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)

Post-renal transplant hypertension remains a common problem. The most frequent causes now are chronic rejection and cyclosporine-induced hypertension. Before the development of cyclosporine, renin-dependent hypertension was the dominant pathophysiological mechanism but now, with the widespread use of cyclosporine, a salt-dependent mechanism is the major one. In severe "inappropriate" hypertension, potentially surgically remediable causes such as renal artery stenosis of the allograft artery or renin release from the native kidneys should be considered. Cyclosporine causes hypertension in normal subjects and in all solid organ transplants. The most likely mechanism is renal vasoconstriction with subtle retention of sodium chloride together with systemic vasoconstriction. The vasoconstriction, as yet, is not associated with any specific vasoconstricting agent nor does there appear to be a specific antagonist. Indeed, increased sensitivity to many different vasoconstrictors has been demonstrated. The major site of vasoconstriction appears to be in the afferent arteriole, and optimum antihypertensive therapy is probably provided by calcium channel blockers if the hypertension is due to cyclosporine. Because post-renal transplant hypertension is often multifactorial in origin, however, it is not surprising that the use of combined antihypertensives is often necessary.
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PMID:Pathophysiology and treatment of posttransplant hypertension. 193 42

Diabetic patients treated with insulin injected subcutaneously are characterized by peripheral hyperinsulinaemia and an increased mass of total body exchangeable sodium. We hypothesized that this may cause, at least in part, the glomerular hyperfiltration seen in the diabetic state. Six normal subjects were studied on 2 days in random order. Day A: Basal state for 40 min, hyperinsulinaemic euglycaemic clamp for 1 h (insulin infusion rate 2 mU kg-1 min-1 and 50% glucose infusion) and hyperinsulinaemic euglycaemic clamp combined with volume expansion (2 1 isotonic sodium chloride) for 2 h. Day B: as day A, but without insulin and glucose infusion. During combined volume expansion and hyperinsulinaemia an increase in glomerular filtration rate (GFR) (128 +/- 6 vs 117 +/- 8 ml min-1 1.73 m-2, p less than 0.01) and lithium clearance (CLi) (50 +/- 4 vs 33 +/- 5 ml min-1 1.73 m-2, p less than 0.01) was observed compared with basal conditions. GFR and CLi were unchanged during day B. Insulin infusion reduced renal sodium excretion. Absolute proximal tubular reabsorption was unchanged on both days. Insulin infusion without volume expansion caused a decrease of 24% in the fractional distal sodium excretion. Superimposed volume expansion and the concomitant increase in GFR and CLi was accompanied by a subsequent enhanced fractional distal sodium excretion of 27%. The changes in plasma concentrations of aldosterone, renin, angiotensin II, atrial natriuretic peptide and catecholamines did not explain the differences in GFR. An increase in GFR of 10%, comparable with that observed in diabetic patients, was induced by combined hyperinsulinaemia and volume expansion in euglycaemic normal subjects. The enhanced GFR is probably a compensatory response to the sodium retention induced by the action of insulin on the distal tubules.
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PMID:Effects of insulin on renal haemodynamics and sodium handling in normal subjects. 194 21

Overall 78 men were examined. Of these, 30 presented with borderline arterial hypertension (BAH), 30 with stage I essential hypertension (EH), and 18 healthy subjects served as control. To assess osmoregulating and natriuretic renal functions, water and water plus salt were administered (at a rate of 22 ml water or isotonic sodium chloride per kg bw). Use was made of classic approaches in this case, with the determination of K+, Na+ excretion, blood plasma and urine osmolarity, calculation of the concentration index, clearance of osmotic-active substances and free water, total reabsorption of Na in the distal parts of nephron and intensity of that process. Besides, flame photometry was employed to measure blood K+, Na+ concentration and RIA to examine plasma renin activity. The data obtained indicate the heterogeneity of the patients with BAH and stage I EN according to the response to water and water and salt administration. Approximately 1/3 of the patients showed a tendency towards water retention in the body as well, which is common to patients with the volume-dependent form of arterial hypertension. In that case the compensatory potentialities of modulating renin-angiotensin system activity were preserved.
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PMID:[The osmoregulatory and natriuretic functions of the kidneys in the early stages of the evolution of hypertension]. 194 58

