14 results on '"Salazar, F."'
Search Results
2. Interaction between angiotensin II and nitric oxide in control of renal hemodynamics in conscious...
- Author
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Alberola, Antonio M. and Javier Salazar, F.
- Subjects
- *
ANGIOTENSINS , *NITRIC oxide , *KIDNEY physiology , *BIOCHEMICAL mechanism of action - Abstract
Studies the interaction between angiotensin II and nitric oxide in the control of renal hemodynamics in conscious dogs. Kidney functions; Sodium excretion; Endothelial factors.
- Published
- 1994
3. Role of nitric oxide in the renal hemodynamic response to a meat meal.
- Author
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Javier Salazar, F. and Alberola, Antonio
- Subjects
- *
NITRIC oxide , *KIDNEY physiology , *HEMODYNAMICS , *DOG physiology , *PHYSIOLOGY - Abstract
Tests the hypothesis that nitric oxide is involved in the renal hyperemic responses to a meat meal in dogs. Vasodilation and hyperfiltration after ingesion of a meat meal; Effects of a meat meal on renal hemodynamics; Intrarenal infusion of NG-nitro-L-arginine methyl ester to inhibit nitric oxide synthesis within the kidney.
- Published
- 1994
4. Interactions between angiotensin and nitric oxide in the renal response to volume expansion.
- Author
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Llinás MT, González JD, and Salazar FJ
- Subjects
- Angiotensin-Converting Enzyme Inhibitors pharmacology, Animals, Arginine analogs & derivatives, Arginine pharmacology, Captopril pharmacology, Dogs, Female, Hemodynamics, Lithium urine, Male, NG-Nitroarginine Methyl Ester, Natriuresis drug effects, Nitric Oxide antagonists & inhibitors, Nitric Oxide Synthase antagonists & inhibitors, Renal Circulation, Renin-Angiotensin System physiology, Angiotensin II physiology, Blood Volume, Kidney drug effects, Nitric Oxide physiology
- Abstract
This study examined, in anesthetized dogs, the possible interactions between nitric oxide (NO) and angiotensin II (ANG II) in mediating the renal response to an extracellular volume expansion (ECVE). It was found that the intrarenal maintenance of ANG II levels (group 1) or the intrarenal NO synthesis inhibition (group 2) did not induce changes in renal hemodynamics but reduced (P < 0.05) the ECVE-induced increments in sodium excretion and fractional lithium excretion (FeLi). In the third group, ANG II synthesis was inhibited during NO synthesis blockade. It was found in this group that the NO synthesis inhibition reduced the ECVE-induced increment in sodium excretion (P < 0.05) but did not modify the ECVE-induced increment in FeLi. These results suggest that the increase of proximal sodium reabsorption induced by the No synthesis inhibition is mediated by endogenous ANG II levels. In the fourth group, it was observed that NO synthesis inhibition, during the intrarenal maintenance of ANG II levels, induced a decrease of renal blood flow (P < 0.05) and reduced the natriuretic response to ECVE to a lower level (P < 0.05) than that observed in groups 1 and 2. The results of this group suggest that endogenous NO modulates the vasoconstrictor and antinatriuretic effects of ANG II during an ECVE. In summary, the results of this study suggest that there is an important interaction between NO and ANG II in mediating the renal response to an ECVE.
- Published
- 1995
- Full Text
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5. Role of prostaglandins and nitric oxide in mediating renal response to volume expansion.
