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)

It has been shown that the severity of experimentally induced acute renal failure (ARF) is inversely related to dietary sodium chloride intake, and the effects have been attributed to the concurrent changes in renal renin. In the current study, renal renin of rats was increased by chronic sodium deprivation and decreased by chronic sodium loading and DOCA administration. In two nephrotoxic models (mercuric chloride, uranyl nitrate), giving previously sodium-deprived rats 1% sodium chloride to drink for 48 hours prior to ARF induction greatly attenuated the severity without any reduction in their high renal renin. Conversely, giving previously sodium-loaded rats tap water to drink for 4 to 5 days prior to AFR induction greatly enhanced the severity without any increase in their subnormal renal renin. Therefore, the changes in severity of ARF resulting from changes in dietary sodium are not mediated by changes in renal renin. Significant inverse correlations were found between mean peak BUN values during the follow-up period (5 to 7 days) and the 24-hour urinary sodium excretions prior to ARF induction in both models, suggesting that sodium intake and/or excretion at the time of induction is a good predictor of the severity. The effects of sodium chloride in both models were predominantly expressed during the maintenance phase, and consisted of attenuation of the severity (both models) and hastening of the recovery (mercuric chloride model). Possible mechanisms by which dietary sodium produced its effects, independently of its effects on the renin-angiotensin system, are discussed.
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PMID:Sodium-chloride-induced protection in nephrotoxic acute renal failure: independence from renin. 39 16

The effects of treatment with a spironolactone derivative (SC 14266) for 9 experimental weeks on blood pressure and plasma renin activity (PRA) were investigated in unilaterally nephroadrenalectomized rats drinking 1% saline ("unilater nephrectomy"), unilaterally nephroadrenalectomized and contralaterally adrenal-enucleated rats drinking 1% saline ("adrenal enucleation") and intact rats drinking tap water ("normal"). The development of hypertension in "adrenal enucleation" rats was prevented by treatment with SC 14266 and the drug did not significantly affect the blood pressure in either "unilateral nephrectomy" or "normal" rats. SC 14266 did not influence a low level of basal PRA and the blunted response of PRA to furosemide administration in either "unilateral nephrectomy" or "adrenal enucleation" rats. On the other hand, PRA after furosemide administration in "normal" rats receiving SC 14266 was significantly higher than that in those rats treated with vehicle. The results suggest that the mineralocorticoid(s) secreted by the enucleated adrenal has a hypertensogenic property but no effect on the suppression of renin secretion under a high sodium intake and the unilateral nephrectomy.
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PMID:Effect of a spironolactone derivative (SC 14266) on Plasma renin activity in adrenal regeneration hypertension. 99 34

1. Complete ligation of the aorta between the origins of the two renal arteries in the rat produces a predictable form of accelerated hypertension. Changes in the blood pressure, plasma renin activity and renal histological lesions have been studied. 2. Group 1 rats and their control group (group 2) received tap water, and group 3 and its control group (group 4) received sodium chloride solution (0-154 mol/l) in place of tap water, for 4 weeks before aortic ligation. In the experimental groups 1 and 3, complete ligation was carried out. In groups 2 and 4 the aorta and renal arteries were exposed, but not ligated. Interlobular artery lesions were studied on a blind basis and graded 0-4 according to severity. 3. Groups 1 and 3 developed severe hypertension. In group 1 the raised mean arterial pressure showed a significant correlation with increased plasma renin activity. Both mean arterial pressure and plasma renin activity also showed a significant correlation with changes in interlobular arteries. In group 3 the raised mean arterial blood pressure did not show a significant correlation with the depressed plasma renin activity, or with changes in interlobular arteries. A significant correlation was, however, found between plasma renin activity and interlobular artery lesions in group 3. 4. These results suggest that the renin-angiotensin system may influence renal vascular lesions through some mechanism independent of the blood pressure.
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PMID:Accelerated hypertension in the rat: relation between renin, renal vascular lesions, salt intake and blood pressure. 107 10

To clarify the role of the enucleated adrenal in the suppression of plasma renin activity (PRA) in adrenal regeneration hypertension (ARH), PRA response to furosemide administration was compared at the 9th experimental week in three groups of rats, which had been subjected to (a) sham operation (control), (b) unilateral nephrectomy, (c) unilateral nephrectomy plus contralateral adrenal enucleation, and given on tap water or high sodium intakes. Urine volume and sodium, and changes in body weight and hematocrit, determined 90 min after administration of furosemide, did not show any significant differences among any of the experimental groups. The basal PRA was significantly decreased in rats of the other groups as compared to the control rats drinking tap water. A decrease in basal PRA was much more pronounced in the unilaterally nephrectomized rats with or without an enucleated adrenal, drinking saline. After furosemide administration, PRA significantly increased in the control rats drinking saline as well as in the unilaterally nephrectomized rats drinking tap water, with or without an enucleated adrenal, but the PRA values in these three groups were only half those of the control rats drinking tap water. An insignificant increase in PRA was found in unilaterally nephrectomized (plus or minus enucleation) rats drinking saline. These findings suggest that the lack of a PRA response in ARH may be due to the pronounced suppression of the juxtaglomerular cells caused by a high sodium intake and the reduction of the renal mass, independently of the corticosteroid(s) secreted by the enucleated adrenal.
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PMID:Suppressed plasma renin activity in adrenal regeneration hypertension. 112 88

