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)

Renin has been identified biochemically and immunohistochemically in the adrenal gland. We examined the subcellular distribution and behavior of adrenal renin. By differential centrifugation of adrenal capsules, we found renin mainly in mitochondrial fractions. By Percoll density gradient centrifugation of this fraction, dense granules were separated from mitochondria and microsomes. The renin activity in the dense granules from the capsules of nephrectomized rats was 15 times greater than that of the intact rat. Immunohistochemical studies revealed that the dense granules increased in number after bilateral nephrectomy. Immunogold staining of these granules showed unequivocally the presence of renin in these granules. Adrenal capsules in organ culture were found to release renin at a steady rate. Renin release from bilaterally nephrectomized rat adrenals was 46 times faster than from the organs of intact animals. The mechanism of the control of renin secretion from the adrenal gland was different from the kidney in that the secretion was stimulated by potassium chloride (10 mM) or angiotensin II (10(-9)-10(-7) M) but not by ACTH (10(-9)-10(-7) M), suggesting stimulation by intracellular calcium. These results provide evidence that the adrenal synthesizes renin, stores it in specific secretory granules and secretes it in a regulated manner.
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PMID:Presence of renin secretory granules in rat adrenal gland and stimulation of renin secretion by angiotensin II but not by adrenocorticotropin. 284 64

Intracellular recordings were made in juxtaglomerular granulated (JG) cells and in vascular smooth muscle (VSM) cells in afferent arterioles of hydronephrotic mouse kidneys. Both cell types did not differ in their passive and active electrical membrane properties; membrane potential was about -58 mV, input resistance exceeded 400 M omega, and JG as well as VSM cells showed spontaneous depolarizations resembling excitatory junction potentials and active responses observed in smooth muscle cells of other blood vessels in various species. These depolarizations, attributed to spontaneous transmitter release from adrenergic terminals, were extremely polymorphous and quite frequent. Epinephrine, norepinephrine, phenylephrine, arginine vasopressin, and angiotensin II depolarized JG and VSM cells, but isoproterenol and orciprenaline had no effect. A hyperpolarizing action of catecholamines was never observed. It is suggested that, in this in vitro preparation, isoproterenol increases renin secretion by a mechanism independent of membrane potential changes. Depolarizations mediated by alpha-mimetic agents, arginine vasopressin, and angiotensin II, as well as by the junctional activity may inhibit renin secretion by an increased calcium influx into JG cells.
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PMID:Intracellular recordings from renin-positive cells of the afferent glomerular arteriole. 286 96

Adrenaline may increase noradrenaline release and enhance sympathetic pressor effects through activation of pre-synaptic beta 2-adrenoceptors. Conversely, blockade of beta 2-receptors could lead to a fall in blood pressure. To test this hypothesis we performed a double-blind placebo controlled crossover study in nine patients with mild hypertension, comparing the effects of the beta 2-selective blocker ICI 118,551, 50 mg t.i.d. with those of propranolol, 80 mg t.i.d. Two hours after the first dose of ICI 118,551 or propranolol, plasma noradrenaline and blood pressure remained unchanged while heart rate and renin were reduced. After 1 week, blood pressure was significantly reduced by both drugs. The beta 2-selectivity of ICI 118,551 was confirmed by isoprenaline infusion studies. After 1 week of treatment ICI 118,551 had no effect on the beta 1-receptor mediated shortening of electromechanical systole (QS2I), the rise in systolic pressure and rise in renin, whereas these responses were blocked by a dose factor of eight after propranolol. ICI 118,551 and propranolol equally blocked the beta 2-receptor mediated fall in diastolic pressure and the rise in noradrenaline. We conclude that beta 2-selective blockade by ICI 118,551 lowers blood pressure. This finding is compatible with a role of pre-synaptic beta 2-receptors in blood pressure control.
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PMID:Compound ICI 118,551, a beta 2-adrenoceptor antagonist, lowers blood pressure. 290 20

