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)

The effect of thyroid hormone on renin productiona and release by rat kidney slices was studied. Rat kidney slices were incubated in Warburg flasks containing Krebs-Ringer-Phosphate- Glucose- Dextran solution at 37 C for 5 hours. Renin content, renin released into the incubation media and oxygen consumption were measured. Kidney slices actively secreted renin. Kidney slices of hyperthyroid rats released more renin, and kidney slices of hypothyroid rats released less renin than normal kidneys (p less than 0.001). The addition of 1-thyroxine to the incubation medium increased significantly (p less than 0.001) renin release by kidney slices from normal and hypothyroid rats. Thyroid hormone affects renin release through a mechanism independent of the ouabain-sensitive sodium pump and protein synthesis, since ouabain and cycloheximide did not modify renin release or production. The results of this study suggest that thyroid hormone plays a role in renin release from the juxtaglomerular cells.
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PMID:The effect of thyroid hormone on renin production and release by rat kidney slices. 61 72

Angiotensin II (AII)-like immunoreactivity (LIR) was detected by immunostaining in 7.5 +/- 1.1% of cells obtained by redispersion of pituitary cell aggregates from 15- to 20-day-old female rats, cultured for 5-7 days in serum-free medium supplemented with thyroid hormone and dexamethasone. Also, renin-LIR was retained in these cultures. As shown by double immunostaining of paraffin-embedded sections of the aggregates, this AII-LIR was localized only in gonadotrophs. AII-LIR was detected at least up to 5 weeks in culture. On reversed-phase, high-performance liquid chromatography (HPLC), this AII-LIR co-migrated with authentic AII. In perifused aggregate cell cultures of 15- to 20-day-old female rat pituitary maintained in serum-free medium supplemented with dexamethasone (DEX) and triiodothyronine (T3), AII stimulated GH release. AI and AIII had a similar effect. To evaluate the possible involvement of endogenous AII in the local regulation of GH release, gonadotrophs were stimulated with luteinizing hormone-releasing hormone (LHRH). LHRH displayed a transient inhibitory effect on GH release, which was followed by a rebound of GH release after withdrawal of the peptide. Treatment of aggregates with pertussis toxin reversed this inhibitory effect into a significant stimulation of GH release. In aggregates cultured in serum-supplemented medium, LHRH provoked a significant stimulation of GH release which was still followed by a post-stimulus rebound release. In hemipituitaries from 5-day-old rats, a significant stimulatory effect of LHRH on GH release was found without rebound secretion. To evaluate the possible involvement of endogenous AII in the effects of LHRH on GH release, the influence of (Sar1,Ala8)AII, a peptide AII receptor antagonist, and of DUP753, a non-peptide AII receptor blocker was tested in various in vitro conditions. The effect of LHRH on GH release in aggregates cultured either in serum-free medium supplemented with DEX and T3 or in serum-supplemented medium was not affected by (Sar1,Ala8)AII, not even after enhancing the LHRH-induced GH release by treatment of the aggregates with pertussis toxin. A hundred times lower concentration of (Sar1,Ala8)AII, however, abolished the AII-induced changes in GH release. Also DUP753 (10 microM) failed to block LHRH-induced GH release in aggregates. (Sar1,Ala8)AII also failed to block the effect of LHRH on GH release from hemipituitaries. It is concluded that LHRH has inhibitory and stimulatory effects on GH release in cultured pituitary cell aggregates.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin II is retained in gonadotrophs of pituitary cell aggregates cultured in serum-free medium but does not mimic the effects of exogenous angiotensins and luteinizing-hormone-releasing hormone on growth hormone release. 147 13

In previous studies we found that plasma angiotensinogen levels were reduced by lesions of the hypothalamic paraventricular nuclei. To determine if the decrease was caused by decreased secretion of hormones that normally stimulate angiotensinogen secretion by the liver, we correlated the changes in plasma angiotensinogen produced by paraventricular lesions with changes in plasma LH, ACTH, and thyroid hormones; compared the changes in plasma angiotensinogen and other hormones to those produced by hypophysectomy; and determined the effects of treatment with ACTH and T4 in animals with paraventricular lesions. In male Sprague-Dawley rats, bilateral lesions destroying more than 50% of the paraventricular nuclei decreased plasma angiotensinogen to 787 +/- 52 ng angiotensin-I/ml in 7 days compared to 1576 +/- 142 ng angiotensin-I/ml in sham-operated controls. Plasma T3 and T4 were also reduced, whereas there were no statistically significant changes in plasma ACTH or LH. Hypophysectomy produced a comparable decline in plasma angiotensinogen and thyroid hormone levels. Daily administration of a single dose of ACTH had no effect on plasma angiotensinogen in rats with paraventricular lesions, but T4 treatment restored plasma angiotensinogen to normal levels. The data indicate that the decline in circulating angiotensinogen produced by lesions of the paraventricular nuclei is caused by the decrease in the secretion of thyroid hormones produced by these lesions. They also demonstrate that in addition to regulating circulating renin via the sympathetic nervous system, the brain has an effect on circulating angiotensinogen via neuroendocrine control of thyroid function.
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PMID:Neuroendocrine regulation of plasma angiotensinogen. 164 50

