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 changes in arterial blood pressure and plasma cortisol concentration in response to exogenous angiotensin II (AII) and to manipulation of the endogenous renin-angiotensin system (RAS) have been examined in the flounder, Platichthys flesus. Intravenous [Asp1Val5]AII was pressor in a dose-dependent manner over the range of 0.25-250 micrograms/kg. Sequential blood sampling revealed steroidogenic stimulation, measured as change in plasma cortisol concentration, by doses of AII greater than 2.5 micrograms/kg. Enhanced circulating cortisol levels were measured some time after recovery of normal systemic blood pressure, suggesting that the change in plasma steroid concentration was not entirely dependent on the change in systemic blood pressure. Administration of the vasodilator papaverine produced immediate hypotension followed by gradual recovery in blood pressure, which was accompanied by a sustained increment in circulating cortisol. Both blood pressure recovery and the increased plasma steroid concentration were inhibited by prior treatment with the angiotensin converting enzyme inhibitor captopril. These results are consistent with a physiologically important role for the RAS in the control of plasma cortisol levels which complements its demonstrated pressor and dipsogenic actions in the flounder: the RAS may thus afford an integrating influence on the mechanisms of body fluid homeostasis in this euryhaline species.
Gen Comp Endocrinol 1990 Jun
PMID:The renin-angiotensin system and the regulation of plasma cortisol in the flounder, Platichthys flesus. 218 79

1. The antinociceptive effect of compound 48/80 was reversed by the pretreatment with an angiotensin-converting enzyme (ACE) inhibitor, Hoe 498, in a dose-dependent manner and with a opiate receptor antagonist, naloxone (5.0 mg/kg, s.c.) in rats. 2. The increase of plasma beta-endorphin-like immunoreactivity produced through s.c. administration of compound 48/80 was attenuated by the pretreatment with Hoe 498 but not with naloxone. 3. The present data suggest the possible involvement of renin-angiotensin system in compound 48/80-induced analgesia in rats.
Gen Pharmacol 1989
PMID:The role of renin-angiotensin system in compound 48/80-induced analgesia in rats. 252 74

The role of a renin-angiotensin-like system (RAS) in the regulation of blood pressure and drinking has been investigated in the elasmobranch, Scyliorhinus canicula. Injection of exogenous angiotensin II produced, as expected, a vasopressor response, though injection of the converting enzyme inhibitor, Captopril, alone produced little change in resting blood pressure. Papaverine, a smooth muscle relaxant, reduced blood pressure which completely recovered within 30 min. A subsequent injection of Captopril produced a rapid vasodepressor response with no recovery over 2 hr. The low basal levels of drinking in dogfish were not altered by Captopril injection but angiotensin II-induced increased drinking and papaverine administration resulted in markedly stimulated water intake, which was inhibited by coadministration with Captopril. Captopril inhibition of the recovery in blood pressure and associated dipsogenic response following the papaverine-induced hypotension is consistent with the activation of a RAS-like system in the dogfish. This and other evidence supporting the presence of a RAS-like system in elasmobranchs are discussed in relation to other vertebrates.
Gen Comp Endocrinol 1989 May
PMID:The renin-angiotensin system and vascular and dipsogenic regulation in elasmobranchs. 265 53

