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)

1. The effects of external medium calcium concentration, the ionophore A(23187) and lanthanum on the rate of renin release in vitro were studied with particular emphasis on results obtained from isolated superfused glomeruli of rat kidneys.2. The response to reduction in superfusate calcium concentration from 2 mM was a graded and reversible increase in the rate of renin release. An increase in release was detectable at 0.2 mM calcium; a threefold increase was found 36 min after a change from 2 mM calcium to calcium-free superfusate. A similar relative increase in release resulted from reductions from 0.1 mM to zero calcium, but the absolute amounts of renin released were greater in this latter series. Renin release from kidney cortical slices similarly increased in response to calcium-free incubation medium.3. The effects of A(23187) on renin release were modest. Changing from 2 mM calcium during control periods to calcium-free Ringer with A(23187) added caused an attenuated and more delayed increase in release than the change to calcium-free Ringer without ionophore. This difference in response was abolished when glomeruli were superfused with 0.1 mM calcium during the preceding 1 hr control period. There was no significant difference in renin release from glomeruli exposed to calcium-free EGTA-Ringer with and without A(23187) in the 2 mM calcium series; in the 0.1 mM calcium series the increase in release following a shift to calcium-free EGTA-containing superfusate with A(23187) added was significantly greater than in the absence of the ionophore.4. Addition of lanthanum (1 or 0.05 mM) to calcium-containing as well as calcium-free superfusate resulted in a significant depression of renin release. Subsequent removal of the lanthanum did not restore the rate of release unless EGTA was added; in the latter case a massive increase in renin release occurred resulting in a marked depletion of the remaining renin content of the glomeruli.5. It is concluded that calcium influences renin release by a direct action on the juxtaglomerular cells. The data support the previous suggestion that basal renin release is a function of active, calcium-dependent cell volume regulation - swelling causing an increase in the release; and further suggest that membrane-bound calcium has a direct effect on the cell membrane permeability to renin.6. The results exclude that calcium-stimulated exocytosis is responsible for basal renin release from the juxtaglomerular cells adhering to isolated glomeruli.
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PMID:Studies on the mechanism of renin release from isolated superfused rat glomeruli: effects of calcium, calcium ionophore and lanthanum. 41 32

1. Renin release from isolated dog renin granules was limited to within 20% of the total renin during incubation at 37 degrees C in isotonic medium and did not depend on the external concentration of renin. 2. Although the renin granules were osmotically and mechanically fragile, they were quite stable at 0 degrees C in isotonic medium. 3. The bulk of renin activity appeared in the supernatant when the granules were ruptured by osmotic lysis. About 8% of the total renin still remained in the membrane fraction of the granules after treatment by freezing and thawing. 4. Therefore stored renin in the granules can be described as comprising three components: a readily released soluble form; a soluble but hard-to-release form; a membrane-bound form.
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PMID:Renin release from renin granules in the dog. 66 62

Small-volume resuscitation with hypertonic saline in combination with dextran appears to be very successful in experimental animals, where better results are achieved than in animals treated with a traditional infusion regime. This effect is apparently related to improved organ blood flow due to reflex vasodilatation. This reflex is based on the arrival of hypertonic solution in the pulmonary circulation. The expansion of intravascular volume would seem to be of secondary importance. Atrial natriuretic peptide (ANP) is released from secretory granules located in atrial cardiocytes. Atrial distention appears to be the predominant stimulus triggering ANP production. In addition to the natriuretic and diuretic effects, ANP leads to vasodilation, especially when vascular tone is elevated; the sympathetic reflex seems to be attenuated. Cyclic Guanosine Monophosphate (cGMP) is an intracellular messenger and is partly released by ANP in the membrane-bound form. Renin excretion is highly influenced by ANP. The object of this study was to evaluate the influence of a hypertonic solution on this hormonal regulatory system. METHOD. This study compared a hypertonic sodium chloride solution (7.5%) in combination with hydroxyethyl starch (6%) (HH) to Ringer's lactate (RL). Six healthy volunteers received 4 ml/kg HH and 1 week later 500 ml RL. The infusion was administered in 20 minutes via a central venous catheter 70 cm in length. Blood pressure, heart rate, hemoglobin (Hb), hematocrit (Hk), colloid osmotic pressure (COP), sodium (Na+), chloride (Cl-), and plasma osmolarity were measured before starting and 5 and 30 min following infusion. At the same times ANP, cGMP, and plasma renin were also determined. RESULTS. Both groups showed no change in blood pressure or heart rate. The decrease of Hb, Hk, and COP in the HH and RL groups indicated the expansion of circulating plasma volume. HH infusion caused significant increases in ANP and cGMP, whereas plasma renin declined significantly. After RL infusion, ANP and renin values were very similar to the HH group except in one volunteer, who showed an extreme increase in ANP (760 pg/ml) 5 min after HH infusion. cGMP did not increase significantly in the RL group. On comparison of the two groups, only a significant difference in plasma osmolarity and in sodium and chloride levels was noted. CONCLUSION. We found that hypertonic NaCl (7.5%) with HH was well tolerated. Release of ANP and cGMP after HH infusion in healthy volunteers was not as high as expected, and the vasodilatory effect of hypertonic solutions was not explained by ANP or cGMP release in this investigation.
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PMID:[Plasma levels of atrial natriuretic peptide, cyclic guanosine monophosphate and renin following 7.5% NaCl + 6% hydroxyethyl starch or Ringer's lactate. A comparative study of 6 normal subjects]. 170 29