- Author
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Salazar FJ, Llinas MT, Gonzalez JD, Quesada T, and Pinilla JM
- Subjects
- Animals, Arginine pharmacology, Blood Pressure drug effects, Dogs, Extracellular Space physiology, Female, Glomerular Filtration Rate drug effects, Homeostasis, Kidney drug effects, Male, NG-Nitroarginine Methyl Ester, Natriuresis drug effects, Nitric Oxide antagonists & inhibitors, Potassium urine, Reference Values, Regional Blood Flow drug effects, Renal Artery drug effects, Renal Artery physiology, Renal Circulation drug effects, Renal Circulation physiology, Arginine analogs & derivatives, Hemodynamics drug effects, Indomethacin pharmacology, Kidney physiology, Meclofenamic Acid pharmacology, Nitric Oxide physiology, Prostaglandins physiology
- Abstract
The objective of the present study was to examine, in anesthetized dogs, the possible interaction between prostaglandins (PG) and nitric oxide (NO) in mediating the renal response to an extracellular volume expansion (ECVE). The renal response to ECVE was examined during 1) intrarenal infusion of a PG synthesis inhibitor, 2) intrarenal administration of a NO synthesis inhibitor, and 3) simultaneous inhibition of PG and NO synthesis in the right kidney. Compared with the control group, the ECVE-induced increments in sodium excretion and fractional excretion of lithium were not affected by the PG synthesis inhibition. The NO synthesis inhibition did not induce changes in renal hemodynamics but reduced (P < 0.05) the ECVE-induced increments in sodium excretion and fractional excretion of lithium. When PG and NO synthesis were simultaneously inhibited in the right kidney during ECVE, there were no significant differences between the renal hemodynamics of both kidneys. However, compared with the left kidney, the ECVE-induced changes in sodium excretion and fractional excretion of lithium were reduced in the right kidney. The reduction of the natriuretic response to ECVE was greater (P < 0.05) than in the dogs where only NO synthesis was inhibited. Our results suggest a major interaction between NO and PG in mediating the renal hemodynamic and excretory responses to an increase in extracellular volume.
- Published
- 1995
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- View/download PDF
6. Role of nitric oxide in the renal hemodynamic response to a meat meal.
- Author
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Salazar FJ, Alberola A, Nakamura T, and Granger JP
- Subjects
- Animals, Arginine pharmacology, Blood Pressure drug effects, Dogs, Glomerular Filtration Rate drug effects, Hemodynamics drug effects, NG-Nitroarginine Methyl Ester, Regional Blood Flow drug effects, Renal Circulation drug effects, Time Factors, Vascular Resistance drug effects, Arginine analogs & derivatives, Dietary Proteins, Eating, Hemodynamics physiology, Kidney blood supply, Meat, Nitric Oxide physiology, Renal Circulation physiology
- Abstract
Ingestion of a high-protein meat meal results in significant increases in renal plasma flow (RPF) and glomerular filtration rate (GFR). The mechanism involved in this hemodynamic response to the meat meal has not yet been fully elucidated. The present study was designed to test the hypothesis that nitric oxide (NO) is involved in the renal hyperemic responses to a meat meal. To test this hypothesis, renal hemodynamic response to a meat meal (10 g/kg) was determined in conscious, chronically instrumented dogs with (n = 9) and without (n = 7) an intrarenal NO synthesis inhibition with NG-nitro-L-arginine methyl ester (L-NAME, 3 micrograms.kg-1.min-1 intrarenally). Under control conditions, the meat meal resulted in significant renal hyperemia. Three hours after ingestion of the meat meal, GFR (43 +/- 3 to 59 +/- 6 ml/min) and RPF (128 +/- 10 to 160 +/- 17 ml/min) progressively increased by approximately 40 and 25%, respectively. In contrast, pretreatment with intrarenal infusion of L-NAME abolished the GFR (48 +/- 6 to 52 +/- 6 ml/min) and RPF (129 +/- 20 to 121 +/- 17 ml/min) increases induced by the meat meal. Pretreatment with L-arginine (0.5 mg.kg-1.min-1) plus L-NAME (3 micrograms.kg-1.min-1) did not modify the meat meal-induced changes in GFR (41 +/- 4 to 66 +/- 6 ml/min) and RPF (127 +/- 9 to 182 +/- 14 ml/min). In summary, a meat meal in dogs results in marked increases in RPF and GFR. Intrarenal NO synthesis inhibition abolished the RPF and GFR responses to the meat meal.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1994
