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PubMed1997

Comparison of responses to T-kinin and bradykinin in the mesenteric vascular bed of the cat.

Responses to T-kinin and bradykinin were compared in the mesenteric vascular bed of the cat. Under constant-flow conditions, injection of T-kinin and bradykinin into the perfusion circuit induced similar dose-related decreases in perfusion pressure. Responses to T-kinin and bradykinin were inhibited by the kinin B2 receptor antagonist Hoe-140, but were not altered by the B1 receptor antagonist des-Arg9-[Leu8]-BK, the histamine H1 antagonist pyrilamine, the histamine H2 receptor antagonist cimetidine, or the H3 receptor antagonist thioperamide. Vasodilator responses to T-kinin and bradykinin were attenuated by the nitric oxide synthase inhibitor, N omega Nitro-L-arginine methyl ester (L-NAME), but were not altered by the cyclooxygenase inhibitor, sodium meclofenamate, or the K+ ATP channel antagonist, U37883A. These data suggest that vasodilator responses to T-kinin and bradykinin are mediated by kinin B2 receptor stimulated release of nitric oxide from the endothelium, but that the activation of kinin B1 receptors, the release of vasodilator prostaglandins, or the opening of K+ ATP channels are not involved in the response to T-kinin in the mesenteric vascular bed of the cat.

Adamantane↗
PubMed1986

Benefits and risks of nonsteroidal antiinflammatory drugs in steroid-resistant nephrotic syndrome.

In this paper we discuss the effects of nonsteroidal antiinflammatory drugs on proteinuria and the specific risks of these drugs in patients with nephrotic syndrome. We summarize the results of a prospective uncontrolled trial of meclofenamate in severe steroid-resistant nephrotic syndrome secondary to focal glomerular sclerosis and idiopathic membranous nephropathy. This study examined the effect of meclofenamate on proteinuria, serum albumin levels, serum cholesterol, serum triglycerides, renal function, BP, liver function tests, and hematologic values. We also sought and evaluated adverse reactions due to this medication. We offer some suggestions for selective use and careful supervision of NSAIDs in the nephrotic syndrome.

Anti-Inflammatory Agents↗
PubMed1985

Comparison of meclofenamate sodium with buffered aspirin and placebo in the treatment of postsurgical dental pain.

The efficacy of meclofenamate sodium (Meclomen) at two different doses was compared with that of buffered aspirin and placebo in the control of postsurgical pain in a double-blind, randomized study of 205 patients. Meclofenamate sodium, 200 mg, was significantly better than meclofenamate sodium, 100 mg, in some efficacy parameters. Both doses of meclofenamate sodium were superior to buffered aspirin in most parameters of efficacy, and more effective than placebo in every parameter.

Acetaminophen↗
PubMed1997

Sensory nerve-mediated inhibitory responses in airways of F344 rats.

We recently described a sensory nerve inhibitory system that mediates relaxation in the airways of Sprague-Dawley rats. Results of several studies have shown that this system protects the lungs against injury induced by toxic stimuli. Whether a similar inhibitory system exists in the airways of Fischer 344 (F344) rats is unknown. Because this rat strain is used extensively in lung toxicological research, the purpose of this study was to determine whether a sensory nerve inhibitory system exists in intrapulmonary bronchi and tracheae isolated from F344 rats. In intrapulmonary bronchi at resting tone, substance P (1.0 microM) evoked a transient contraction that was inhibited by the 5-HT2A receptor antagonist, ketanserin. Exposing airway segments to compound 48/80 to degranulate mast cells also abolished substance P-induced contractions. Inhibition of cyclooxygenase with meclofenamate augmented markedly the contraction to substance P in the intrapulmonary bronchi. In intrapulmonary bronchi that were contracted with bethanechol, substance P evoked a biphasic response characterized by an increase in tension above that induced by bethanechol followed by relaxation. Incubation of the airways with ketanserin abolished the contractile portion of the response; relaxation responses were augmented after ketanserin. In contracted intrapulmonary bronchi that had been treated with compound 48/80, substance P and capsaicin caused relaxation responses that were inhibited markedly or were nearly abolished by the NK1 receptor antagonist, RP67580, by meclofenamate, and by denuding the epithelium. Capsaicin-induced relaxation responses also were abolished by desensitization of C-fibers with capsaicin. Only ketanserin-sensitive contractile responses were observed in response to substance P in tracheal segments. We conclude that a sensory nerve inhibitory system exists in the intrapulmonary airways of F344 rats. The presence of this inhibitory system in F344 rat airways may play a protective role against lung injury induced by inhaled toxicants.

