Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. An increase in plasma chloride concentration (PC1) decreases renal blood flow (RBF) and glomerular filtration rate (GFR) and inhibits the intrarenal release of renin and angiotensin II (AII). Captopril was administered to indomethacin-treated dogs to assess the role of AII independent of prostaglandins (PGs) in the haemodynamic response to hyperchloraemia. Studies were performed on kidneys that were denervated by autotransplantation. 2. Anaesthetized greyhounds received an intrarenal infusion of 0.616 M-sodium acetate, which was changed to 0.616 M-NaCl (hyperchloraemia). These infusions increased the plasma sodium and osmolality at the experimental kidney by 7-11% throughout but increased the PCl during the hypertonic NaCl infusions only (122 +/- 3 to 136 +/- 3 mM). 3. In vehicle-treated dogs (n = 8), hyperchloraemia reduced the GFR (1.4 +/- 0.1 to 1.0 +/- 0.1 ml min-1 kg-1; P less than 0.05) and the RBF (13.0 +/- 1.4 to 8.3 +/- 0.6 ml min-1 kg-1; P less than 0.01); these changes were reversible on return to the 0.616 M-sodium acetate infusion. Hyperchloraemia reduced the release of AII into renal lymph (2.5 +/- 0.9 to 1.2 +/- 0.4 pg min-1 kg-1; P less than 0.01). 4. Indomethacin (0.6 mg kg-1 and 0.2 mg kg-1 h-1 intrarenally; n = 4) blunted (P less than 0.05) the Cl--induced fall in RBF (10.4 +/- 1.1 to 8.2 +/- 0.6 ml min-1 kg-1) without changing significantly the fall in GFR or the release of AII into renal lymph.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Renal haemodynamics during hyperchloraemia in the anaesthetized dog: effects of captopril. 307 84

1. A haemorrhage volume/plasma renin activity (PRA) response relationship was established for five levels of acute haemorrhage ranging from 1.5 to 15 ml/kg in conscious rats. In addition, the effects of chronic indomethacin and/or acute propranolol administration on the PRA response to 5 and 10 ml/kg haemorrhage was assessed. 2. Mean arterial pressure decreased in a haemorrhage volume dependent manner which was not significantly altered by indomethacin and/or propranolol. 3. Haemorrhage volumes of 1.5 and 3.0 ml/kg did not significantly alter PRA. At haemorrhage volumes of 5.0 ml/kg and higher, PRA increased in a volume-dependent manner. Propranolol decreased basal PRA levels but had little effect on the response to haemorrhage. Indomethacin had no effect on basal PRA, but attenuated the response to haemorrhage somewhat. When propranolol and indomethacin were combined, the PRA response to haemorrhage was significantly attenuated. 4. The conscious cannulated rat model exhibits predictable and reproducible renin responses to haemorrhage and is an excellent model for studying the control of renin secretion.
 ...
PMID:Renin response to graded haemorrhage in conscious rats. 307 79

We studied the effects of a specific thromboxane (TX) synthetase inhibitor (U-63,557A) and a cyclooxygenase inhibitor on furosemide-induced renin release. Furosemide (2.0 mg X kg-1) was injected into Sprague-Dawley rats pretreated with indomethacin (10 mg X kg-1, i.v.), U-63,557A (1.0-32.0 mg X kg-1, i.v.), or vehicle (Na2CO3 0.03 M). Plasma renin activity was measured in blood samples collected 0, 10, 20, and 40 min after the injection of furosemide. Blood was also collected after the administration of vehicle, indomethacin, or U-63,557A for serum TXB2, a measure of platelet TXA2 synthesis. The results demonstrated that plasma renin activity rose with time following furosemide in the various groups of rats; indomethacin suppressed the furosemide-induced increments in plasma renin activity, while U-63,557A at doses of 4-8 mg X kg-1 augmented it. At doses below 4 mg X kg-1 or above 8 mg X kg-1, U-63,557A did not augment renin secretion. Indomethacin and U-63,557A reduced serum thromboxane by 81 and 90%, respectively. Thus, these experiments suggest that thromboxane synthetase inhibition, within a narrow dosage range, potentiates furosemide-induced renin release while cyclooxygenase inhibition suppresses it.
 ...
PMID:Effect of cyclooxygenase and thromboxane synthetase inhibition on furosemide-stimulated plasma renin activity. 310 53