Kidney extract from rats which were adrenalectomized and given tap water was dialyzed, salted out, ultrafiltrated or heated. A given dose of each extract or fractionized material was administered to uninephrectomized rats subcutaneously every 12 hours for 10 days. The relationship between renin content of each sample and final blood pressure level following repeated injections as an index of its hypertension-inducing potency was analyzed. There was no apparent discrepancy between the two of each sample. No evidence was obtained for the existence of other renal substance than renin which might be implicated in producing hypertension.
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PMID:Hypertension-inducing potency and renin content of variously treated kidney extract. 115 98

1) To clarify the role of adrenal enucleation on plasma renin activity (PRA), plasma renin substrate (PRS), PRA response to furosemide administration and vacular reaction to renin in adrenal regeneration hypertension (ARH), serial changes of PRA and PRS during adrenal regeneration, PRA response to furosemide administration, and pressor response to exogenous renin in ARH were investigated by comparison with those of intact rats, unilaterally adrenalectomized rats, and unilaterally nephroadrenalectomized rats with contralateral adrenalectomy or with contralateral adrenal exploration (control) on both tap water and high sodium intake. 2) The control rats drinking saline, when compared with intact rats drinking tap water, showed significant decreases in PRA and, concomitantly, significant increases in PRS throughout the experimental period. In the unilaterally nephroadrenalectomized rats drinking saline, two days after adrenal enucleation or adrenalectomy, a significant increase in PRA, with a concomitant decrease in PRS, was observed. Those changes were less pronounced in the adrenal enucleated group than in the adrenalectomized group. Ten days later PRA markedly decreased to the control level in both groups. PRS rose to the control level on the 10th day after adrenal enucleation without increasing further, while that in the adrenalectomized group remained as low as before. 3) No significant differences in any of the experimental groups were found in diuresis, natriuresis, or in changes in body weight and hematocrit during the one and a half hours after furosemide administration performed at the 9th experimental week. The basal PRA was significantly decreased in the other groups with unilateral nephroadrenalectomy and/or a high sodium intake as compared with the unilaterally adrenalectomized rats drinking tap water. The decrease in basal PRA was much more pronounced in the unilaterally nephroadrenalectomized rats drinking saline, with or without adrenal enucleation. After furosemide administration, PRA significantly increased in the unilaterally adrenalectomized rats drinking saline as well as in the unilaterally nephroadrenalectomized rats drinking tap water, with or without adrenal enucleation, while PRA values in three groups were only a half of the unilaterally adrenalectomized rats drinking tap water. An insignificant increase was found in the unilaterally nephroadrenalectomized rats drinking saline, independent of adrenall enucleation. 4) Pressor responses to hog renin in rats with ARH at the 10th postoperative day, and the 4th and 9th postoperative week did not show any significant differences as compared with those of intact rats drinking tap water and unilaterally nephroadrenalectomized rats drinking saline. 5) The effects of adrenal enucleation on PRA, PRS, PRA response to furosemide administration and pressor response to renin in ARH were discussed based on the observed results.
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PMID:[Studies on the renin-angiotensin system in adrenal regeneration hypertension (author's transl)]. 117 93

The mechanism for reduced voluntary water intake during water immersion was studied in eight men (19-25 yr of age) immersed to the neck while sitting for 3 h at 34.5 degrees C or in air at 28 degrees C when euhydrated (Eu-H2O and Eu-air, respectively) and hypohydrated (Hypo-H2O and Hypo-air) by 3.6% body weight loss. Thirst sensations (degree of thirst, mouth dryness and taste, drinking desirability, and stomach fullness) were similar at the beginning of Hypo-air and Hypo-H2O test periods. Initial drinking of tap water (15 degrees C) was 216 +/- 30 ml/7 min (P less than 0.05) with Hypo-air, decreased to 108 +/- 28 ml/7 min (P less than 0.05) with Hypo-H2O, and was 10-50 ml/10-30 min thereafter. Intake was less than 10 ml/10-30 min in Eu-air, and there was no drinking in Eu-H2O. Within the first 10 min of immersion, compared with Hypo-air findings, the significant reduction in drinking in the Hypo-H2O experiment was associated with unchanged plasma Na+, plasma osmolality, heart rates, and mean arterial pressures; the different responses were increased cardiac output, plasma volume, and atrial natriuretic peptides and decreased plasma renin activity and arginine vasopressin. Thus the extracellular pathway, as opposed to the osmotic pathway, appears to be the major mechanism for immersion-induced suppression of drinking.
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PMID:Effect of dehydration on thirst and drinking during immersion in men. 153 47