The renin angiotensin system is an important system for the regulation of blood pressure and salt and water homeostasis. As a pathogenetic factor it is involved in the development of several forms of renal hypertension and, furthermore, it participates in the pathogenesis of primary and secondary hypertension. The regulation of the activity of the system is under the control of neuronal and hormonal mechanisms and depends on blood pressure and plasma concentrations of sodium chloride. With the development of converting enzyme inhibitors and their vasodilator, diuretic and sympatholytic actions a new important antihypertensive principle for lowering blood pressure was found. In this context also local renin angiotensin systems which have been described for several tissues have to be discussed as a possible target of action for converting enzyme inhibitors.
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PMID:[Pathophysiology of the renin-angiotensin system]. 210 55

An increased venous tone responsible for changes in systemic hemodynamics has been described in borderline hypertensive patients along with the release, in response to intravenous sodium chloride, of an endogenous sodium ion/potassium ion adenosine triphosphatase (Na+/K+ ATPase) inhibitor with vasoconstrictive properties. The hemodynamic and humoral effects of a 2-hour intravenous saline infusion were studied in 25 borderline hypertensives characterized on the basis of their forearm venous distensibility (VV30) in normal (n = 15) and low (n = 10) VV30. VV30 was slightly reduced by saline in the entire hypertensive group (1.47 vs 1.36 ml/100 ml; p less than 0.05), whereas blood pressure and plasma Na+/K+ ATPase inhibitor were unchanged. Normal VV30 showed a sudden increase in plasma Na+/K+ ATPase inhibitor in response to saline associated with an increase in blood pressure, a forearm arterial and venous constriction, and a sluggish suppression in plasma renin activity, whereas low VV30 exhibited a completely opposite pattern. The changes in plasma Na+/K+ ATPase inhibitor inversely correlated to VV30 decreases in borderline hypertensives with normal VV30 (r = -0.49; p less than 0.05), whereas they did not in all hypertensive patients. Atrial natriuretic peptide response to saline infusion was delayed in normal VV30 and inversely related to the changes in Na/K+ ATPase inhibitory activity (r = -42; p less than 0.05) attained after 2 hours of infusion in the entire hypertensive population. Results of this study suggest the ability of acute volume expansion to reduce peripheral venous distensibility in borderline hypertensive patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pattern of peripheral venous response to volume expansion in borderline systemic hypertension. 214 96

Nifedipine and verapamil (10 mg/kg orally) were found to induce a significant increase of renin activity, a decrease of aldosterone and ionized calcium levels in blood plasma in spontaneously hypertensive rats. A preliminary administration of a hypertonic solution of sodium chloride decreased renin activity, ionized calcium and aldosterone levels that contributed to the enhancement of the hypotensive effect of calcium antagonists. It was established that nifedipine by its effect on the parameters of hemodynamics and the condition of renin-angiotensin system as well as the blood plasma ionized calcium level is superior to verapamil.
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PMID:[The effect of fenigidin (nifedipine) and verapamil on renin activity, the levels of ionized calcium and aldosterone in the blood plasma and on the hemodynamic indices of rats with spontaneous hypertension]. 218 50

Eight normal women took part in a randomized crossover study to investigate the effect of dietary supplementation with 105 mEq sodium chloride (NaCl) for 3 days or equimolar sodium citrate (NaCit) after salt depletion. NaCit supplement induced greater urinary sodium and potassium excretions than did the NaCl supplement (197 +/- 10 v 107 +/- 19 mEq/3 days for sodium, P less than .01, 130 +/- 7 v 96 +/- 6 mEq/3 days for potassium, P less than .01, respectively) and less body weight gain (+0.6 +/- 0.1 v +1.6 +/- 0.1 kg, P less than .01). Suppressions of plasma norepinephrine, renin activity and aldosterone concentration were significantly smaller with NaCit than with NaCl supplement. We conclude that the anionic component of sodium salts may have some effects on renal sodium handling and modulates volume expansion and humoral factors.
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PMID:Chloride ion plays an important role in sodium induced volume expansion in normal humans. 219 64