We studied the effects of inhibition of either prostaglandins or the role of prostanoids and the renin-angiotensin system on renal function in rats with congenital unilateral hydronephrosis. Wistar rats with congenital unilateral hydronephrosis were infused with normal saline (control), captopril dissolved in normal saline or indomethacin dissolved in a solution of sodium chloride and sodium carbonate. In the control group both glomerular filtration rate (GFR) and effective renal plasma flow were reduced in the right hydronephrotic kidney (RHK) compared with the normal left kidney. Indomethacin did not improve renal function in the RHK. Captopril significantly improved GFR in the RHK. These results support the conclusion that the renin-angiotensin system is an important mediator of reduced GFR in congenital unilateral hydronephrosis in rats.
 ...
PMID:Reversible vasoconstriction in rats with congenital unilateral hydronephrosis. 315 23

13 1/2 year old boy with short stature and pubertal delay had infrequent episodes of tetany. Biochemical determinations demonstrated low plasma and high urinary magnesium and potassium levels, hypocalciuria, slightly increased plasma bicarbonate, slightly reduced fractional distal reabsorption of chloride and sodium, high plasma renin activity and high urinary excretion of prostaglandins (E2, F2 alpha). The other parameters of renal functions were normal. Endocrine evaluation of short stature and pubertal delay was normal. Intracellular magnesium and potassium levels in lymphocytes and erythrocytes were within normal limits. Cyclooxygenase blockade with Indomethacin 2.5 mg/kg daily during 4 weeks normalized urinary excretion of prostaglandins and corrected in part low plasma and high urinary potassium levels, but had no effect on magnesium, calcium, sodium and chloride handling. These data raise the possibility that tubular hypomagnesaemia-hypokalaemia could be solely explained by a low renal threshold for magnesium.
 ...
PMID:Metabolic studies in primary tubular hypomagnesaemia-hypokalaemia. 327 28

Certain nonsteroidal anti-inflammatory drugs antagonize the action of antihypertensive therapy. Indomethacin has been shown to abrogate the antihypertensive effect of beta-adrenergic receptor blockers, diuretics, converting enzyme inhibitors, and several antihypertensive drug combinations, and the accumulated evidence on piroxicam indicates that it also raises arterial pressure in treated patients. In contrast, sulindac and aspirin do not reverse the effects of antihypertensive drugs, and currently available data indicate that they are the safest cyclooxygenase inhibitors for use in hypertensive patients. In the absence of definitive information on the array of other nonsteroidal anti-inflammatory drugs, they should be considered to pose a risk similar to indomethacin until proved otherwise. The magnitude of the elevation in blood pressure varies between patients, ranging from no effect to dangerous hypertensive responses. Generalized inhibition of the cyclooxygenase enzyme has opposing effects on arterial pressure, lowering renin on one hand and causing sodium retention on the other. Some evidence suggests that cyclooxygenase inhibition causes the greater increments in pressure in patients who initially have low plasma renin activity (often the elderly). The potential for cerebral vascular catastrophes attends these drug interactions in which platelet function also is suppressed by cyclooxygenase inhibition.
 ...
PMID:Antagonism of antihypertensive drug therapy by nonsteroidal anti-inflammatory drugs. 328 Apr 91

