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)

Angiotensin II (Ang II) controls renal plasma flow, which depends on perfusion pressure and on renal vascular resistances; the glomerular filtration rate of single nephrons (SNGFR) also depends on these two parameters. The glomerulus can synthesize all components of the renin-angiotensin system. Renin is produced by mesangial cells and cells of afferent arterioles, angiotensinogen by mesangial cells, and angiotensin I-converting enzyme (ACE) by endothelial and mesangial cells. Ang II binds to afferent and efferent arterioles and to mesangial cells, which subsequently contract and enhance their production of vasodilator prostaglandins. Ang II participates in the regulation of the SNGFR by acting on arteriolar resistance, on the glomerular capillary surface area, and finally on the ultrafiltration coefficient. The synthesis of renin is initiated when the cAMP concentration increases under the influence of hormones (parathyroid hormone, catecholamines), of mediators (e.g., prostanoids), or of changes in composition of tubular fluid (in sodium, chlorine, or calcium) detected by the macula densa. Moreover, renin synthesis is stimulated by decreases in intracellular calcium concentration. The renin-angiotensin system plays an important role in the regulation of glomerular filtration. A decrease in renal plasma flow is followed by an increase in glomerular efferent arteriole resistance, so that perfusion pressure and glomerular filtration remain constant. Furthermore, if the decrease in renal plasma flow is more marked, vasodilator prostaglandins, whose synthesis is stimulated by Ang II, dilate afferent arterioles, which sustains glomerular filtration. Prostaglandins are also apt to bind to the juxtaglomerular apparatus and to increase the intracellular cAMP level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of the renin-angiotensin system in the regulation of glomerular filtration. 248 24

51 patients with mild essential hypertension (EH) were randomly divided into two groups; the first group (31 patients) was treated with 1 g. of oral calcium during a period of 8 weeks; the second group received a placebo. The treated with calcium showed a significant decrease in blood pressure (BP), the maximal reduction being of 6 mm Hg in the systolic pressure (SBP) and 3 mm in the diastolic (DBP) at the end of the 8th week. We found a substantial positive relationship between the decrease in SBP and seric renin activity (p less than 0.05), as well as a significant negative relationship (p less than 0.05) between DBP and the seric level of parathyroid hormone (PTH). During the administration of the oral calcium supplement, the BP decreased in an inverse proportion to the plasmatic renin and seric level of PTH.
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PMID:[Effect of an oral calcium supplement in the treatment of slight-to- moderate essential arterial hypertension]. 249 21

After burn trauma, a very marked endocrine response occurs. Almost all the known hormones take part in it. Their response influences very much the postburn metabolic changes and participates in the integration of the body's response with the nervous and immune systems. In this review, mainly the changes in various hormone levels are described, as well as the possible role of the acute phase response after burn trauma, and the communications between the endocrine and immune systems, the cells of the latter are able to respond to various hormonal stimuli and to secrete various hormones themselves. Some of the hormones are very sensitive indicators of the burn stress, e.g., the T3 levels (very low), testosterone in males (very low), dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) (very low), ADH, catecholamines, renin and angiotensin II, cortisol (high), 17-beta-estradiol in males (usually elevated). Other hormones are usually elevated, but not always (ACTH, aldosterone, prolactin, glucagon, immunoreactive insulin, beta-endorphin, rT3, 11-beta-hydroxyandrostenedione), but there are hormones that are unually low (T4, FSH, androstenedione, progesterone--the latter especially in females). Calcitonin, parathyroid hormone, growth hormone are sometimes elevated, as well as LH (measured with RIA methods). TSH is usually normal, the biologically measured LH was reported to be low. The levels of the sensitive indicators of burn stress may be used to evaluate the effect of treatment: if the burn patient is properly treated, the indicators may become earlier normal.
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PMID:Endocrine changes after burn trauma--a review. 251 73