- Full Text
- View/download PDF
7. Role of prostaglandins on the renal effects of angiotensin and interstitial pressure during volume expansion.
- Author
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Pinilla JM, Alberola A, González JD, Quesada T, and Salazar FJ
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- Angiotensin-Converting Enzyme Inhibitors pharmacology, Animals, Captopril pharmacology, Cyclooxygenase Inhibitors pharmacology, Diuresis drug effects, Dogs, Extracellular Space drug effects, Female, Kidney physiology, Lithium urine, Male, Natriuresis drug effects, Prostaglandin Antagonists, Angiotensin II pharmacology, Extracellular Space physiology, Hydrostatic Pressure, Kidney drug effects, Prostaglandins physiology, Sodium Chloride pharmacology
- Abstract
This study was undertaken to determine, in anesthetized dogs, the role of renal prostaglandins (PG) in mediating the natriuretic response to increased renal interstitial hydrostatic pressure (RIHP) during extracellular volume expansion (ECVE) with isotonic saline. It was also determined if the intrarenal angiotensin II (ANG II) effects during ECVE are potentiated by the inhibition of PG synthesis. ECVE induced similar elevations of RIHP, natriuresis, and fractional lithium excretion in dogs treated (n = 7) and not treated with a PG synthesis inhibitor (n = 5). In other experimental groups, the effects of the intrarenal maintenance of ANG II levels (n = 6) by infusing captopril and ANG II into the right renal artery were compared with those induced by the simultaneous infusion of captopril, ANG II, and a PG synthesis inhibitor (n = 6). In response to ECVE, renal blood flow and glomerular filtration rate were similar in both kidneys when ANG II levels were maintained constant and were significantly higher in the left kidney when ANG II levels were maintained constant and PG synthesis was inhibited in the right kidney. However, when compared with the left kidney, the ECVE-induced increments of natriuresis and RIHP in the right kidney were reduced by the same magnitude when intrarenal ANG II was maintained constant with (36 and 53%, respectively) and without (40 and 54%, respectively) the simultaneous PG synthesis inhibition. Our results indicate that during ECVE, renal PGs do not play an important role in mediating the RIHP-induced increments in natriuresis and decrements in proximal sodium reabsorption. (ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1993
- Full Text
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8. Role of intrarenal angiotensin II in mediating renal response to volume expansion.
- Author
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Pinilla JM, Perez MC, Hernandez I, Quesada T, García-Estañ J, and Salazar FJ
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- Angiotensin II administration & dosage, Angiotensin II physiology, Animals, Atrial Natriuretic Factor metabolism, Captopril administration & dosage, Captopril pharmacology, Diuresis, Dogs, Female, Glomerular Filtration Rate drug effects, Homeostasis, Hydrostatic Pressure, Infusions, Intra-Arterial, Kidney drug effects, Male, Natriuresis, Renal Artery physiology, Renal Circulation drug effects, Renin blood, Saralasin administration & dosage, Saralasin pharmacology, Angiotensin II pharmacology, Kidney physiology
- Abstract
Natriuresis induced by extracellular volume expansion (ECVE) is accompanied by a decrease in renin release and by an increase of renal interstitial hydrostatic pressure (RIHP). This study was undertaken to examine, in anesthetized dogs, the relative role of intrarenal angiotensin II (ANG II) changes in mediating natriuresis, diuresis, and increases in RIHP induced by two different levels of volume expansion (1.5 and 5% body wt in 45 min) with isotonic saline. Intrarenal ANG II levels were maintained in the right kidney throughout the experiment by simultaneously infusing captopril (0.8 micrograms.kg-1.min-1) and ANG II (1 ng.kg-1.min-1) into the right renal artery. In response to 5% ECVE, increases in RIHP, natriuresis, and diuresis were inhibited in the right kidney by 55, 40, and 47% respectively, when compared with the left kidney. Significant increases occurred in plasma atrial natriuretic peptide (ANP) levels during 5% ECVE. Maintenance of constant intrarenal ANG II levels during 1.5% ECVE completely abolished the increment of RIHP and diuresis and inhibited the natriuretic response by 80% in the right kidney when compared with the left kidney. Plasma ANP levels did not change during the 1.5% ECVE. No differences between kidneys were found when the intrarenal effects of ANG II were blocked with saralasin before saline loading. These results suggest that increases in RIHP, natriuresis, and diuresis during ECVE are partially mediated by decreases in intrarenal ANG II levels. Furthermore, these results indicate that the role of intrarenal ANG II levels in mediating the renal response to ECVE is more important when plasma ANP levels do not change than when they are increased.