The mechanisms of the cardiovascular and renin responses to vasoactive intestinal polypeptide (VIP) are unclear. Rabbit studies suggest that VIP-induced tachycardia is largely beta-adrenoceptor mediated, but that the renin response may be partially prostaglandin-dependent. To examine the relative importance of prostaglandins and reflex sympathetic activation in the haemodynamic and renin responses to VIP infusion in man, we completed two randomised single-blind crossover studies in two groups of six healthy male volunteers (aged 24-35 years). We recorded the effects of indomethacin and propranolol pretreatment on VIP-related changes in heart rate (HR), blood pressure (BP), forearm vascular resistance (FVR), plasma renin activity (PRA), plasma noradrenaline (PNA) and plasma arginine vasopressin (AVP) concentrations. Intravenous VIP (calculated dose: 6 pmol kg-1 min-1) produced cutaneous flushing, increased HR and PRA, decreased FVR, but did not alter mean arterial BP or AVP levels. Indomethacin (375 mg over 3 days) lowered basal PRA and propranolol (circa 40 mg i.v. over 60 min) decreased resting HR and increased FVR. Although indomethacin and propranolol reduced the absolute rise in PRA and HR, respectively, during VIP infusion, the percentage changes were no different from control. Neither drug altered the flush response to VIP and propranolol did not affect the fall in FVR. We conclude that the measured cardiovascular responses to VIP infusion in man are probably direct and do not involve a significant contribution from reflex sympathetic stimulation, nor prostaglandin release.
 ...
PMID:Effects of indomethacin and (+/-)-propranolol on the cardiovascular and renin responses to vasoactive intestinal polypeptide (VIP) infusion in man. 329 24

The effects of captopril on the forearm hemodynamics in patients with severe congestive heart failure were studied, using strain-gauge plethysmography. To determine whether prostaglandins are involved in the captopril actions, indomethacin, an inhibitor of prostaglandin synthesis, was administered. In 8 patients, captopril (25 mg) decreased mean blood pressure (P less than 0.01) and venous pressure (P less than 0.05); forearm blood flow (P less than 0.05) and maximum venous volume (P less than 0.05) were increased; forearm vascular resistance (P less than 0.05) and forearm venous tone (P less than 0.05) were decreased. Venous distensibility was improved with captopril (P less than 0.05). All the hemodynamic changes were attenuated by indomethacin (50 mg). Captopril increased circulating bradykinin (P less than 0.05), prostaglandin E2 (P less than 0.05) and 6-keto-prostaglandin F1 alpha (P less than 0.05). Indomethacin did not affect bradykinin level but blocked the increase in prostaglandins. These data suggest that captopril dilates both arterial and venous vessels not only by blocking the renin-angiotensin system but by increasing local or circulating vasodilator prostaglandins.
 ...
PMID:Effects of captopril on peripheral hemodynamics in severe congestive heart failure. 330 Oct 83

The possible role of vasodilatory prostanoids in the antihypertensive action of captopril was investigated in spontaneously hypertensive rats (SHR). Captopril (100 mg/kg/day for 5 days) decreased systolic blood pressure and increased water consumption, urine excretion and plasma renin activity (PRA). It also enhanced the urinary excretion of the prostacyclin metabolite 6-keto-PGF1 alpha, but did not change the excretion of PGE2. Indomethacin (3 mg/kg/day), given both alone and in combination with captopril, reduced markedly the urinary excretions of 6-keto-PGF1 alpha and PGE2 but did not alter PRA, compared with corresponding groups without indomethacin. The suppression of prostanoid synthesis caused by indomethacin did not affect the antihypertensive effect of captopril or the basal blood pressure in SHR. Neither did indomethacin influence drinking or urine excretion in SHR not receiving captopril, but it reduced the dipsogenic and diuretic effects of captopril. The results suggest that captopril augments the production of vasodilatory prostacyclin. Yet prostanoids have no significant role in the antihypertensive mechanism of captopril in SHR.
 ...
PMID:Effects of indomethacin on hormonal and blood pressure responses to captopril in spontaneously hypertensive rats. 331 83

Three cases of primary amyloidosis and 2 cases of familial amyloidosis complicated by asympathicotonic orthostatic hypotension are reported. Blood pressure measurements on a tilting table, plasma renin activity and plasma aldosterone or catecholamine concentrations enabled localisation of the lesion of the baroreceptor reflex in some cases. When the pre- and post-synaptic efferent sympathetic pathway was intact, treatment associating Tyramine and Tranylcypromine may provide these bedridden patients some autonomy of movement. When this pathway is affected by the disease the association of Indomethacin, Dihydroergotamine and 9-alpha-fluorohydrocortisone may be tried.
 ...
PMID:[Amyloidosis and orthostatic hypotension. Physiopathology, therapeutic attempts. Apropos of 5 cases]. 345 Feb 11


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>