In mammals, a well-documented inverse relationship exists between oral salt intake and plasma renin activity (PRA). We carried out this study to determine if a similar relationship exists in the freshwater turtle Pseudemys scripta. Three groups of turtles (N = 8 for each group) were fed different amounts of salt dissolved in distilled water (2 cc/kg). The high salt group received 580 mg (10 mEq) NaCl/kg twice per week, the medium salt group received 290 mg (5 mEq) NaCl/kg twice per week, and the low salt (control) group received 2 cc/kg distilled water twice per week with no salt. The animals were weighed weekly and blood was collected by cardiac puncture after 3 and 6 weeks of salt loading and again 3 weeks after termination of the salt loading. PRA and plasma electrolytes (PNa, PK, PCl) were determined. The low salt (control) group showed no changes in any of the measured variables throughout the 9-week study. At 3 weeks the following mean values were obtained for the control group: PNa, 119.5 +/- 7.2 mEq/liter; PK, 5.0 +/- 1.0 mEq/liter; PCl, 74.1 +/- 2.6 mEq/liter; PRA, 1.0 +/- 0.2 ng/ml/hr. In the medium salt group, no significant changes were seen until 3 weeks after termination of the salt loading when PNa and PRA were elevated to 137.9 +/- 3.6 mEq/liter and 1.9 +/- 0.2 ng/ml/hr, respectively (P less than 0.05 compared to control). In the high salt group, PNa (136.5 +/- 6.5 mEq/liter) was elevated after 3 weeks of salt loading. At 6 weeks, PNa (136.8 +/- 4.9 mEq/liter) remained elevated in the high salt group and PCl (86.3 +/- 1.3 mEq/liter) and PRA (1.7 +/- 0.2 ng/ml/hr) also increased significantly (P less than 0.05 compared to control in each case). Three weeks after termination of salt loading, PNa (136.8 +/- 3.3 mEq/liter). PCl (88.0 +/- 1.6 mEq/liter), and PRA (1.9 +/- 0.2 ng/ml/hr) remained elevated (P less than 0.05 in each case) in the high salt group while PK dropped to 3.5 +/- 1.6 mEq/liter (P less than 0.05). The results show that after 6 weeks of salt loading sufficient to raise PNa in the turtle, PRA was significantly elevated.
Gen Comp Endocrinol 1989 Dec
PMID:Salt intake and plasma renin activity in the freshwater turtle. 268 40

1. The effects of the angiotensin-converting enzyme (ACE) inhibitor lisinopril on plasma vasoactive intestinal polypeptides (VIP) and plasma noradrenaline, adrenaline and dopamine were studied in 12 patients with congestive heart failure over two consecutive 48-hr periods. The first day in each period served as a treatment day and the second as a control day. 2. A parallel monitoring was made of various hormonal parameters related to the renin-angiotensin-aldosterone system, and a right-heart catheter was used to monitor haemodynamics at rest. 3. Potent inhibition of the renin-system (as demonstrated by decreases in angiotensin converting enzyme (ACE) activity, angiotensin II and plasma aldosterone) together with improved haemodynamics (decreases in mean right atrial pressure, mean pulmonary arterial pressure, mean pulmonary capillary wedge pressure and mean systemic arterial pressure) were recorded. 4. Plasma VIP was significantly increased by a mean of 20.3% (P less than 0.01) on the lisinopril treatment days compared with the control days, whereas circulating catecholamines showed no significant pattern of change. 5. It is postulated that the potent vasodilatory neuromodulator VIP is implicated in the ACE inhibitor effects. 6. The ACE is a non-specific peptidase that previously has been implicated in the potentiation of other vasoactive endogenous systems (kinins and enkephalins).
Gen Pharmacol 1987
PMID:Increase in vasoactive intestinal polypeptides (VIP) by the angiotensin converting enzyme (ACE) inhibitor lisinopril in congestive heart failure. Relation to haemodynamic and hormonal changes. 282 21

The changes in body fluid economy and endocrine status associated with exposure of the Nile crocodile, Crocodylus niloticus, to hypertonic media have been related to the responses to altered renin-angiotensin system (RAS) activity observed in fresh water (FW) animals. Animals held in hypertonic media for 7 days showed a 18.2% body weight loss and raised plasma and urinary sodium, potassium, chloride, and osmotic concentrations. Within 6 hr of return to FW rapid imbibition had largely restored body weight and produced significant plasma dilution. Although plasma sodium, chloride, and osmotic concentrations remained higher than in FW controls, plasma levels of corticosterone, aldosterone, and arginine vasotocin were not significantly altered. Angiotensin I (AI) administration in FW crocodiles stimulated drinking and raised plasma aldosterone levels by comparison with animals given the converting enzyme inhibitor, Captopril, together with AI. The compensatory drinking behaviour exhibited by the Nile crocodile may thus involve the RAS. The RAS also appears to influence interrenal steroidogenesis and thus may afford an integrative role in crocodile fluid management as it does in homeotherms.
Gen Comp Endocrinol 1989 Mar
PMID:Endocrines and osmoregulatory mechanisms in the Nile crocodile, Crocodylus niloticus. 292 77