- Published
- 1991
- Full Text
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9. Hemodynamic effects of chronic infusion of rANP in renal hypertensive rats.
- Author
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Fenoy FJ, Quesada T, García-Salom M, Romero JC, and Salazar FJ
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- Animals, Atrial Natriuretic Factor blood, Blood Pressure, Infusions, Intravenous, Male, Rats, Rats, Inbred Strains, Time Factors, Atrial Natriuretic Factor pharmacology, Hemodynamics drug effects, Hypertension, Renovascular physiopathology
- Abstract
The purpose of this study was to evaluate the hemodynamic effects induced by an infusion of synthetic rat atrial natriuretic peptide (rANP, 0.5 micrograms/h iv) during 5 consecutive days in conscious normotensive and two-kidney, one-clip hypertensive (2K,1C) rats. Changes in plasma ANP (pANP) levels and plasma renin activity (PRA) were also determined. The administration of ANP in 2K,1C rats induced a significant decrease in mean arterial pressure (MAP) from 169 +/- 3 to 138 +/- 3, and 149 +/- 3 mmHg by 2 and 5 days of infusion, respectively. This hypotension was accompanied by a significant fall in cardiac index (CI) from 400 +/- 16 to 348 +/- 14 ml.min-1.kg-1 after 2 days of ANP treatment. However, CI returned to the basal levels at the third day, and a significant decrease in total peripheral resistance (TPR) was observed by 3 and 5 days of ANP infusion. The administration of the same dose of ANP in normotensive rats did not induce changes in MAP, but CI decreased (P less than 0.001) transitorily during the first 2 days and returned to control values thereafter. Basal pANP levels were significantly elevated in the hypertensive animals (176 +/- 40 pg/ml) when compared with the normotensive rats (82 +/- 10 pg/ml). The ANP infusion resulted in lower (P less than 0.05) pANP levels in hypertensive (1,017 +/- 234 pg/ml) than in normotensive rats (3,466 +/- 975 pg/ml). PRA did not change in any group during the administration of ANP.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1989
- Full Text
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10. Renal effects of ANP without changes in glomerular filtration rate and blood pressure.
- Author
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Salazar FJ, Fiksen-Olsen MJ, Opgenorth TJ, Granger JP, Burnett JC Jr, and Romero JC
- Subjects
- Animals, Dogs, Dose-Response Relationship, Drug, Female, Kidney Cortex blood supply, Male, Prostaglandins urine, Regional Blood Flow drug effects, Sodium metabolism, Atrial Natriuretic Factor pharmacology, Blood Pressure drug effects, Glomerular Filtration Rate drug effects, Kidney drug effects
- Abstract
The aim of the present study was to determine if atrial natriuretic peptide (ANP)-induced natriuresis is dependent on increases in glomerular filtration rate (GFR). Intrarenal blood flow distribution and urinary excretion of prostaglandins were also determined during the infusion of a dose of ANP that does not induce changes in GFR and mean arterial pressure (MAP). It was found that the intrarenal infusion of ANP (8-33) at a dose of 0.05 micrograms X kg-1. min-1 in seven anesthetized dogs did not produce any change in GFR or MAP, but its natriuretic effect was similar to that obtained by a larger dose (0.3 micrograms X kg-1 X min-1, n = 5) that produces significant changes in both MAP and GFR. The natriuresis induced by the lower dose of ANP was associated with a redistribution (P less than 0.05) of renal blood flow (RBF) from the superficial to the juxtamedullary cortex and with an increase (P less than 0.05) in urinary excretion of prostaglandins E2 (PGE2) (0.8 +/- 0.2 to 2.4 +/- 1.0 ng/min) and 6-keto-F1 alpha (6-keto-PGF1 alpha) (2.8 +/- 0.6 to 5.5 +/- 1.7 ng/min). Renin secretion rate decreased from 610 +/- 165 to 279 +/- 61 ng angiotensin I/min. These results show that the natriuresis induced by ANP is not necessarily produced by an increase in GFR and is associated with a redistribution of RBF to the deep cortex and an increase in urinary excretion of PGE2 and 6-keto-PGF1 alpha.