Analgesics↗
PubMed2000

[Effect of cyclooxygenase inhibition on the adaptation of coronary blood flow to tachycardia].

BACKGROUND: The role of different endothelium-derived vasoactive substances in the regulation of coronary circulation during tachycardia is not well defined. In order to elucidate the contribution of prostacyclin to the adaptation of coronary blood flow to tachycardia, the effect of meclofenamate, a cyclooxygenase inhibitor on the coronary blood flow response to rapid atrial pacing was analyzed in a porcine model. METHODS: A group of seventeen pigs were instrumented for coronary blood flow, aortic pressure and atrial pacing. Heart rate was increased by 20 beats every 5 minutes. Coronary blood flow and aortic pressure were measured, and coronary resistance calculated, basally and at each pacing interval, before and after saline serum (n = 6), meclofenamate 5 mg/kg, i.v. (n = 7) or meclofenamate 35 mg/kg, i.v. (n = 4). RESULTS: Neither saline nor meclofenamate modified the normal increase of coronary blood flow provoked by rapid atrial pacing (163 +/- 28% increase before versus 172 +/- 29% after saline; 159 +/- 21% increase before versus 161 +/- 22% after meclofenamate low doses and 201 +/- 39% before vs 172 +/- 36 after meclofenamate high doses). There were no differences in the response of coronary vascular resistance to tachycardia before and after meclofenamate (44% reduction vs 40% respectively). CONCLUSION: Cyclooxygenase blockade does not modify the response of coronary circulation to rapid atrial pacing, suggesting that prostacyclin does not play a limiting role in the regulation of coronary blood flow during tachycardia in this model.

Animals↗
PubMed1980

Furosemide-induced vasodilation: importance of the state of hydration and filtration.

The circumstances under which furosemide increases renal blood flow was examined in mongrel dogs as it may relate to a tubuloglomerular feedback mechanism. Two maneuvers, desoxycorticosterone (DOCA) plus salt treatment and inhibition of tubular fluid flow, were used in the dogs to evaluate the renal vascular effects of furosemide because these maneuvers have been reported to blunt the tubuloglomerular feedback in micropuncture studies. In addition, we also used two structurally different nonsteroidal antiinflammatory drugs to assess the importance of prostaglandins to achieve furosemide's renal vasodilatation. Furosemide (5 mg/kg, i.v.) increased renal blood flow in volume-depleted animals from a baseline flow of 141 +/- 28 ml/min to a maximum of 176 +/- 35 ml/min at 6 min after furosemide administration. If the animals were pretreated with a high-salt diet and i.m. DOCA for 5 days, furosemide administration produced no renal vascular effects but still caused a large diuresis, and these dogs still had a responsive renal vascular bed to infused prostaglandin E2. In addition, kidneys rendered non-filtering in volume-depleted animals had no renal vascular response to furosemide. Volume-depleted animals, pretreated with either indomethacin or sodium meclofenamate, did not have a renal vascular response to furosemide although they did have a diuretic response and a responsive renal vasculature to prostaglandin E2. From our data, we hypothesize that the renal vascular response to furosemide is secondary to a tubular mechanism mediated by a vasodilatory prostaglandin. Because furosemide has been shown to disrupt the tubuloglomerular feedback mechanism, and the two maneuvers, DOCA plus salt treatment and lack of filtration, blunt the tubuloglomerular feedback response as well as inhibit the renal vascular response to furosemide, we further hypothesize that furosemide-induced renal vasodilation may be secondary to the disruption of an active tubuloglomerular feedback mechanism.

Animals↗
PubMed1982

Prostaglandin synthesis inhibition during volume expansion: collecting duct function.

The aim of this study was to examine the possible role of renal prostaglandins in the response of the inner medullary collecting duct (IMCD) to acute volume expansion. Collecting duct microcatheterization and clearance studies were carried out in anesthetized rats, volume-expanded with isotonic Ringer's solution. In volume-expanded control animals, there was no significant sodium or chloride reabsorption between the beginning and end (papillary tip) of the IMCD. Administration of indomethacin or meclofenamate prior to and during volume expansion in two other groups of rats resulted in significant water, sodium, and chloride reabsorption along the IMCD and markedly blunted the diuretic, natriuretic and chloriuretic response to volume expansion. Because delivery to the beginning of the duct was not significantly decreased, enhanced reabsorption in the IMCD largely accounted for the decrease in natriuresis and chloriuresis. Inner medullary tissue fluid chloride concentration increased after inhibition of prostaglandin synthesis. The results indicate that renal prostaglandins, perhaps by directly decreasing sodium chloride reabsorption, have an important role in the decrease in collecting duct reabsorption of sodium and chloride observed with acute volume expansion.