Components of the renin angiotensin system have been identified in many nonmammalian vertebrates. However, in many of these animals, including reptiles, the physiological functions and importance of the system remain unclear. To aid in the study of the system in a reptile we modified a commercially available radioimmunoassay (RIA) kit containing antibody against human angiotensin I (ANG I) for use in the freshwater turtle, Pseudemys scripta. Cross-reactivity between anti-human ANG I antibodies (Rainen Angiotensin I RIA Kit, New England Nuclear) and turtle ANG I was demonstrated. Cross-reactivity with the antibody in two other human ANG I assay kits (Travenol-Genentech and Biotecx) was very limited. Blood for assay was collected from conscious turtles in EDTA, centrifuged, and the plasma frozen at -20 degrees. Turtle ANG I was generated by incubation at 0.5 ml plasma at pH 5.5 for 2 hr at 30 degrees with addition of dimercaprol and 8-hydroxyquinoline. Angiotensin generation increased with temperature and with generation time. The recovery of turtle ANG I added to turtle plasma prior to incubation was 92-97%. The assay procedure was used to measure plasma renin activity (ng/ml/hr incubation) from unstimulated turtles.
Gen Comp Endocrinol 1988 Jun
PMID:Measurement of plasma renin activity in the freshwater turtle. 304

1. To investigate the possible effects of potassium canrenoate (PC) on plasma renin activity (PRA) and on renal prostaglandins (PGS) and kinins under elevated sodium and/or potassium intakes, a single dose of PC was administered to four groups of Wistar male rats. 2. They were fed a normal diet (C), a diet supplemented with 4% of NaCl, (Na), with 1% of KCl: (K) or both supplements (NaK). 3. PRA and urinary PGS excretion did not show changes after PC administration, but total urinary kinins showed higher values after the treatment in all groups. 4. A diuretic but not natriuretic effect was observed only in C animals. 5. In conclusion, the single dose of PC was able to stimulate urinary kinins and to spare potassium independently of dietary electrolyte supplements that were able to block the diuretic effect of the drug.
Gen Pharmacol 1988
PMID:Acute effect of potassium canrenoate administration on renin-angiotensin, kallikrein-kinin and prostaglandin systems. 306 96

Cost effectivenesses of four tests for diagnosing renal artery stenosis were examined. Sensitivity, specificity, cost per patient, and cost per stenosis found for a variety of diagnostic strategies using these tests were retrospectively evaluated using clinical data from 605 hypertensive patients. Cost effectiveness of a given strategy was found to depend on the sequence in which the tests were performed, but to be relatively independent of the exact cost of the tests. Auscultation for a systolic/diastolic abdominal bruit was the most cost-effective test for beginning a diagnostic strategy and showed a 99.6% specificity for stenosis. When the patient has a systolic bruit only or no bruit, plasma renin activity measurement should guide the clinician's choice of whether to test further with intravenous pyelography or renal arteriography. Diagnosis of renal artery stenosis using these tests is estimated to cost between $2,300 and $6,200 per stenosis found, depending on the prevalence of renal artery stenosis.
J Gen Intern Med
PMID:Cost effectiveness in the detection of renal artery stenosis. 249 96

The evidence presented here suggests strongly that the kallikreins-kininogens-kinins-kininase II system has most significant role in regulation of systemic BP. This system is involved in mediation and modulation of renin-angiotensin-aldosterone, PGS and vasopressin in the regulation of sodium water balance, renal hemodynamic and BP. Therefore, reduction in the kinin-formation due to high production of kininase II, and lower formation of tissue kallikrein might result in an increased release of vasoconstrictor angiotensin II on one side, and on the other side much reduced production of PGE, vasodilator. These changes might lead to deranged vascular smooth muscle structures and cell membrane functions, retention of sodium and water, increased plasma volume, and renovascular constriction. These physiological defects might result in the development of essential hypertension (Fig. 4). Although, it is possible now to treat hypertensive conditions with tissue kallikrein and kininase II inhibitors. These discoveries have opened up new vistas to research on the pharmacological applications of kallikreins-kininogens-kinins-kininases in human diseases.
Gen Pharmacol 1988
PMID:Interrelationship between the kallikrein-kinin system and hypertension: a review. 328 Mar 99


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