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Biomedical subjects

C Caramelo

Publications and source records attributed to C Caramelo.

At least 91 records · Page 5Linked to original sources
PubMed1992

Renal and systemic effects of aminoacids administered separately: comparison between L-arginine and non-nitric oxide donor aminoacids.

The present study examined the mechanisms of the renal effect of the NO-donor aminoacid, L-Arg and different non-NO-donor aminoacids, namely L-Asn, L-Ala, L-Gly L-Gln administered separately. In conscious, unrestricted Wistar rats, a bolus of L-Arg produced a short-lasting decrease in mean arterial pressure. No variations in mean arterial pressure were found with either L-Gly, L-Asn, L-Ala or L-Gln. This effect of L-Arg was inhibited by NwNLA, methylene blue and atropine and not affected by meclofenamate. Simultaneously, a dose-response diuretic and natriuretic effect was observed with all the aminoacids. In further experiments with L-Arg and L-Gly, this effect was associated with increased glomerular filtration rate, renal plasma flow, fractional sodium and free water excretion and urinary cyclic guanosine monophosphate. These effects of L-Arg and L-Gly were inhibited by NwNLA. On the contrary, no inhibition by NwNLA was detected on the diuretic, natriuretic and renal hemodynamic effects of L-Gln, and the diuretic and natriuretic effects of L-Asn or L-Ala. Our results show that all the assayed aminoacids were endowed of diuretic and natriuretic capabilities. Such effects were apparently related with a NO-mediated mechanism in the case of L-Arg and L-Gly, but not in the case of L-Gln, L-Asn or L-Ala, therefore suggesting that more than one mechanism is involved in the renal effect of the different aminoacids. Simultaneously, only L-Arg produced a NO-, cyclic guanosine monophosphate-dependent hypotensive effect, which was not shared by the other assayed aminoacids.

Amino Acids↗
PubMed1991

Inhibition by L-arginine of the endothelin-mediated increase in cytosolic calcium in human neutrophils.

The effect of endothelin (ET) on the cytosolic-free calcium [(Ca2+]i) changes in polymorphonuclear leukocytes (PMN) from normal humans and Wistar rats was investigated. ET induced a dose-related [Ca2+]i peak. This [Ca2+]i transient was blunted by TMB-8 (10(-5)M) and by Ca(2+)-free EGTA medium, therefore suggesting a role of both intracellular Ca2+ release and Ca2+ influx in the generation of the [Ca2+]i peak. Preincubation of PMN with the nitric oxide (NO)-donor L-arginine (L-Arg) markedly blocked the ET-induced [Ca2+]i transient in an enantiomerically-specific manner. A similar blunting effect of L-Arg on the fMLP (10(-7)M)-induced [Ca2+]i transient was detected. The L-Arg antagonist, NG-monomethyl-L-arginine (L-NMMA), reverted the L-Arg blocking effect on both ET- and fMLP-induced [Ca2+]i transients. These data suggest that ET has a potential role in activating Ca2+ mobilization in PMN, an effect that can be inhibited by L-Arg.

Arginine↗
PubMed1991

Peritonitis with CDC group IVc-2 bacteria in a patient on continuous ambulatory peritoneal dialysis.

A case of CDC group IVc-2 peritonitis in a patient on continuous ambulatory peritoneal dialysis (CAPD) is described. To the authors' knowledge, this is the first case reported of CAPD peritonitis in which a member of this unusual group of bacteria was isolated as the sole microorganism. As this microorganism is usually resistant to most antibiotics commonly used to treat peritonitis in patients on CAPD, microbiological investigations with identification and antimicrobial susceptibility tests are mandatory.

Gram-Negative Aerobic Bacteria↗
PubMed1991

Glomerular binding and contractile response to angiotensin II in rats with chronic experimental cirrhosis of the liver.