Animals↗
PubMed1984

Pressure natriuresis and prostaglandin secretion by perfused rat kidney.

Isolated rat kidneys respond to elevations of perfusion pressure with an increase in glomerular filtration rate (GFR), filtration fraction (FF), and sodium excretion (UNaV) and a fall in fractional sodium reabsorption (FRNa). Significant linear correlations exist between each of these dependent variables and the renal artery pressure (P). In control kidneys, pressure natriuresis is seen to result both from an increase in filtered sodium load and a decrease in FRNa. In kidneys treated with indomethacin in doses which curtail the release into the perfusate of prostaglandin E2 (PGE2) and the prostacyclin metabolite, 6-keto-PGF1 alpha, the regression lines relating GFR, FF, and UNaV to P are shifted to the right. Thus, prostaglandin-inhibited kidneys require higher pressures than control kidneys to maintain comparable rates of filtration and sodium excretion. Total renal vascular resistance (RVR) is also higher in inhibited kidneys. These findings suggest that in the isolated perfused rat kidney, prostaglandins promote pressure natriuresis by maintaining afferent arteriolar dilation. Their inhibition leads to afferent constriction, which raises RVR, lowers FF and GFR, and reduces sodium excretion.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Effect of cyclosporine administration on renal hemodynamics in conscious rats.

The effect of acute and chronic administration of cyclosporine on systemic and renal hemodynamics was studied in conscious rats. Infusion of cyclosporine in a dose of 20 mg/kg (Cy 20) resulted in a significant fall in renal blood flow (RBF) (3.4 vs. 6.5 ml/min/g, P less than 0.05) and a rise in renal vascular resistance (RVR) (36.9 vs. 20.6 mm Hg/ml/min/g, P less than 0.05). Infusion of cyclosporine at a dose of 10 mg/kg (Cy 10) did not result in a significant change in RBF or RVR. Both doses of cyclosporine resulted in stimulation of plasma renin activity (PRA) from control values of 5.6 +/- 0.8 ng/ml/hr to 11.6 +/- 2.0 with 10 mg/kg and 26.7 +/- 5.6 with 20 mg/kg. Urinary 6-keto-PGF1 alpha excretion increased from control values of 14.0 +/- 2.0 ng/6 hr to 22.7 +/- 2.2 with 10 mg/kg and 25.0 +/- 2.0 with 20 mg/kg. Similar effects on RBF, RVR, PRA, and 6-keto-PGF1 alpha excretion were seen after chronic administration of cyclosporine (20 mg/kg i.p. for 7 days). Pretreatment of animals with captopril did not prevent the fall in RBF after cyclosporine, suggesting that the vasoconstriction was not mediated by angiotensin II. Animals treated with meclofenamate demonstrated reduction in RBF with 10 mg/kg cyclosporine (4.3 vs. 7.0 ml/min/g, P less than 0.05), suggesting that prostaglandins protect against the vasoconstrictor effect of cyclosporine. Administration of phenoxybenzamine after cyclosporine improved RBF (5.0 vs. 3.4 ml/min/g) and restored RVR to normal. Similarly, renal denervation dramatically reduced the fall in RBF after cyclosporine (innervated right kidney 3.6 vs. denervated left kidney 6.0 ml/min/g, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Effects of lithium on cAMP generation in cultured rat inner medullary collecting tubule cells.