Brattleboro rats, homozygous for hypothalamic diabetes insipidus (DI), compared to their Long Evans (LE) controls, revealed typical changes in water-sodium-potassium balance: hypernatremia and hyperosmolality and hypokalemia. Plasma renin activity was significantly increased (79%) and plasma concentration of aldosterone was significantly lower (--36%) in DI rats than in LE rats. Concomitantly aldosterone excretion in DI rats was increased sevenfold. Adrenal blood flow rates were not statistically different in both groups of rats but the aldosterone concentrations in the adrenal venous effluent were significantly lower (--66%) in DI rats than in LE rats, suggesting that the in vivo production rate of aldosterone was reduced in DI rats. Plasma concentration of ACTH was significantly decreased (by 25%) in DI rats. The reasons for the dissociation between the changes of aldosterone production and the variations of renin-angiotensin system activity were discussed.
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PMID:Water-electrolyte balance and hypothalamo-pituitary-adrenocortical function in rats with inherited diabetes insipidus (Brattleboro strain). 301 46

Adrenal responses to angiotensin II (ANG II) are enhanced with restriction of sodium intake. To determine whether increased circulating ANG II levels are responsible for the enhanced responsiveness, the adrenal and blood pressure responses to ANG II in human subjects were assessed four times: in balance on a high and a low salt diet and before and after the administration of a converting enzyme inhibitor (enalapril). Before enalapril administration, sodium restriction significantly increased (p less than 0.02) plasma renin activity, ANG II, and aldosterone levels; the aldosterone response to ANG II was enhanced twofold (p less than 0.01); and the blood pressure response to ANG II infusion was reduced significantly (p less than 0.05). Despite a fixed and low plasma ANG II concentration when enalapril was employed, the adrenal response to ANG II on the low salt diet was enhanced to the same degree as that observed before administration of the converting enzyme inhibitor. Conversely, enalapril substantially altered the blood pressure response to ANG II with sodium restriction, completely preventing the reduction in responsiveness. If the subjects were first given enalapril and then sodium intake was restricted, ANG II levels did not change significantly but renal excretion of both sodium and potassium was substantially modified. The rate at which renal excretion of sodium fell to match intake was retarded strikingly (p less than 0.001); conversely, renal retention of potassium increased significantly (p less than 0.03) as low salt balance was attained. Possibly because of the potassium retention, aldosterone levels rose, but significantly less than when enalapril was absent.
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PMID:Role of angiotensin II in the hormonal, renal, and electrolyte response to sodium restriction. 302 57

Renin heterogeneity has been described in rat kidney and plasma. In this study, we used the isoelectric focusing method to 1) characterize the adrenal renin forms in control rats, in rats on low- and high-Na diets, and in nephrectomized rats; and 2) examine their resemblance with plasma renin. Active renin (AR) and inactive trypsin-activatable renin (IR) were measured in adrenal homogenates and plasma. Aliquots were subjected to isoelectric focusing gels. Activation with trypsin (5 mg/ml) was performed before or after isoelectric focusing. Results showed that adrenal glands contained AR and IR. The content of adrenal AR increased significantly only in rats fed a low-Na diet. Following anesthesia, nephrectomy, or high-Na intake, the content of adrenal AR and IR was not significantly changed. In plasma, an inverse relationship between AR and IR was found. Adrenal glands contained six forms of AR focusing at the same pH as those of plasma AR but in different proportions. After activation of IR in adrenal glands, two additional renin forms focusing at pH 6.4 and 6.1 were found, whereas after activation of plasma IR, two peaks focusing at pH 5.9 and 4.8 were significantly enhanced. Adrenal AR forms were modified by alterations of salt and water balance differently than plasma AR. These results support the hypotheses of an endogenous production of renin forms by the adrenal gland.
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PMID:Multiple renin forms in the adrenal gland. 305 4

The effects of environmental air temperature of 6 degrees C and 26 degrees C on catecholamines (CA) and circulation were studied in eight male subjects during rest and during bicycle exercise at WOBLA for 45 min each. We found that resting at 6 degrees C increased the norepinephrine (NE) levels to the same levels as endurance exercises at 6 degrees C. The increase of CA levels was 2.5 to 3 times higher during work at 26 degrees C compared with 6 degrees C. During both rest and exercise at 6 degrees C we found a higher stroke volume of the heart and a reduced heart rate (HR) with no or only small effects on the oxygen uptake and blood lactate levels compared with 26 degrees C. Measurements of the skin temperatures showed large differences both at rest and during work; those of core temperature showed no changes at rest and a slightly more pronounced increase during work at 26 degrees C compared with 6 degrees C. The behavior of CA, plasma renin activity (PRA), plasma aldosterone (PA), and circulation were studied in 13 top class swimmers and 12 recreational swimmers during immersion into water of 27 degrees C for 10 min. The recreational swimmers were additionally immersed into water of 21 degrees C and 33 degrees C. Even immersion at 33 degrees C induced a small but significant increase of NE levels and of blood pressure (BP) values with no effect on the HR and blood lactate values. Epinephrine (EPI) showed a tendency to decrease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of temperature and water immersion on plasma catecholamines and circulation. 305 72