- Published
- 1986
- Full Text
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11. Possible modulatory role of angiotensin II on atrial peptide-induced natriuresis.
- Author
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Salazar FJ, Granger JP, Fiksen-Olsen MJ, Bentley MD, and Romero JC
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- Animals, Blood Pressure, Dogs, Female, Glomerular Filtration Rate, Male, Regional Blood Flow, Angiotensin II pharmacology, Atrial Natriuretic Factor pharmacology, Natriuresis drug effects
- Abstract
Studies showing that atrial natriuretic peptides (ANP) induce a suppression of the renin-angiotensin system suggest that there might be a modulatory influence of angiotensin II (ANG II) on the natriuretic effect of the ANP system. To evaluate this possibility we assessed, in anesthetized dogs, the net increments in fractional excretion of sodium (FENa) and lithium (FELi) produced by ANP and by the inhibition of ANG II formation with captopril. These agents were infused at separate time periods into the renal artery at a maximal level that has been shown not to alter glomerular filtration rate (GFR). ANP caused an increment in FENa of 4.0 +/- 0.2, whereas captopril caused a much smaller increase of 0.2 +/- 0.04, indicating that most of the natriuretic effect of ANP is unlikely to be solely accounted for by inhibition of ANG II. The administration of both ANP and captopril produced increases in the FELi used as a marker for proximal tubular reabsorption. An infusion of ANG II superimposed on the infusion of captopril reduced the FENa from 1.5 +/- 0.3 to 0.8 +/- 0.1. Under these conditions the administration of ANP produced an increment of 2.7 +/- 0.4 in the FENa. This increase in FENa is 32.5% less than the net increase obtained when ANP was given in the absence of ANG II, whereas under these conditions FELi remained statistically unchanged. These results suggest that the modulatory activity of ANG II on the natriuretic affect of ANP could be negligible under normal conditions.
- Published
- 1987
- Full Text
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12. Effects of hypertonic saline infusion and water drinking on atrial peptide.
- Author
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Salazar FJ, Granger JP, Joyce ML, Burnett JC Jr, Bove AA, and Romero JC
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- Animals, Arginine Vasopressin blood, Blood Pressure drug effects, Dogs, Female, Hematocrit, Kinetics, Male, Water, Water-Electrolyte Balance, Atrial Natriuretic Factor blood, Drinking, Saline Solution, Hypertonic pharmacology, Sodium Chloride pharmacology
- Abstract
This study was undertaken to define the changes in plasma levels of atrial natriuretic peptide (ANP) induced by hypertonic saline infusion followed by spontaneous water drinking and to determine whether these changes in ANP are correlated with changes in right atrial pressure (RAP) and plasma levels of vasopressin (AVP). Conscious dogs (n = 5) were infused with hypertonic saline (6%) at a rate of 1.4 ml/min for 4 h. Water was withheld for the first 2 h and administered ad libitum for the final 2 h. Hypertonic saline infusion induced increases (P less than 0.05) in plasma osmolality (posM), pAVP, mean arterial pressure (MAP), and RAP (1.9 +/- 0.6 to 3.1 +/- 0.7 mmHg). These changes were accompanied by an increase of pANP (68 +/- 14 to 120 +/- 33 pg/ml, P less than 0.05). Spontaneous water drinking (1,410 +/- 127 ml) returned posM and pAVP to control levels and produced a further and significant increment in RAP (150%) and pANP (100%). During the water-drinking phase MAP was not further altered, and hematocrit decreased by 11.1% (P less than 0.05). A positive linear correlation (P less than 0.001) was found between increases in RAP and pANP. The administration of an AVP vasopressor antagonist in a similar protocol, and before hypertonic saline infusion, inhibited the increase of MAP, but it did not alter the changes of posM, hematocrit, RAP, nor pANP. These results suggest that changes in the release of ANP during increases in posM and after spontaneous water drinking are predominantly controlled by changes in RAP.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1986
- Full Text
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13. Atrial natriuretic peptide levels during acute and chronic saline loading in conscious dogs.