The effects of lithium (Li) on the cAMP system in rat inner medullary collecting tubule cells were studied. While acute exposure to 5 mM Li was without effect, 10 mM, 25 mM and 50 mM Li significantly decreased AVP-stimulated cAMP formation. In contrast, cells grown in 5 mM Li for 72 hours which caused no morphologic changes enhanced cAMP formation (fmol/microgram protein) in response to both 10 nM AVP (114.5 +/- 9.2 vs. 71.6 +/- 7.4, P less than 0.005) and 100 nM AVP (182 +/- 14 vs. 120 +/- 8.3, P less than 0.001), N = 16. A similar enhancement was observed when cAMP formation was stimulated by a post-receptor agonist, cholera toxin. The role of eicosanoids was examined with 5 microM meclofenamate which reversed Li-enhanced cAMP formation in response to both AVP and cholera toxin. To define the eicosanoid responsible, cyclooxygenase products were measured. Prostaglandin E2 and thromboxane B2 synthesis were unchanged by Li, but the production of prostacyclin was significantly (P less than 0.02) increased. Prostacyclin (3 microM) mimicked the effect of Li to enhance the response to 10 nM AVP as cAMP levels increased from 100 +/- 11 to 173 +/- 13, P less than 0.05. The experiments suggest that acute exposure of Li at concentrations of 10 mM or greater inhibit cAMP formation but prolonged Li exposure enhances cAMP formation by increasing the formation of prostacyclin.

Animals↗
PubMed1993

Prostaglandin synthesis inhibition stimulates lithium reabsorption in Henle's loop in rats.

The effect of prostaglandin (PG) synthesis inhibition on tubular lithium (Li) handling in the rat was studied by micropuncture at the late proximal (LPT) and early distal (EDT) tubules. Animals received no treatment (N = 7), meclofenamate (MECLO; 5 mg/kg i.p. and 5 mg/kg i.v.; N = 7) or indomethacin (INDO, 1 mg/kg i.v.; N = 6). Whole kidney fractional Li excretion fell from 26.2 +/- 1.5% in control rats to 12.8 +/- 1.3% and 14.6 +/- 1.3% in MECLO and INDO treated rats. Fractional delivery of Li to the LPT was not affected by PG synthesis inhibition. All of the rise in tubular Li reabsorption took place between the LPT and EDT; at the EDT fractional Li delivery fell from 32.3 +/- 2.0% in the control group to 19.1 +/- 1.6% and 20.0 +/- 1.4% in the rats given MECLO or INDO. Water reabsorption between the LPT and EDT also increased. The tubular fluid/plasma Li concentration ratio ([T/P]Li) at the LPT was approximately 1.15 in all groups of rats. At the EDT, this ratio was approximately 1.06 in control rats, but only approximately 0.82 (P < 0.01) in rats subjected to PG synthesis inhibition. The finding that the [T/P]Li fell from values exceeding unity at the LPT to values below unity at the EDT during PG synthesis inhibition indicates that reabsorption of Li between these sites was stimulated to a greater extent than that of water. This dissociation strongly suggests that at least part of the increased Li reabsorption between the LPT and EDT took place in the water-impermeable thick ascending limb.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1994

Renal autacoids are involved in the stimulation of renin gene expression by low perfusion pressure.

This study aimed to examine the role of local autacoids for the regulation of renin secretion and renin gene expression by the renal perfusion pressure. To this end the effects of unilateral reduction of renal perfusion by 0.2 mm clips on plasma renin activity and on renal renin mRNA levels were examined in rats treated with the cyclooxygenase inhibitor meclofenamate (8 mg/kg body wt, twice a day), with the NO-synthase inhibitor nitro-L-arginine-methylester (L-NAME, 40 mg/kg body wt, twice a day) or with a combination of both. L-NAME alone decreased basal PRA values from 9.9 to 5.4 ng Ang I/hr x ml, while meclofenamate alone and the combination meclofenamate/L-NAME had no consistent effect on basal PRA. Unilateral renal artery clipping increased PRA values from 9.9 ng Ang I/hr x ml to 34, 27, and 16 ng Ang I/hr x ml in vehicle, meclofenamate, and L-NAME treated animals, respectively, but did not increase PRA in meclofenamate/L-NAME treated rats (9.5 ng Ang I/hr x ml). Renal renin mRNA levels in the clipped kidneys increased 4.8-, 2.6-, 2.5- and 1.8-fold in the clipped kidneys in vehicle, meclofenamate, L-NAME and meclofenamate/L-NAME injected animals, respectively. These findings indicate that both the inhibition of prostaglandin synthesis and of the formation of endothelium-derived relaxing factor (EDRF) attenuate the increase of renin gene expression and of renin secretion in response to acute unilateral renal hypoperfusion and that the effects of both maneuvers are additive.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Control of renin gene expression in 2 kidney-1 clip rats.