To determine whether administration of chloride corrects chloride-depletion metabolic alkalosis (CDA) by correction of plasma volume contraction and restoration of glomerular filtration rate or by an independent effect of chloride repletion, CDA was produced in normal men by the administration of furosemide and maintained by restriction of dietary sodium chloride intake. Negative sodium balance (-112 +/- 16 meq) and reduced plasma volume (2.53 versus 2.93 liters, p less than 0.05) developed. The cumulative chloride deficit of 271 +/- 16 meq was then repleted by oral potassium chloride (267 +/- 19 meq) over 36 hours with continued serial measurements of glomerular filtration rate, effective renal plasma flow, plasma volume, body weight, and plasma renin and aldosterone levels. CDA was corrected, even though body weight, plasma volume, glomerular filtration rate, and renal plasma flow all remained reduced and plasma aldosterone was elevated; urinary bicarbonate excretion increased during correction. Administration of an identical potassium chloride load to similarly sodium-depleted but not chloride-depleted normal subjects produced no change in acid-base status. It is concluded that chloride repletion can correct CDA by a renal mechanism without restoring plasma volume or glomerular filtration rate or by altering sodium avidity.
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PMID:On the mechanism by which chloride corrects metabolic alkalosis in man. 245 Apr 56

Gordon's syndrome was diagnosed in a 19-year-old woman who had hypertension, hyperkalemia and hyperchloremic acidosis. In family screening, hyperkalemia and hyperchloremic acidosis were also found in the patient's mother and brother. The proband and her brother were studied and showed normal glomerular function with normal renal sodium conservation and urine acidification mechanisms. The levels of plasma aldosterone were normal in both subjects. The renin activity was low in the proband but normal in the brother. Both the basal and the volume-stimulated plasma concentration of atrial natriuretic peptide was low in the two patients. As compared with controls, the kaliuretic response to infusion of sodium chloride was not decreased in the patients. Hydrochlorothiazide promptly corrected the acidosis and the hyperkalemia as well as normalized the raised blood pressure of the proband. We suggest that a deficiency of atrial natriuretic peptide rather than an unusual avidity for sodium chloride reabsorption by the renal tubules plays a significant pathogenetic role in Gordon's syndrome.
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PMID:A deficient response of atrial natriuretic peptide to volume overload in Gordon's syndrome. 252 4

In order to clarify the possible relationship between changes in blood pressure after salt loading, membrane sodium transport and renin profile, 19 patients with essential hypertension (8 patients with low renin hypertension and 11 patients with normal renin hypertension), admitted to our hospital, were studied. We also examined the correlation of changes in intracellular sodium concentration after salt loading between erythrocytes and lymphocytes. After a control period of one week, all subjects were placed on a low salt intake for one week followed by one week of a high salt intake. Percent increases in mean blood pressure and intracellular sodium concentration in erythrocytes and in lymphocytes after salt loading were greater in low renin hypertensive patients than in normal renin hypertensives. Percent changes in intracellular sodium concentration in erythrocytes inversely correlated with those in ouabain sensitive sodium efflux rate constant and positively correlated with those in intracellular sodium concentration in lymphocytes. These results suggest that an increase in sodium chloride sensitivity of blood pressure in patients with low renin hypertension may be due to the inhibition of Na+-K+ pump in vascular smooth muscle cell membrane.
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PMID:Sodium chloride sensitivity, intracellular sodium concentration in erythrocytes and lymphocytes, and renin profile in essential hypertension. 265 38


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