Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

In four-month-old spontaneously hypertensive rats (SHR) the effect of a calcium blocking agent verapamil on blood pressure, ventricular contractility indices, parathyroid hormone (PTH), plasma renin activity (PRA), plasma and adrenal corticosterone content and catecholamines in hypothalamus, myocardium and adrenal gland was evaluated. Calcium and phosphorus in plasma were also determined. Verapamil treatment resulted in a significant decrease in systolic and diastolic blood pressure and a reduction in maximum left ventricular pressure. Verapamil exerted a negative inotropic effect, evaluated by a decrease in dP/dt max and dP/dt neg. PRA was elevated, calcium tended to decrease, and no changes in PTH and phosphorus were found. The hypotensive effect of verapamil in SHR was accompanied by a decrease in plasma and adrenal corticosterone content, and a fall in catecholamine concentration in adrenal glands and myocardium.
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PMID:Effect of calcium blocking agent verapamil on blood pressure, ventricular contractility, parathyroid hormone, calcium and phosphorus in plasma, catecholamines, corticosterone and plasma renin activity in spontaneously hypertensive rats. 328 65

In order to clarify the relationship and the pathophysiological role of renal dopamine, kallikrein-kinin and prostaglandin systems in essential hypertensives, the effects of dopamine on these systems and renal sodium handling were investigated. Basal levels of kallikrein, kinin and prostaglandin E2 in essential hypertensives were significantly lower than those in normotensives. Those of kallikrein and kinin were obviously more suppressed in the low renin group than in the normal renin group, but no significant difference in prostaglandin E2 was found in either subgroup. Urinary dopamine excretion was significantly lower in the low renin essential hypertensives, while no significant difference was found between normotensives and normal renin essential hypertensives. Kallikrein activity and prostaglandin E2 were significantly increased in essential hypertensives by dopamine infusion, and no significant difference was found in kallikrein-quantity and kinin between normotensives and essential hypertensives after the infusion. These increases of kallikrein and kinin were significantly higher in the low renin group than in normal renin group, but those of prostaglandin E2 were not. Urine volume, urinary sodium excretion and fractional excretions of sodium and inorganic phosphorus were all increased in both normotensives and essential hypertensives after dopamine infusion. The increases of these were significantly greater in essential hypertensives than in normotensives, and greater in the low renin group than the normal renin group. From these results, it was suggested that the dopamine, kallikrein-kinin and prostaglandin E2 system have a close relationship with each other, and the suppression of these systems may contribute to the pathophysiology of essential hypertension, especially in the low renin group.
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PMID:The pathophysiological role of renal dopamine, kallikrein kinin and prostaglandin systems in essential hypertension. 332 11

The stress response in humans commonly includes elevations in plasma concentrations of glucocorticoids, catecholamines, glucagon, growth hormone, aldosterone, and renin, resulting in alterations in the metabolism of glucose and other energy substrates, and in increased sodium and water retention. In severe illness, triiodothyronine and sometimes thyroxine are decreased without evidence of clinical hypothyroidism. Antidiuretic hormone may be elevated in bacterial meningitis and other central nervous system disorders, as well as in acute asthma, chronic ventilator therapy, pneumothorax, atelectasis, and postoperatively. Increased ADH concentration can lead to significant hypoosmolality and hyponatremia with adverse effects on the patient. In the setting of severe intracerebral insults, ADH may be inappropriately low, resulting in diabetes insipidus. Insulin concentrations may be inappropriately low for serum glucose concentration, or insulin may have diminished receptor responsiveness in seriously stressed patients. Either situation leads to hyperglycemia. Disturbances in calcium, phosphorus, and magnesium homeostasis may occur relatively frequently in the critically ill patient in response to therapeutic interventions, or illness-induced altered metabolism. It is not always clear when an altered metabolic or hormonal state is an appropriate response to a stress, or represents decompensation of the body's mechanisms for coping with that stress. It is important, however to recognize the common responses of the organism to severe illness, and to monitor for treatable abnormalities which occur.
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PMID:Endocrine manifestations of critical illness in the child. 354 20

In order to investigate the pathophysiological role of the renal kallikrein-kinin system in renin subgroups of essential hypertension, the quantity and activity of urinary kallikrein, urinary kinin excretion, and correlations of kallikrein and kinin excretions with renal sodium handling in the renal tubules were studied in 17 normal subjects, 23 patients with normal renin and 12 patients with low renin essential hypertension. Urine samples were collected by the 2-hour clearance method in the early morning. The quantity and activity of urinary kallikrein, and the urinary excretion of kinin were significantly lower in both low and normal renin patients than in normal subjects. Comparing the normal renin and the low renin group, no significant difference was found in the quantity of urinary kallikrein, while the activity of urinary kallikrein and urinary kinin excretion were significantly lower in low renin patients than in normal renin ones. Fractional excretions of sodium (FENa) and inorganic phosphorus (FEP), which reflect renal tubular and proximal tubular sodium reabsorption, respectively, were significantly lower in the low renin patients than in the normal renin ones. A significantly positive correlation was observed between the urinary kallikrein activity or urinary kinin excretion and FENa or FEP in both normal subjects and normal renin patients, but not in low renin patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of the renal kallikrein-kinin system in sodium metabolism in normal and low renin essential hypertension. 635 50

