) and plasma aldosterone in the adrenal cortex hyperactivity. Studies on 50 hypertensive patients. 636 2

The effects of two different amounts of pure rat angiotensinogen were investigated in a closed circuit isolated perfused rat kidney. In response to angiotensinogen, circulating levels of angiotensin I (AI) and angiotensin II (AII) immunoreactive materials were found to increase in a time and dose-dependent manner. Vasoconstrictor and renin inhibitory effects were observed in parallel with the increase in AII. Glomerular filtration rate decreased after administration of angiotensinogen to a greater extent than renal flow and filtration fraction. The characterization by high performance liquid chromatography of peptides generated showed the liberation of AI, des-Asp1AI, AII and des-Asp1AII (AIII). These findings demonstrate that administration of angiotensinogen in an isolated perfused kidney model generates AI and that renal converting enzyme and aminopeptidases are able to convert AI to AII, AI to des-Asp1AI, and des-Asp1AI and/or AII to AIII. Changes in circulating level of angiotensinogen influence the activity of the renin-angiotensin system and, therefore, renal function.
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PMID:Effects of circulating renin substrate on renal function in isolated perfused rat kidney. 640 Jan 16


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