Congestive heart failure is characterized by both disturbances in electrolyte homeostasis and neuro-hormonal regulation. Total body potassium is reduced, and this reduction bears a modest relation to activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Patients with decompensated heart failure show increases in both plasma epinephrine and plasma norepinephrine, whereas patients with chronic stable heart failure usually have an increase only in plasma norepinephrine. High levels of circulating epinephrine may contribute to the development of hypokalemia by activating skeletal muscle and liver membrane beta 2-adrenergic receptors, which in turn stimulate intracellular cyclic adenosine monophosphate to activate the membrane-bound Na+K(+)-adenosine triphosphatase pump. The net result is that potassium flux across the cell membrane from the extracellular to the intracellular space increases, setting the stage for hypokalemia and possibly serious ventricular arrhythmias. Other mechanisms that may contribute to the development of hypokalemia in heart failure include the kaliuresis brought on by excessive levels of aldosterone. Moreover, it is likely that the activity of facilitated by concomitant activation of the renin-angiotensin system. Increased sympathetic nerve activity may then release additional renin from the kidney (by way of a beta 2-adrenergic mechanism). Therefore, both the sympathetic nervous system and the adrenal medulla may interact to cause hypokalemia in patients with heart failure. Because hypokalemia is known to predispose patients to ventricular arrhythmias, it may be prudent to aggressively maintain serum potassium levels in patients with heart failure in the range of 4 to 5 mEq/liter.
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PMID:Interaction of the sympathetic nervous system and electrolytes in congestive heart failure. 230 25

The Na,K-ATPase activity of erythrocyte membranes is markedly increased in normal-renin essential hypertensives. A temporal shift of the chronobiology of the erythrocyte-membrane-bound Na,K-ATPase in these patients is described. The disorder causes a loss of synchronism between the circadian rhythms of aldosterone and Na,K-ATPase. Such uncoupling phenomenon may explain the inversion of the day/night sodium excretion ratio and other disturbances of sodium metabolism found in essential hypertensives.
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PMID:Chronobiological evidence for an uncoupling of the Na,K-ATPase to aldosterone in normal renin hypertension. 254 13

Although renin-secreting tumors are rare, they must be considered in the differential diagnosis of hypertension associated with hypokalemia, which occurs commonly in the hypertensive population. The finding of an ovarian renin-secreting tumor emphasizes the potential importance of the ovary as an extrarenal source of renin; the local ovarian renin-angiotensin system may play a key role in reproductive function by regulating vascular reactivity, local blood flow, steroidogenesis and other physiologic effects. In the illustrative case presented, a renin-secreting ovarian leiomyosarcoma was obtained from a women who presented with hypertension and hypokalemia. Plasma prorenin levels were markedly elevated. Tumor excision was quickly followed by a fall in prorenin levels and tumor recurrence was accompanied by an increase in prorenin levels. Active renin concentration in the tumor homogenates was similar to that found in kidney homogenates while the tissue prorenin concentration was approximately 20 times that found in kidney tissue. When cultured for up to 4 weeks, ovarian tumor cells secreted greater than 95% prorenin. Immunoblot analysis demonstrated that tumor renin had a molecular weight of 47,000, similar to that of human recombinant prorenin. Immunohistochemical staining of tumor tissue with antibodies against human renal renin at the electron microscopic level demonstrated the presence of renin primarily in membrane-bound vesicles and rarely in dense-core secretory granules. These findings suggest that prorenin in this ovarian tumor was secreted by the constitutive pathway, which is mediated by these amorphous vesicles.
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PMID:Extrarenal renin-secreting tumors: insights into hypertension and ovarian renin production. 267 94