- Author
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Salazar FJ, Romero JC, Burnett JC Jr, Schryver S, and Granger JP
- Subjects
- Animals, Consciousness, Dogs, Female, Time Factors, Atrial Natriuretic Factor blood, Sodium Chloride pharmacology
- Abstract
The purpose of the present study was to determine if acute and chronic increases in sodium intake by isotonic saline infusion are accompanied by changes in plasma concentrations of atrial natriuretic peptide (PANP). Acute saline loading (5% body wt) over a 30-min period in seven conscious chronically instrumented dogs produced a significant increase in PANP (48 +/- 5 to 119 +/- 24 pg/ml, P less than 0.05). However, chronic and progressive increments of sodium intake from 5 to 75 to 300 meq/day for 7 days, each by isotonic saline infusion, were examined in the same group of dogs and had no significant effect on PANP. PANP's were 37 +/- 7, 39 +/- 8, and 33 +/- 5 pg/ml when sodium intake was changed from 5 to 75 to 300 meq/day, respectively. The increase of sodium intake from 5 to 75 meq/day produced decreases of plasma renin activity (PRA) (2.5 +/- 0.5 to 1.5 +/- 0.4 ng angiotensin I X ml-1 X h-1, P less than 0.05), plasma aldosterone concentration (PAC) (19.3 +/- 5.4 to 2.9 +/- 0.4 pg/ml, P less than 0.05), and urinary excretion of prostaglandin E2 (760 +/- 131 to 320 +/- 58 pg/min, P less than 0.05). Further increase of sodium intake to 300 meq/day induced decreases of PRA and PAC to undetectable levels and an increase of urinary excretion of 6-ketoprostaglandin F1 alpha (649 +/- 95 to 1,056 +/- 148 pg/min, P less than 0.05). Before the completion of the study, sodium intake was decreased from 300 to 75 meq/day.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1986
- Full Text
- View/download PDF
14. Hemodynamic alterations in chronically conscious unrestrained diabetic rats.
- Author
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Carbonell LF, Salom MG, Garcia-Estañ J, Salazar FJ, Ubeda M, and Quesada T
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- Animals, Blood Glucose analysis, Body Weight, Chronic Disease, Consciousness, Diabetes Mellitus, Experimental blood, Diabetes Mellitus, Experimental drug therapy, Insulin therapeutic use, Male, Motor Activity, Rats, Rats, Inbred Strains, Streptozocin, Diabetes Mellitus, Experimental physiopathology, Hemodynamics drug effects
- Abstract
Important cardiovascular dysfunctions have been described in streptozotocin (STZ)-diabetic rats. To determine the influence of these changes on the hemodynamic state and whether insulin treatment can avoid them, different hemodynamic parameters, obtained by the thermodilution method, were studied in STZ-induced (65 mg/kg) diabetic male Wistar rats, as well as in age-control, weight-control, and insulin-treated diabetic ones. All rats were examined in the conscious, unrestrained state 12 wk after induction of diabetes or acidified saline (pH 4.5) injection. At 12 wk of diabetic state most important findings were normotension, high blood volume, bradycardia, increase in stroke volume, cardiac output, and cardiosomatic ratio, and decrease in total peripheral resistance and cardiac contractility and relaxation (dP/dtmax and dP/dtmin of left ventricular pressure curves). The insulin-treated diabetic rats did not show any hemodynamic differences when compared with the control animals. These results suggest that important hemodynamic alterations are present in the chronic diabetic state, possibly conditioning congestive heart failure. These alterations can be prevented by insulin treatment.
- Published
- 1987
- Full Text
- View/download PDF
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