1. The effects of angiotensin II on glomerular filtration rate and renal plasma flow were studied in surgically instrumented conscious control and cirrhotic rats. In addition, angiotensin II binding and the contractile response to angiotensin II were studied in glomeruli isolated from cirrhotic and control rats. 2. Cirrhotic rats had a higher glomerular filtration rate and a higher renal plasma flow than control animals. A non-pressor dose of angiotensin II induced small but significant decreases in glomerular filtration rate and renal plasma flow in both control and cirrhotic rats, the effect on renal plasma flow being the most pronounced. 3. Plasma renin and aldosterone concentrations were similar in control and cirrhotic rats. 4. The cross-sectional area of glomeruli from cirrhotic rats was 42% greater than that of glomeruli from control animals. Angiotensin II (10(-9) mol/l) decreased the cross-sectional area of glomeruli from control animals by 6.4 +/- 0.9% and of glomeruli from cirrhotic rats by 6.6 +/- 0.8% (P = not significant for comparison between control and cirrhotic animals). 5. There were no differences between control and cirrhotic rats in the affinity of angiotensin II for its glomerular receptors. However, the angiotensin II receptor density was higher in cirrhotic than in control rats, thereby producing an increased total angiotensin II binding in cirrhotic rats. 6. Since no functional differences between control and cirrhotic animals were present in the response to angiotensin II, even though angiotensin II binding was increased, a post-receptor blockade of the angiotensin II signal could be present in cirrhotic rats.

Angiotensin II↗
PubMed1991

Mechanisms of renal effects of different agents stimulating production of cGMP.

The effect of agents stimulating the production of guanosine 3',5'-cyclic monophosphate (cGMP) by different mechanisms was compared in conscious unrestrained Wistar rats by administration of infusions of acetylcholine (ACh), sodium nitroprusside (SNP), and atrial natriuretic peptide (ANP). ACh (10 micrograms.kg-1.min-1, n = 8), SNP (200 micrograms.kg-1.min-1, n = 8), and ANP (0.5 micrograms.kg-1.min-1, n = 7) induced natriuresis (urinary Na gradient: 399, 499, and 504 microeq/h, respectively; P less than 0.001 with respect to baseline) and diuresis (urine volume gradient: 0.87, 0.82, and 0.92 ml/h, respectively; P less than 0.001). Urinary cGMP increased (P less than 0.001) with the three agents (delta pmol cGMP/min: ACh 22.3, SNP 42.5, and ANP 48.4); in addition, a parallel increase in renal cGMP content was observed with the three agents (ACh 1.6, SNP 2.8, and ANP 3.5 times with respect to controls; P less than 0.05). Mean arterial pressure did not change with the aforementioned dose of ANP but decreased by 10 and 40% with ACh and SNP, respectively. Glomerular filtration rate increased by a similar magnitude with the three compounds. The competitive inhibitor of L-arginine, N omega-nitro-L-arginine (L-NNA), significantly decreased the diuretic, natriuretic, and hypotensive effects of ACh without affecting the actions of SNP and ANP.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

Effects of extra- and intracellular pH on vascular action of arginine vasopressin.

Compared with control studies performed at an extra-cellular pH (pHe) of 7.4, when vascular smooth muscle cells (VSMC) were preincubated in an acid extracellular medium (pHe 7.0) for 60 min the maximal arginine vasopressin (AVP)-induced sustained cellular contraction was reduced, whereas preincubation in an alkaline extracellular medium (pHe 7.8) enhanced the vascular action of AVP. These changes in VSMC contraction were accompanied by a parallel decrease in AVP receptor affinity and cytosolic free calcium ([Ca2+]i) mobilization in the acid medium, increased AVP receptor affinity, and [Ca2+]i mobilization in alkaline medium. Because the changes in pHe were parallelled by changes in pHi, studies were performed in which only pHi was altered by administering the proton ionophore, carbonyl cyanide m-chlorophenylhydrazone (CCCP) (10(-6) M for 10 min). CCCP inhibited VSMC contraction in the absence of changes in AVP receptor binding and AVP-induced [Ca2+]i mobilization but abolished the AVP-induced cellular alkalinization. The results therefore indicate that in a nonbicarbonate buffer alterations in pHe may modulate the vascular responses to AVP by altering hormone receptor affinity, [Ca2+]i mobilization, and pHi.

Adenosine Diphosphate↗
PubMed1991

Mechanisms of rapid desensitization to arginine vasopressin in vascular smooth muscle cells.