We studied the expression of angiotensinogen and renin genes in rats treated with 3,3',5-triiodo-L-thyronine (T3) at doses of 0.1 and 1 mg/kg of body weight. Liver angiotensinogen mRNA increased by 2 to 3 times 8 to 12 hours after T3-treatment. This increase was dose-related. Plasma angiotensinogen concentration (PAC) increased 12 hours after T3-treatment. Brain and renal angiotensinogen mRNA levels and the renal renin mRNA level remained the same throughout the experimental periods. These results suggest that the thyroid hormone initially increases angiotensinogen mRNA and leads to an increase in the production of angiotensinogen in the liver followed by an elevation of PAC.
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PMID:Effects of thyroid hormone on angiotensinogen and renin messenger RNA levels in rats. 217 6

Plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA) and aldosterone were consecutively measured during methimazole treatment in patients with hyperthyroidism due to Graves' disease. ANP values of untreated hyperthyroid patients varied greatly from patient to patient, but decreased progressively with a decrease of serum thyroid hormone concentration during methimazole treatment. PRA was elevated in hyperthyroid patients but less aldosterone was secreted as evidenced by lower aldosterone/PRA ratio in these patients than in normal subjects and in hypertensive patients treated with thiazide. In addition, aldosterone/PRA ratio increased progressively with a decrease of ANP during methimazole treatment. The data indicated that ANP secretion was increased and ANP thus secreted depressed aldosterone secretion in hyperthyroid patients. Propranolol depressed pulse rate but failed to affect ANP secretion. It is suggested that thyroid hormone specifically acts on myocytes to stimulate ANP secretion but physiologic significance of such increased ANP secretion remains to be solved.
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PMID:Plasma atrial natriuretic peptide, plasma renin activity and aldosterone during treatment of hyperthyroidism due to Graves' disease. 253 Nov 14

The development of recombinant DNA technology has introduced new directions for the study of the angiotensinogen molecule. The cloning and sequencing of the human and rat cDNAs demonstrate the similarity of angiotensinogen to various serine protease inhibitors produced by the liver and was the beginning of studies looking for new physiological roles of angiotensinogen, in addition to the substrate for renin. The determination of the nucleotide sequence of these cDNAs also allowed the identification of angiotensinogen mRNA in many tissues in addition to the liver that is the major site of synthesis. This multilocalization of angiotensinogen is one of the arguments for the presence and the function of local renin-angiotensin systems. Finally, the hepatic biosynthesis of angiotensinogen is regulated by many different hormonal factors including glucocorticoid, estrogen, thyroid hormone, insulin, and angiotensin II. The cloning of the angiotensinogen gene offers the opportunity to study this regulation at the transcriptional level. We present in this paper a review of the literature concerning the new aspects of angiotensinogen using molecular biological tools and its regulation together with the characterization of the human angiotensinogen gene.
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PMID:Regulation of angiotensinogen gene. 256 14

The effect of thyroxine (T4) replacement on the increased renal beta-adrenergic receptor number and the increased beta-adrenergic dipsogenic responsiveness of fasted rats was studied in male Sprague-Dawley rats. Food deprivation significantly decreased serum thyroxine (T4) and triiodothyronine (T3) levels, increased the dipsogenic response to isoproterenol, and elevated renal beta-adrenergic receptor concentration. Daily administration of T4 (40 micrograms/kg) to food-deprived rats restored serum thyroid levels to normal. Thyroxine replacement also reduced the increased beta-adrenergic dipsogenic responsiveness in the food-deprived rats to control levels. In addition, daily administration of thyroxine reduced the beta-adrenergic receptor concentration in renal cortices to that observed in controls. Thyroid treatment tended to decrease the isoproterenol-induced renin release in food-deprived rats and increase the response in the control rats. These results suggest that the relative hypothyroid state observed in the food-deprived rat may be responsible for the increased concentration of renal beta-receptors and the associated activation of the renin-angiotensin system, which may be partially responsible for the observed increased dipsogenic response induced by isoproterenol. Collectively, the data reaffirm the interaction of thyroid hormone and beta-adrenergic responsiveness, although it is of interest that, in regard to renal beta-receptors, the concentrations are decreased to normal by thyroid treatment, whereas previous studies in hypothyroid rats demonstrate an increase to normal of cardiac beta-receptors. This would suggest thyroid hormone may normalize a response in an opposite direction depending on the direction of the disturbance.
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PMID:Thyroxine, renal beta-adrenergic receptors, and dipsogenesis in food-deprived rats. 282 30