Acute laminitis-hypertension was produced by carbohydrate overloading of the gastrointestinal tract in 12 adult horses. Obel grade 3 (OG3) lameness developed 40 hours (+/- 3.5, SEM) after overfeeding. At OG3 lameness, mean plasma volume was significantly decreased (P less than 0.005) when compared with base-line values. Before OG3 lameness, transient decreases in serum phosphorus and calcium were recorded. Mild hyponatremia also developed before OG3 lameness and persisted. After establishment of OG3 lameness, persistent hypokalemia and increased plasma aldosterone concentration occurred coincidently. Transient increase in plasma hydrocortisone (cortisol) and renin activity and transient hypochloremia were also recorded during the syndromal phase. Changes in plasma volume and serum electrolytes are discussed and related to the pathogenesis of acute equine laminitis. The alterations in plasma renin activity and aldosterone concentration were interpreted as homeostatic adjustments to fluid and electrolyte imbalances. Differences between the horse and pony during onset of experimental alimentary laminitis are also discussed.
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PMID:Plasma volume, electrolyte, and endocrine changes during onset of laminitis hypertension in horses. 675 27

Labetalol, a blocker of alpha- and beta-adrenoreceptors, was tried on 45 patients with severe (29 cases) or mild to moderate (16 cases) hypertension. After an initial period of dosage adjustment and a 2 months treatment in effective doses, there was a significant fall in supine blood pressure from mean values of 207/132 to 170/106 mmHg. In 23 patients hypertension was controlled by labetalol alone in doses of 400 and 1800 mg per day. True failures were rare (16%). Digestive disorders and postural hypotension were the most frequently encountered side-effects; they obliged to discontinue treatment in 4 cases, but were compatible with it in 11 cases. In 22 patients the fall in BP was accompanied by a significant (p less than 0,001) decrease in plasma renin activity from 123 to 44 ng/l/min supine and from 144 to 83 ng/l/min standing. Studies of the renal function showed no changes during oral therapy. Following intravenous injection of 50 mg labetalol to 20 subjects, inulin and PAH clearances remained unaltered, and there was a significant, though transient (1 hour), decrease in chloride, sodium and phosphorus excretion. Effective in lowering blood pressure be used and well tolerated by the kidneys, labetalol can safely be used for the treatment of severe hypertension with organic renal involvement.
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PMID:[Effects of labetalol, a new alpha- and beta-adrenoreceptor blocking drug, on arterial pressure, renal function and renin activity (author's transl)]. 700 20

Our understanding of the physiology and biochemistry of acid-base and fluid-electrolyte regulations has greatly expanded in recent years. Key physiologic principles have emerged that now permit rational diagnosis and therapy of clinical disorders of serum electrolyte concentration. This paper describes diagnostic strategies based upon these principles. The etiology of the myriad factors in hyponatremia is best derived by first measuring serum tonicity and then assessing extracellular fluid volume. The hyper-, iso- and hypotonic hyponatremia are defined, and the hypotonic group is subclassified into hypo-, iso- and hyper volemic forms. The hypernatremias are best categorized by their state of volume expansion. Classification into the hypo-, hyper- and isovolemic hypernatremias simplifies their diagnosis. Metabolic acidoses are classified in terms of the anion gap. Clinical and chemical aspects of increased and normal anion gap acidoses are described. Metabolic alkaloses require a source of new bicarbonate and its retention by the kidney. The means by which new alkali is synthesized and urinary loss prevented serve to effectively classify the alkaloses. Hypokalemic syndromes are defined in terms of associated changes in body potassium. The potassium-depleted states are further subclassified by whether normotension or hypertension is associated. Hyperkalemia is produced by redistribution of cellular and extracellular potassium or by increased body potassium. Defects in the renin-angiotensin-aldosterone-distal renal tubule effector arm usually underlie hyperkalemic states, which are than classified in terms of this regulatory hormonal cascade. Classifications for disordered serum concentrations of calcium, magnesium, phosphorus and uric acid are presented. Hormonal, metabolic and renal regulatory factors form the basis for an organized approach to these disorders.
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PMID:Diagnostic strategies in disorders of fluid, electrolyte and acid-base homeostasis. 703 39