This study characterized the rapid desensitization induced by arginine vasopressin (AVP) in vascular smooth muscle cells (VSMC) in culture. The Ca2+ mobilization response and, in some experiments, the intracellular pH changes were used as a probe for the desensitization phenomenon. In VSMC, AVP desensitization was homologous, concentration dependent, and occurred in less than 30 s. The desensitization was complete with 10(-7) M AVP. Receptor occupancy was a critical factor in the maintenance of desensitization, since complete hormone washing by acid glycine buffer produced an earlier (less than 5 min) recovery of the cell response, whereas partial hormone washing with saline (pH 7.4) required 15 min to produce any significant recovery. Protein kinase C activation was a significant mechanism in AVP desensitization, because protein kinase C downregulation inhibited the desensitization phenomenon. Receptor internalization was, however, not important for the desensitization phenomenon, since it still occurred at 4 degrees C. Treatment with pertussis toxin did not affect the Ca2+ mobilization response but decreased the AVP-mediated intracellular alkalinization, therefore suggesting that a Gi or Go protein may be involved in some but not all the aspects of the AVP signal transduction and the desensitization phenomena.

Animals↗
PubMed1990

Interaction of arginine vasopressin and angiotensin II on Ca2+ in vascular smooth muscle cells.

The non-osmotic release of arginine vasopressin (AVP) is associated with the concomitant activation of the renin-angiotensin and sympathetic nervous systems. In vivo studies suggest that a positive interaction may occur between AVP and angiotensin II (Ang II), and other Ca2+ mobilizing hormones. In the present study, the cellular mechanisms of this interaction between AVP and Ang II in vascular smooth muscle cell (VSMC) were examined. These results support the existence of a positive interaction between AVP and Ang II on Ca2+ mobilization in VSMC. In fact, the challenge of VSMC with combined AVP and Ang II, in a range from 5 x 10(-11) to 10(-8) M, enhanced cytosolic free Ca2+ ([Ca2+]i) and 45Ca2+ efflux in a more than additive manner. This potentiation, which was not dependent of the presence of extracellular calcium, correlated with an increased VSMC shape change. Moreover, the combination of subthreshold doses of AVP and Ang II (5 x 10(-11) M), which do not release Ca2+ alone, evoked a Ca2+ mobilizing response. A subthreshold dose of Ang II also shifted to the left the concentration-response curve of the AVP-mediated 45Ca2+ efflux. Since there were no changes in receptor binding of either hormone by the other hormone and the interaction of the two hormones on the production of inositol phosphatides was additive, the AVP and AII positive interaction on Ca2+ mobilization on VSMC may occur at the level of the intracellular Ca2(+)-releasing mechanism itself. Such an interaction can occur at hormone concentrations below the Ca2+ release threshold and may explain an increased functional response to the combination of pressor hormones compared to that of each hormone alone.

Angiotensin II↗
PubMed1990

Effect of inhibition of Na+/K(+)-adenosine triphosphatase on vascular action of vasopressin.

The present study was undertaken to examine the cellular interaction between a Na+/K(+)-ATPase inhibitor, ouabain, and arginine vasopressin (AVP) in rat vascular smooth muscle cells (VSMC) in culture. Preincubation with 10(-5) M ouabain for 60 min increased basal cytosolic free Ca2+ [( Ca2+]i) concentration and intracellular 45Ca2+ uptake. Ouabain, however, did not affect basal 45Ca2+ efflux or AVP-stimulated 45Ca2+ efflux. As assessed by cell shape change, preincubation with 10(-5) M ouabain for 60 min also enhanced the sustained cellular contractile effect of a submaximal (10(-8) M AVP, 21.5% vs. 30.5%, P less than 0.01) but not maximal dose of 10(-6) M AVP. Preincubation with 10(-5) M ouabain for 60 min did not change AVP-induced V1-specific surface receptor binding or AVP-induced inositol phosphate production but did however potentiate the mobilization of [Ca2+]i induced by a submaximal (10(-8) M AVP, 301 vs. 385 nM, P less than 0.01) but not a maximal dose of AVP. These effects of ouabain on the mobilization of [Ca2+]i were abolished by incubation in Ca2(+)-free buffer or 5 X 10(-5) M verapamil. Ouabain (10(-5) M) also enhanced the sustained cellular contractile effect of a direct protein kinase C activator, phorbol 12-myristate 13-acetate. The present results therefore indicate that the inhibition of Na+/K(+)-ATPase may enhance the vascular action of AVP, and perhaps other vasoconstrictors, by increasing the AVP-induced mobilization of [Ca2+]i and by potentiating the activity of protein kinase C stimulated by AVP through enhancing basal and AVP-stimulated cellular Ca2+ uptake.

Animals↗
PubMed1989

Effect of dietary sodium intake on the pressor reactivity to angiotensin II in rats with experimental cirrhosis of the liver.