Normal-renin essential mesor hypertensives are characterized by a consistent increase in erythrocyte membrane-bound Na/K-ATPase activity. Low-renin essential hypertensives exhibit, in contrast, a lower activity in Na/K-ATPase of cell membranes. This study documents a third disorder characterized by a temporal shift in the rhythmic activity of the erythrocyte membrane-bound Na/K-ATPase in normal-renin hypertensives. The disorder causes the synchronism with the aldosterone circadian rhythm to be invariably lost. The uncoupling phenomenon could be invoked to explain the inversion in the day-night sodium excretion rate found in essential hypertensives. In addition, it suggests that the circadian rhythm in Na/K-ATPase is under the control of cycling factors other than aldosterone.
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PMID:Internal desynchronization between circadian rhythms of plasma aldosterone and erythrocyte membrane-bound Na/K-ATPase. 281 94

Morphological changes in the macula densa have been studied during the infusion of diuretic agents into the renal artery of anesthetized dogs. The kidneys were fixed by rapid high pressure perfusion with glutaraldehyde. Large basolateral intercellular spaces were seen between macula densa cells in control kidneys, but the number and extent of these spaces were strikingly reduced during the natriuresis and diuresis induced by the infusion of frusemide, ethacrynic acid or mannitol. Natriuresis and diuresis produced by the intravenous infusion of large volumes of 0.9% NaCl solution also resulted in closure of these spaces. No simple relationship existed between changes in plasma renin activity and closure of the spaces between macula densa cells during these procedures. A distinctive, membrane-bound, vesicle-containing structure was identified between the basolateral processes of the cells of each macula densa; the function of this structure awaits elucidation. We suggest that changes in the size of the basolateral intercellular spaces of the macula densa reflect changes in fluid flux between the distal tubule and the interstitium of the juxtaglomerular apparatus.
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PMID:Morphological changes in the renal macula densa during natriuresis and diuresis. 311 Aug 85

Using an antibody to pure human renin and the technique of ultrastructural immunocytochemistry we have localized renin in the granular epithelioid cells of three juxtaglomerular apparatuses and one interlobular artery. The staining reaction of the cells was the same in both sites: we found that crystalline protogranules, rounded membrane-bound granules and storage granules intermediate in morphology all stained positively for renin. We also demonstrated immunoreactive renin in dilated cisternae of rough endoplasmic reticulum in the granular cells in both sites. We present these observations as morphological evidence that granular epithelioid cells synthesize and store renin both in the juxtaglomerular apparatus and in the larger arteries in the kidney.
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PMID:New morphological evidence for the synthesis and storage of renin in the human kidney: an ultrastructural immunocytochemical study. 639 24

A basolateral membrane (BLM) enriched fraction of the homogenized rat kidney contained kallikrein and prekallikrein which differ from urinary kallikrein. Triton X-100 (0.1%) or melittin (10(-7) - 10(-5)M) solubilized the membrane-bound enzyme. Prekallikrein was activated by trypsin and plasmin. Active kallikrein and activated prekallikrein cleaved the chromogenic substrate S-2266 and released bradykinin from kininogen. Aprotinin and antiserum to rat urinary kallikrein inhibited BLM kallikrein. Gel electrophoresis separated activated BLM prekallikrein and kallikrein; prekallikrein even after activation moved slower (Rf = 0.3) in electrophoresis at an alkaline pH than active kallikrein (Rf = 1). Gel filtration resolved BLM kallikrein to two proteins of low (4 X 10(4) M) and high (1.5 X 10(5) M) molecular weight. After isoelectric focusing of the activated BLM fraction, two kallikreins with pIs of 3.9 and 5.3 were obtained. The BLM fraction also contained renin which became active after Triton treatment. Renin activity was not enhanced by trypsin or acid pH indicating that there was no prorenin present. Thus, BLM of rat kidney contains a kallikrein which is different from urinary kallikrein. This kallikrein, when released from basal membrane, may appear in renal lymph and venous effluent.
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PMID:Kallikrein and prekallikrein of the isolated basolateral membrane of rat kidney. 675 27


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