Effects of high salt intake on the early onset of hypertension were examined in two-kidney, one-clip rats. They were divided into high salt and control groups which were supplied with 1.0% NaCl and tap water, respectively, as a drinking solution for 12 days after clipping the left renal artery. The high salt group showed a lower plasma renin concentration and a higher plasma atrial natriuretic peptide (ANP) along with an attenuation of the magnitude of early hypertension, as compared with the control group. A significant positive correlation between blood pressure and plasma renin concentration and an inverse correlation between plasma renin concentration and ANP were shown. Cortical renal renin content was comparable between the two groups. In another two groups of sham-clipped rats, the high salt group did not differ from the tap water-drinking group in any of the parameters examined, except that ANP was significantly higher. These results demonstrate that high salt intake attenuates the developmental phase of hypertension in two-kidney, one-clip rats by increasing the ANP and suppressing the release of renin.
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PMID:High salt intake attenuates the development of hypertension in two-kidney, one-clip Goldblatt rats. 182 73

Male Sprague-Dawley rats were uninephrectomized and given either deoxycorticosterone (DOC) pivalate (12.5 mg three times weekly) and 1% NaCl/0.2% KCl to drink for 4 weeks (DOC-treated), after which DOC was stopped and tap water substituted (post-DOC), or tap water to drink throughout (controls), DOC treatment increased blood pressure, serum sodium, plasma atrial natriuretic peptide (P-ANP) and plasma deoxycorticosterone (P-DOC) (P less than 0.05), while serum potassium, plasma renin and plasma angiotensin II were lower (P less than 0.05) than in control animals. Plasma vasopressin (P-AVP) was also raised but not significantly. These changes persisted for up to 4 weeks post-DOC and, in the case of plasma renin, plasma angiotensin II, P-AVP and P-ANP, for up to 12 weeks. Total body sodium was also increased at 2 weeks post-DOC (P less than 0.05). Rats which were adrenalectomized after 4 weeks of DOC treatment in which DOC injections were stopped, then drank either NaCl/KCl or tap water; blood pressure and P-DOC remained elevated while plasma renin remained suppressed. There were more deaths in rats given NaCl/KCl (five of six) than in the group given water (one of six). Rats treated with a subcutaneous DOC silastic implant had a comparable rise in blood pressure to rats given DOC injections. However, after removal of the implant, while blood pressure remained elevated, P-DOC levels were not raised and plasma renin rose to control levels after 4 weeks. These findings indicate that, in rats given DOC injections, post-DOC hypertension results from sodium and fluid retention as a consequence of chronic hangover of exogenously administered DOC.
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PMID:Hormone and electrolyte changes in post-deoxycorticosterone salt hypertension in rats. 196 84

1. The influence of deoxycorticosterone acetate (DOCA)-salt hypertension on brain atrial natriuretic factor (ANF) in rats was investigated to elucidate the role of central ANF in a renin-independent model of experimental hypertension. 2. Sprague-Dawley rats were subjected to uninephrectomy and given either tap water or saline [1% (w/v) NaCl] to drink plus weekly injections of either saline or DOCA (25 mg/kg, subcutaneously). After 32 days, the rats were decapitated and 18 different brain nuclei were removed by a micropunch technique. 3. The systolic blood pressure of the DOCA-salt rats was significantly higher than that of control rats [154 +/- 3 mmHg vs 104 +/- 2 mmHg (20.53 +/- 0.40 kPa vs 13.86 +/- 0.27 kPa), P less than 0.001]. 4. Plasma ANF levels were significantly (P less than 0.01) higher in DOCA-salt hypertensive rats compared with control rats. 5. In DOCA-salt hypertensive rats, the ANF content was increased in the organum vasculosum of the lamina terminalis (31.4 +/- 2.1 vs 22.1 +/- 2.5 pg/mg of protein, P less than 0.05), the subfornical organ (32.5 +/- 5.0 vs 24.2 +/- 2.4 pg/mg of protein, P less than 0.05), the medial amygdaloid nucleus (49.0 +/- 6.4 vs 34.0 +/- 2.0 pg/mg of protein, P less than 0.05) and the locus coeruleus (86.9 +/- 4.1 vs 64.4 +/- 4.2 pg/mg of protein, P less than 0.01) compared with control rats. The ANF content of 14 other brain areas investigated did not alter after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor content of brain nuclei in deoxycorticosterone acetate-salt hypertension in the rat. 253 Oct 54


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