The present experiments were designed to evaluate vascular reactivity to angiotensin II in rats with experimental cirrhosis of the liver (induced with CCl4 and phenobarbital) before ascites appearance. The systemic pressor response to angiotensin II in conscious animals and the contractile effect of angiotensin II in isolated femoral arteries were studied. In addition, the effect of high sodium intake on these parameters was also analyzed. Both renin and aldosterone plasma concentrations were similar in control and cirrhotic rats on the normal or on the high sodium diet. Basal mean arterial pressure was higher in control rats than in cirrhotic rats on the normal sodium (116 +/- 4 vs. 101 +/- 4 mmHg (1 mmHg = 133.3 Pa), p less than 0.05) or on the high sodium diet (118 +/- 7 vs. 98 +/- 6 mmHg). No differences in plasma renin activity or plasma aldosterone were found between control and cirrhotic rats. Upon injection of angiotensin II, control rats show a dose-dependent increase in mean arterial pressure which is higher in high sodium than in normal sodium rats. Cirrhotic rats showed a lower hypertensive response to angiotensin II than their corresponding control rats. In addition, no difference between pressor responses to angiotensin II was observed when normal sodium and high sodium cirrhotic rats were compared. On application of angiotensin II, femoral arteries of control and cirrhotic rats exhibited a dose-dependent contraction. However, maximal contraction was higher in high sodium control rats (145 +/- 12 mg) than in normal sodium control rats (99 +/- 6 mg, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1989

Interstitial dynamics in rats with early stage experimental cirrhosis of the liver.

Pathogenesis of edema in cirrhosis of the liver is still incompletely understood. The present study was designed to examine interstitial fluid dynamics in cirrhotic, non-ascitic rats, measuring interstitial fluid pressure by means of a subcutaneous plastic capsule in basal conditions during extracellular fluid volume expansion with Ringer solution and during albumin infusion. Urine flow and sodium excretion and plasma and interstitial fluid volumes were simultaneously measured. Cirrhotic rats exhibited reduced urine flow and sodium excretion, both in basal conditions and in response to expansion maneuvers. Plasma and interstitial fluid volumes were higher in cirrhotic than in control animals. Remarkable alterations were present in capsular pressures in cirrhotic rats. In the control rats, basal capsular pressure values were negative, and they increased after Ringer infusion and markedly decreased with albumin infusion. In contrast, in cirrhotic rats, basal capsular pressures were in the positive range and they remained nearly constant during ringer infusion and albumin administration. These results suggest that in cirrhotic rats there are significant alterations in systemic interstitial dynamics, even before ascites formation. Altered systemic capillary dynamics may therefore be important early changes that precede and thus contribute to the formation of edema in cirrhosis.

Animals↗
PubMed1989

Phorbol esters and arginine vasopressin in vascular smooth muscle cell activation.

Vascular smooth muscle cell (VSMC) contraction is the result of several interacting mechanisms. In this study such interactions in rat aortic VSMC in culture were examined with a focus on the role of protein kinase C-mediated mechanisms. The change in shape of VSMC was used as a functional parameter representative of contraction. The protein kinase C agonist, phorbol myristate acetate (PMA), and arginine vasopressin (AVP) induced a dose-dependent, progressive change in VSMC shape. The effects of PMA differed from AVP in the delay time necessary to reach the plateau of the response and in the absence with PMA of a transient rise in cytosolic free Ca2+ [( Ca2+]i). The effect of PMA was potentiated by the Ca2+ ionophore, ionomycin, and involved a verapamil-inhibitable transmembrane Ca2+ transport system. Protein kinase C inhibition by either isoquinolin-sulfonyl-O-2-methylpiperazine or protein kinase C desensitization significantly reduced the cell shape change induced by either PMA or AVP. In the case of AVP, this inhibitory effect occurred without affecting the [Ca2+]i transient. Therefore, the [Ca2+]i transient appears to be independent of acute protein kinase C regulation, since it is apparently not affected by the absence of protein kinase C activity. Protein kinase C activation by PMA produced intracellular alkalinization that is blocked by the sodium transport antagonist, amiloride. Amiloride also blocked the cell shape change induced by PMA or AVP. The intracellular alkalinization, however, was not necessary for the cell shape change to occur. Specifically, with the use of VSMC preincubated with fetal calf serum, PMA did not induce cellular pH changes but still produced cell shape changes.

Amiloride↗