In order to clarify the role of dopamine on the pathophysiology of essential hypertension, mean arterial pressure (MAP), heart rate (HR), urine volume (UV), urinary sodium excretion (UNaV), endogenous creatinine clearance (Ccr), fractional excretions of sodium (FENa), inorganic phosphorus (FEP) and potassium (FEK), plasma renin activity (PRA), plasma aldosterone concentration (PAC) and plasma noradrenaline concentration (PNA) were measured before and after intravenous infusion of dopamine (3 micrograms/kg/min, 60 min) in normotensive (NT) and essential hypertensive subjects (EHT). Following dopamine infusion, a significant decrease of MAP and an increase of HR were observed in EHT but not in NT. UV, UNaV, Ccr, FENa, FEP and FEK increased significantly in both NT and EHT, and changes in these except for Ccr were significantly greater in EHT than in NT. In EHT, following dopamine infusion, PNA was clearly elevated, but no remarkable change was found in PRA and PAC. A significantly positive correlation was found between delta UNaV and delta FENa or delta FEP, and between delta FENa and delta FEP, while no significant relation was observed between delta UNaV and delta Ccr, delta MAP or MAP before dopamine infusion. A significant inverse correlation between supine PRA before dopamine infusion and delta FENa or delta FEP and a positive correlation between age and delta FENa or delta FEP were also observed in these patients. The changes in UNaV positively correlated with delta FENa and delta FEP in both low renin (group L) and normal renin EHT (group N) and with delta Ccr i group N but not in group L. The mean values of delta FENa, delta FEP and delta FEK were significantly higher in group L as compared with those in age-matched group N. These results suggest that, since the enhanced response to infused dopamine may reflect reduced dopaminergic activity, attenuation of renal dopaminergic activity might exist and be involved through a distribution of water-sodium metabolism, at least in part, in the pathophysiological mechanism in EHT, particularly in group L.
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PMID:Hemodynamic and natriuretic responses to intravenous infusion of dopamine in patients with essential hypertension. 704 16

The fine structural appearance and elemental composition of unfixed chromatin is described for cells of the dinoflagellate Prorocentrum micans prepared by a freeze-drying technique. This involves rapid freezing, cryo-dehydration and resin infiltration of a monolayer of cells dispersed over renin base. The fine structure of the nucleus appears quite different from chemically fixed and dehydrated cells. In stained sections, the chromosomes are seen as pale areas containing diffuse chromatin, and are surrounded by electron-dense nucleoplasm which has a reticulate substructure. X-ray microanalysis reveals the presence of high levels of chromatin-associated Ca and transition metals Fe, Ni, Cu and Zn, in accordance with previous observations on chemically processed cells. Calculation of elemental mass fractions by on-line computer demonstrates an overall ratio of one divalent cation per two phosphorus groups (or per two nucleotides). This ratio is similar to that obtained previously for chemically fixed chromatin, and shows that the precise overall association of metals is not primarily determined by the process of fixation.
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PMID:X-ray microanalysis of unfixed chromatin in dinoflagellate cells prepared by a monolayer cryotechnique. 720 Sep 96

The design and application of alpha-hydroxy phosphonates, a new class of transition state analogs, toward the discovery of novel and potent inhibitors of the aspartyl protease renin is described. Tripeptidic alpha-hydroxy diethyl phosphonate 3, the first example in this series, was found to be a good inhibitor of human renin (IC50 = 29 nM), and preliminary studies led to the choice of alpha-hydroxy dimethyl phosphonate 15 (IC50 = 16 nM) as a base-line compound for further structure-activity relationship study. Corresponding phosphinate (28-30) and phosphine oxide (23 and 24) analogs of 15 were prepared to assess the steric and electronic requirements around the phosphorus center. Evaluation of these analogs suggested that the presence of at least one alkoxy group on phosphorus was a critical requirement for good activity. Inhibitors with leucine at P2 possessed better in vitro activity than the corresponding P2 histidine analogs (15, IC50 = 16 nM vs 37, IC50 = 220 nM; 33, IC50 = 8.5 nM vs 40, IC50 = 41 nM). Compound 34 (IC50 = 31 nM), the P3 aminocaproic analog of 15, showed complete and long-lasting inhibition of plasma renin activity while eliciting a 10-15 mmHg drop in mean arterial pressure when administered intravenously at 1 mumol/kg in conscious, sodium-depleted, cynomolgus monkeys. In summary, the alpha-hydroxy phosphonates represent a promising and structurally novel class of transition state analog inhibitors of human renin.
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PMID:alpha-Hydroxy phosphinyl-based inhibitors of human renin. 747 84


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