This study was done to investigate the mechanisms that underly the changes of renal renin gene expression upon hypoperfusion of one kidney. To this end the left renal arteries of male Sprague-Dawley rats were clipped with 0.2 mm silver clips and renal renin mRNA levels were assayed by RNase protection during the first ten days after clipping. Unilateral reduction of renal blood flow led to transient maximal fivefold increases of renin mRNA levels in the clipped kidneys and to sustained suppression of renin gene expression to 20% of the control value in the contralateral intact kidneys. Inhibition of prostaglandin (PG) formation by meclofenamate or EDRF synthesis by L-NAME markedly attenuated the increase of renin mRNA levels in response to clipping, and a combination of PG/EDRF inhibition almost abolished the increase of renin mRNA levels. Inhibition of PG/EDRF formation did not change the suppression of renin mRNA levels in the contralateral intact kidneys. Neither did renal denervation nor inhibition of macula densa function by furosemide prevent the suppression of renin gene expression in response to unilateral renal artery clipping. Only converting enzyme inhibition by ramipril and blockade of Ang II-AT1 receptors by losartan attenuated the decrease of renin mRNA levels in the contralaterals to clipped kidneys. These findings suggest that intact PG and EDRF synthesis represent stimulatory signals for renin gene expression that are required for the elevation of renin mRNA levels upon unilateral renal hypoperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Cerebral vasoconstriction produced by vasopressin in conscious goats: role of vasopressin V(1) and V(2) receptors and nitric oxide.

To examine the role of vasopressin V(1) and V(2) receptors, nitric oxide and prostanoids in the cerebrovascular effects of arginine vasopressin, cerebral blood flow was electromagnetically measured in awake goats. In 16 animals, vasopressin (0.03 - 1 microg), injected into the cerebral circulation, caused increments of resting cerebrovascular resistance which ranged from 18% (0.03 microg, P<0.01) to 79% (1 microg, P<0.01). Desmopressin (0.03 - 1 microg, four goats) did not affect significantly cerebrovascular resistance. The cerebrovascular resistance increases by vasopressin were reduced significantly by the antagonist for vasopressin V(1) receptors d(CH(2))(5)Tyr(Me)-AVP in a rate depending way (five (six goats) and 15 (four goats) microg min(-1)), and by the mixed antagonist for vasopressin V(1) and V(2) receptors desGly-d(CH(2))(5)-D-Tyr(Et)Val-AVP (5 microg min(-1), four goats), and they were not significantly affected by the antagonist for vasopressin V(2) receptors d(CH(2))(5), D-Ile(2), Ile(4)-AVP (5 microg min(-1), four goats). The inhibitor of nitric oxide synthesis N(w)-nitro-L-arginine methyl ester (L-NAME, 47 mg kg(-1) i.v., five goats) augmented cerebrovascular resistance by 130% (P<0.01), and for 24 h after this treatment the cerebrovascular effects of vasopressin were potentiated. The inhibitor of cyclo-oxygenase meclofenamate (6 mg kg(-1) i.v., five goats) did not modify significantly resting haemodynamic variables measured or the cerebrovascular effects of vasopressin. Therefore, the vasopressin-induced cerebral vasoconstriction may be mediated by vasopressin V(1) receptors, without involvement of vasopressin V(2) receptors, and may be modulated by nitric oxide but not by prostanoids.

Animals↗
PubMed2002

Relaxation by urocortin of human saphenous veins.

Urocortin, an endogenous peptide structurally related to corticotropin-releasing factor (CRF), has potent cardiovascular effects, suggesting that it may be of significance in cardiovascular regulation. The objective of this study was to analyse the effects of urocortin and its action mechanisms on human blood vessels. To this, 3 mm long segments from human saphenous veins were prepared for isometric tension recording in an organ bath. In the segments at basal resting tone, urocortin did not produce any effect, but in the segments precontracted with endothelin-1 (1 - 10 nM), urocortin (1 pM - 10 nM) produced concentration-dependent relaxation. This relaxation was not modified by the inhibitor of nitric oxide synthase NG-nitro-L-arginine methyl ester (L-NAME, 100 microM), but it was potentiated by the cyclo-oxygenase inhibitor meclofenamate (10 microM) and it was reduced by the inhibitors of high-conductance Ca2+-dependent potassium channels tetraethylammonium (TEA, 10 mM) and charybdotoxin (100 nM). These results indicate that human saphenous veins are very sensitive to urocortin, which produces vascular relaxation by a mechanism independent of nitric oxide and dependent of high-conductance Ca2+-dependent potassium channels, and that it may be opposed by the release of vasoconstrictor prostanoids. Therefore, urocortin may be of significance for regulation of the venous circulation in humans.

Adult↗