The purpose of study was to investigate the role of angiotensin II in idiopathic primary aldosteronism (IPA) and to evaluate the interest of angiotensin converting enzyme inhibitors (ACEI) in its management. The study concerned 10 hypertensive patients, mean 49 +/- 11 years with idiopathic primary aldosteronism due to bilateral adrenal hyperplasia: plasma renin activity (PRA) less than 1.5 ng/ml/h and plasma aldosterone (PA) greater than 25 ng/100 ml. Adrenal venography and adrenal vein aldosterone levels demonstrated bilateral hyperplasia. PRA and PA were evaluated in recumbent position, then after 4 hours in upright posture. The next day, a "captopril screening test" was performed with PA assays before and three hours after a single oral administration of captopril (1 mg/kg). Upright PRA and PA were slightly increased and acute administration of captopril reduced significantly PA levels in all patients. Blood pressure (BP was unmodified under captopril. These hormonal results demonstrated that adrenal glomerulosa remained sensitive to low concentrations of angiotensin II, and underlined the potential interest of ACEI in the management of IPA. Brown R. demonstrated already an increase of adrenal sensitivity to angiotensin II infusions, and isolated an aldosterone-stimulating factor (ASF). Plasma aldosterone levels were related to increased ASF concentrations but there was no link between PRA and ASF. Carey R. suggested that ASF acts through an increase of the sensitivity of aldosterone production to angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Influence of angiotensin on the secretion of aldosterone in idiopathic hyperaldosteronism]. 311

Two female patients were admitted for evaluation of hypertension and hypokalaemia. Plasma renin activity was suppressed and plasma aldosterone levels were within the normal value in a 52-year-old woman and below the normal value in the other patient, a 62-year-old woman. Plasma 11-deoxycorticosterone (DOC) levels were as high as 1.13 and 1.47 nmol/l, respectively. Adrenal scintigram and abdominal CT scan clearly showed a right adrenal tumour in the 52-year-old woman. After adrenalectomy plasma DOC level decreased to the normal level of 0.12 nmol/l, and her blood pressure and serum potassium became normal. Abdominal CT scan revealed no finding of adrenal tumour in the older woman. These results indicate that these two patients had hypermineralocorticism with elevation of plasma DOC. One patient had a DOC-producing adrenal adenoma, and the other probably had bilateral adrenal hyperplasia.
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PMID:Hypermineralocorticism without elevation of plasma aldosterone: deoxycorticosterone-producing adrenal adenoma and hyperplasia. 325 72

A 9-year-old boy who complained of fatigue, myalgias, and progressive weakness was found to have a markedly elevated serum creatine phosphokinase (CPK). He developed polyuria with polydipsia and was noted to be hypertensive and severely hypokalemic. Treatment with potassium and spironolactone alleviated his signs and symptoms and normalized the blood pressure and CPK. Initial studies revealed low plasma renin activity that did not increase with change from supine to upright position. Plasma aldosterone was consistently elevated in the supine position, decreased with upright posture, and was not suppressed by administration of dexamethasone. Plasma 18-hydroxycorticosterone also was elevated. Enhanced computerized tomography (CT) revealed a mass in the left adrenal that had not been seen on the initial unenhanced scan. Adrenal vein catheterization confirmed elevated plasma aldosterone on that side. Adrenalectomy was performed, and a well-encapsulated adenoma was found at examination of the surgical specimen. Postoperatively, suppression of plasma renin activity continued for many months without signs of aldosterone deficiency.
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PMID:Aldosterone-producing adenoma presenting with hypokalemic myopathy. Case report and review. 329 4


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