To evaluate the relationship between the elevation of blood pressure and altered bone metabolism, the changes of systolic blood pressure in six experimental models for bone disorders were investigated. Rats used were either parathyroidectomized, ovariectomized, fed with a calcium-deficient diet, fed with a vitamin D-deficient diet, treated with HEBP (1-Hydroxyethylidene-1, 1-bisphosphonate) or treated with streptozotocin. Hypertension developed in 5-week-old male rats fed with a calcium-deficient diet for 2 weeks, which evoked hypocalcemia and nutritional hyperparathyroidism. The blood pressure returned to normal when fed with a normal calcium diet. In parathyroidectomized rats receiving a normal calcium diet, the blood pressure did not rise, though the plasma calcium level decreased to an extent similar to the rats fed with the calcium-deficient diet. These findings seem to indicate that hyperparathyroidism, but not hypocalcemia, was involved in the elevation of blood pressure in rats fed with a calcium-deficient diet. Hypertension was not observed in rats fed with a vitamin D-deficient diet or treated with streptozotocin. These rats showed not only an increase in parathyroid hormone (PTH) but also a decrease in 1,25 (OH)2 D3. These results may suggest that the presence of 1,25 (OH)2D3 as well as the enhanced parathyroid function is necessary for the development of hypertension. The elevated blood pressure was reduced by a calcium antagonist, nifedipine, or by calcium supplementation, but not by an inhibitor of angiotensin-converting enzyme, captopril, or by calcitonin. This may indicate that hypertension due to nutritional hyperparathyroidism responds to the calcium antagonist nifedipine and to calcium supplementation, but does not depend on renin or salt. Furthermore, an acute hypotensive effect by human PTH (1-34) was not observed in the hypertension of calcium-deficient rats, suggesting the difference between acute and chronic effects of PTH. The hypertension developed in the present experiment may be a useful model for pharmacological evaluation of antihypertensive drugs, such as calcium and calcium antagonists.
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PMID:[Pharmacological study on blood pressure in rats with bone disorders]. 253 55

In recent years abnormalities of calcium metabolism have been described in human hypertension. In this study, the relationships between indices of calcium metabolism and the renin-aldosterone system were studied in 39 subjects with untreated essential hypertension. No significant associations were found between the major determinants of calcium metabolism (plasma ionised calcium, parathyroid hormone and 1,25(OH)2-vitamin D) and the renin-aldosterone system. Serum magnesium was, however, positively correlated to plasma renin activity (PRA) (r = 0.38, P less than 0.05) while both 24 h urinary excretion of calcium and cAMP were found to be correlated to both PRA and urinary aldosterone in a positive way (r = 0.39-0.42, P less than 0.01 and r = 0.33-0.57, P less than 0.01, respectively). In this study there was no other evidence of any major influence of the renin-aldosterone status on the calcium balance in human hypertension. The urinary leak of calcium might be determined by the action of the renin-aldosterone system.
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PMID:An association between mineral metabolism and the renin-aldosterone system in human hypertension. 254 51

Basolateral membranes were prepared from rat renal cortex by density gradient centrifugation. Their purity was confirmed by electron microscopy and by marker enzyme enrichment. The basolateral membrane preparation was shown to be derived predominantly from the proximal renal tubule by measurement of hormone-stimulated adenylate cyclase; marked stimulation of adenylate cyclase was found with parathyroid hormone, but not with isoprenaline, antidiuretic hormone or calcitonin. A single class of specific high-affinity [3H]angiotensin II-binding site was identified in the basolateral membrane preparation which, after correction of results for tracer degradation, showed equilibrium dissociation constant of 0.23 nmol/l and binding site concentration of 485.8 fmol/mg protein. Binding sites for [3H]angiotensin II were measured in basolateral membranes prepared from rats fed diets with a low, normal or high sodium content. A trend of increased binding site density with reduced sodium intake was found which did not reach statistical significance. No effect on affinity was demonstrated. Treatment of rats on a low-sodium diet with captopril (500 mg/l drinking water) caused a significant reduction in binding site density; no effect on affinity was demonstrated. These findings suggest that the density of angiotensin II receptors at this site is altered by the activity of the renin-angiotensin system.
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PMID:[3H]angiotensin II binding to basolateral membranes from rat proximal renal tubule: effect of sodium intake and captopril. 254 61