Angiotensin-converting enzyme (ACE) was measured in plasma of patients with Graves' disease and with toxic nodular goiter, as well as in their treated counterparts and in normal controls. A significant elevation of ACE levels and a positive correlation between ACE, thyroxine, and triiodothyronine levels was found in both groups of thyrotoxicosis. Parallel fluctuations of triiodothyronine and ACE levels, albeit with a certain lag of the latter, was observed in patients in whom multiple measurements were taken. ACE levels, which were also determined in hypothyroid patients and in patients with euthyroid goiter on suppression therapy, were in the same range as normal controls and as in treated thyrotoxic patients. We conclude that the pathogenesis of thyrotoxicosis does not play a role in ACE elevation but that increased thyroid hormone seems to induce elevation of ACE. ACE elevation in thyrotoxicosis may constitute an integral part of the renin-angiotensin axis.
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PMID:Comparison of serum angiotensin-converting enzyme in Graves' disease, toxic nodular goiter, and other thyroid conditions. 298 14

Renin in the female mouse submandibular gland (SMG) is known to increase in response to thyroid hormone. In the present study a 500 base-pair renin cDNA was used to quantify renin mRNA, the product of transcription of the Ren-2 gene, in the female mouse SMG in response to thyroid hormone to assess more directly the nature of stimulation of renin biosynthesis. After daily injection for 1 wk renin mRNA increased from control values of 36 +/- 3 SE ng/g tissue to 212 +/- 41 with triiodothyronine (T3; P less than 0.005) and to 217 +/- 33 with thyroxine (T4; P less than 0.005). Treatment of mice with propylthiouracil (PTU) decreased renin mRNA to 1.2 +/- 0.3 (P less than 0.005) and after subsequent injection of T3 for 1 wk renin mRNA increased to 289 +/- 35 ng/g tissue. The time course of the response to a single injection of thyroid hormone indicated a rapid response with significant increases in renin mRNA by 1 h, reaching values 3.5 +/- 0.4 times control (P less than 0.005) by 5 h. Such rapid effects are consistent with a direct nuclear action of thyroid hormone in stimulating transcription of the Ren-2 gene in mouse submandibular gland or in stabilization of nuclear precursor renin mRNA or both.
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PMID:Stimulation by thyroid hormone of renin mRNA in mouse submandibular gland. 352 82

The transcriptional activity of renin genes in the mouse kidney and submandibular gland (SMG) was examined by measurement of renin messenger RNA (mRNA) (nanograms per g tissue) and compared with renin activity (micromoles angiotensin I per h/g tissue). In control adult mice renin mRNA and renin activity (in parentheses) were 1.8 +/- 0.24 (11 +/- 1.1) in male kidney, 3.6 +/- 0.66 (18 +/- 2.8) in female kidney, 230 +/- 34 (903 +/- 59) in male SMG, and 31 +/- 6 (188 +/- 47) in female SMG (mean +/- SE, n = 6). The ratio of renin mRNA among these four tissues was similar to that of renin activity (1:2:100:17, respectively). Although the values in male kidney were one one-hundredth those in SMG, 1000 to 10000 times more SMG cells are involved per gram of tissue so that, per renin-synthesizing cell, kidney values would be 10 to 100 times SMG values. Expression of renin gene(s) in a renal juxtaglomerular cell may thus be higher than in a SMG granular duct cell. Values in adult male SMG were a consequence of a 40-fold rise at puberty, were decreased to 16% (+/- 3.8) by castration, but were not significantly influenced by treatment with testosterone, T4, propylthiouracil, sodium depletion, or spironolactone. Renin mRNA in adult female SMG was 18-fold higher than juvenile values, was increased 10-fold (+/- 1.6) by testosterone (to adult male levels) and 5.5-fold (+/- 0.81) by T4 (P less than 0.005), but was decreased to 42% (+/- 29) of normal by propylthiouracil (P less than 0.05). Propylthiouracil caused a small but significant decrease in testosterone-treated female values. In the kidney renin mRNA was increased 3.0-fold (+/- 0.30) by captopril, 2.3-fold (+/- 0.23) by a low sodium diet, and 1.7-fold (+/- 0.13) by spironolactone after 1 week, whereas T4, testosterone, or propylthiouracil had little or no effect. Sialoadenectomy increased renin mRNA and renin in male but not in female kidney, suggesting that a SMG factor, possibly renin, may have a role in suppression of renin synthesis in male kidney. In conclusion, measurement of renin mRNA suggests that testosterone regulates renin gene expression by a direct effect in male mouse SMG, whereas in the female regulation is by thyroid hormone. In the kidney conditions which increase renin content are accompanied by parallel (5-fold higher) increases in renin mRNA, suggesting enhanced expression of renin gene(s) in renal juxtaglomerular cells in chronic low sodium states.
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PMID:Studies of the regulation of mouse renin genes by measurement of renin messenger ribonucleic acid. 389 95


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