Nifedipine was administered orally to 2 patients with primary hyperparathyroidism before and after parathyroidectomy. The operation lowered serum calcium concentration and parathyroid hormone but did not alter plasma renin activity, plasma aldosterone concentration, and serum magnesium. The hypotensive effects of nifedipine were markedly enhanced with the decrease in serum calcium concentration following parathyroidectomy. Thus, the level of serum calcium concentration may modulate the hypotensive effect of nifedipine in humans.
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PMID:Hypotensive effects of nifedipine in patients with primary hyperparathyroidism: case reports. 259 42

The aim of this study was to assess the effect of hypercalcaemia due to primary hyperparathyroidism on the pressor and aldosterone responses to angiotensin II (Ang II) infusion. Five patients with hyperparathyroidism were studied, before and after parathyroidectomy, and were compared with five normal subjects. After 30 min of equilibration, Asp1-Val5 Ang II was infused in all subjects at stepwise increasing dose rates of 2 and 4 ng/kg per min for 30 min each. In the hyperparathyroid patients the baseline levels of plasma parathyroid hormone and calcium were significantly higher than in the controls, and returned to normal after the parathyroidectomy; plasma aldosterone and renin activity were normal both before and after the parathyroidectomy. Two hyperparathyroid patients had high blood pressure levels, which were normalized after surgery. The increase in the aldosterone response from baseline at each time point of the Ang II infusion was greater in the hyperparathyroid patients before than after the operation (P less than 0.05), and greater than in the normals (P less than 0.05). No difference in the increased response of systolic or diastolic blood pressure was observed between the hyperparathyroid patients, either before or after the parathyroidectomy, and the normal subjects. High levels of extracellular calcium or parathyroid hormone, or both, might play a primary role in the aldosterone hyper-responsiveness to Ang II in the hyperparathyroid patients. The similar pressor response to Ang II in hyperparathyroid patients and the normal subjects suggests that hypercalcaemia does not potentiate the vasoconstrictive action of Ang II.
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PMID:Aldosterone and pressor responses to angiotensin II in primary hyperparathyroidism. 263 14

Patients with essential hypertension, in particular those with low plasma renin activity (PRA), are reported to have lowered plasma-ionized calcium and elevated parathyroid hormone levels. In this study 1 microgram alphacalcidol (1 alpha-hydroxy-vitamin D3) was given in a double-blind, placebo-controlled fashion over four months to 39 subjects with mild to moderate hypertension. There was a significant rise in PRA in the treatment group when compared to placebo (P less than .05), but the mean blood pressure response was similar in the two groups. When the treatment group was divided according to pretreatment PRA it was, however, seen that subjects with low PRA displayed a reduction in diastolic blood pressure, whereas those with high PRA raised their blood pressure compared to placebo. Also subjects with low pretreatment values for plasma-ionized calcium and high levels of parathyroid hormone showed a reduction in diastolic blood pressure. This study supports the idea of a relationship between calcium metabolism and the renin-aldosterone system in essential hypertension and describes a beneficial effect of vitamin D supplementation on blood pressure in low-renin hypertension.
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PMID:Reduction of blood pressure during long-term treatment with active vitamin D (alphacalcidol) is dependent on plasma renin activity and calcium status. A double-blind, placebo-controlled study. 264 69

In a study population that comprised 34 normal black pregnant women, biochemical changes are compared between a group of women who received 1.5 gm of calcium supplementation a day and a group of women who received placebos. The blood pressure-lowering effect of calcium supplementation appears to involve a mechanism that relates parathyroid hormone and plasma renin activity. Other alterations in calcium and magnesium metabolism, as reflected by increased urinary calcium excretion and serum magnesium levels, may also contribute to this effect. Subgroups of study participants with initial (less than 26 weeks' gestation) low levels of serum calcium and plasma renin activity are the ones with the largest reductions in blood pressure. Whether these alterations can produce a reduction in the incidence of pregnancy-induced hypertension is the next question to be answered in this area.
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PMID:Biochemical changes associated with blood pressure reduction induced by calcium supplementation during pregnancy. 264 39


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