Risk factors related to hypertension in a Spanish systemic lupus erythematosus cohort.
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Humans↗
Biomedical subjects
J M Sabio
Publications and source records attributed to J M Sabio.
More about Churg-Strauss syndrome and montelukast treatment.
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Acetates↗
A multicase family with primary Sjögren's syndrome.
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Adult↗
Role of nitric oxide in the systemic circulation of conscious hyper- and hypothyroid rats.
1. N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO biosynthesis, which blocks basal NO production, caused a similar increase of mean arterial pressure (MAP) in control hyper- and hypothyroid rats at the lowest dose, however, smaller pressor effects were observed with increasing doses in hyper- and hypothyroid rats. An additional dose of L-NAME (30 mg/kg), which produced no further increase in pressure, killed 90% of the hyperthyroid rats, whereas hypothyroid and control rats survived this additional dose. 2. The systemic responses to acetylcholine (ACh), an endothelium-dependent vasodilator that stimulates NO production/release, were significantly increased in hypothyroid rats, while hyperthyroid rats showed no significant differences when compared with controls. However, 10(-8) M ACh killed hyperthyroid rats, whereas control and hypothyroid rats survived this dose. 3. The maximal hypotensive response to sodium nitroprusside (SNP), an agonist that generates NO, was similar in intact controls, hyper- and hypothyroid rats. 4. These data indicate that hyper- and hypothyroidism show a reduction in basal NO synthesis/release, this reduced systemic NO tone being essential for life in hyperthyroid rats; whereas the response to ACh is not reduced and the hypotensive response to SNP did not differ between groups, indicating that the responsiveness of the systemic circulation to NO is not altered in either thyroid disorder.
Acetylcholine↗
Pressure-diuresis-natriuresis response in hyperthyroid and hypothyroid rats.
1. Renal responses to changes in renal perfusion pressure were studied in anaesthetized hyperthyroid (thyroxine, 300 micrograms day-1 kg-1) and hypothyroid (methimazole, 0.03% via drinking water) rats to determine whether an abnormality in the pressure-diuresis-natriuresis phenomenon is involved in the resetting of kidney function in these disorders. 2. There were no significant differences between control and hypothyroid rats with respect to the relationships between renal perfusion pressure and absolute or fractional water and sodium excretion. However, in hyperthyroid rats the pressure-diuresis-natriuresis mechanism was impaired. 3. Renal blood flow and glomerular filtration rate were well autoregulated and there were no differences between control and hypothyroid rats at every level of renal perfusion pressure. A significantly lower glomerular filtration rate was observed in hyperthyroid rats when data were expressed per gram kidney weight, but glomerular filtration rate was similar to that of control rats when normalized by body weight. 4. The shift in the pressure-diuresis-natriuresis response of hyperthyroid rats is mainly due to an increase in tubular reabsorption. Blunting of the renal pressure-diuresis-natriuresis mechanism in hyperthyroid rats may represent the functional resetting of the kidney necessary for sustained hypertension. However, a normal pressure-natriuresis response was observed in hypothyroid rats, in which blood pressure was markedly reduced.
Animals↗
Effects of Nw-nitro L-arginine methyl ester on the response to NaCl load in hyper- and hypothyroid rats.
We assessed the effects of the inhibition of endogenous nitric oxide (NO) synthesis with Nw-nitro-L-arginine methyl ester (L-NAME) on water and sodium handling after NaCl load containing the inhibitor at 0, 0.5, 5 and 50 mg/kg in conscious control, hyper- and hypothyroid rats. L-NAME at 0.5 mg/kg caused a similar decrease in diuresis and natriuresis in control and hypothyroid rats, whereas no changes were seen in the hyperthyroid group. The saline load with 5 mg/kg of L-NAME produced no significant changes with respect to the 0 dose in any variable in control and hypothyroid rats, but increased natriuresis in the hyperthyroid group. The highest dose of L-NAME (50 mg/kg) increased the diuretic and natriuretic response in control and hyperthyroid groups, whereas in the hypothyroid group no urinary variable was significantly modified with respect to the 0 dose. These results indicate that the antidiuretic and antinatriuretic effects of L-NAME at low doses are suppressed in hyperthyroid rats, whereas the diuretic and natriuretic effects at high doses are absent in hypothyroid rats. Our findings suggest that the modulatory role of NO on sodium and water excretion is affected in both thyroid disorders. In addition, the highest dose of L-NAME killed hyperthyroid rats, indicating that NO plays an essential role for life in hyperthyroidism.
Animals↗
Contribution of endothelium derived relaxing factors to acetylcholine induced vasodilatation in the rat kidney.
OBJECTIVE: The aim was to evaluate the contribution of nitric oxide (NO) and endothelium derived hyperpolarising factor (EDHF) to the endothelium dependent, acetylcholine induced vasodilatation in isolated perfused rat kidney. METHODS: The renal response to acetylcholine was compared in phenylephrine preconstricted renal vasculature under basal conditions and after the infusion of N omega-nitro-L-arginine (L-NAME), an inhibitor of NO synthesis, and tetraethylammonium, a non-specific blocker of potassium channels that inhibits acetylcholine induced hyperpolarisation. These inhibitors were given alone and together. In another experiment, the renal response to acetylcholine was compared when the vasculature was preconstricted with phenylephrine or with 40 and 80 mM KCl under basal conditions and after the infusion of L-NAME. All experiments were done in the presence of indomethacin. RESULTS: Inhibition of NO generation with L-NAME reduced the vasodilator responses to acetylcholine by approximately 50%, and enhanced the response to sodium nitroprusside in the isolated perfused kidney preconstricted with phenylephrine. Infusion of tetraethylammonium also decreased the response to acetylcholine by approximately 50% and increased vasodilatation responses to sodium nitroprusside. The simultaneous administration of both inhibitors (L-NAME and tetraethylammonium) had a summational effect which almost completely suppressed acetylcholine induced vasodilatation. Increasing concentrations of extracellular potassium produced a dose related decrease in acetylcholine induced vasodilatation. These attenuated responses were almost abolished after the infusion of L-NAME. CONCLUSIONS: Our results suggest that the vasodilator response to acetylcholine in isolated perfused rat kidneys is subserved by EDHF and nitric oxide, both endothelium derived mediators participating to a similar extent.
Acetylcholine↗
Increased endothelium-dependent renal vasodilation in cirrhotic rats.
We have evaluated the renal blood flow (RBF) response of cirrhotic rats to endothelium-dependent [acetylcholine (ACh)] and -independent [sodium nitroprusside (NP)] vasodilators. In anesthetized rats, ACh dose dependently increased RBF, but the response of the cirrhotic rats (n = 6) was significantly higher than that of the controls (n = 6). NP also increased RBF in a dose-dependent manner, but there were no differences between both groups. NG-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg i.v.) significantly reduced the responses to ACh in both groups, but those of the cirrhotic rats were still higher than those of the controls. In experiments performed in isolated perfused kidneys, preconstricted with phenylephrine, dose-response curves for ACh and NP were obtained in the presence of indomethacin. Both ACh and NP decreased renal perfusion pressure dose dependently, but only the response of the cirrhotic rats (n = 5) to ACh was significantly higher than that of the controls (n = 5). L-NAME (100 microM) significantly reduced the responses to ACh and increased those of NP and abolished the differences between groups, except at the high dose of ACh. These results demonstrate an elevated endothelium-dependent vasodilator response in the cirrhotic kidney, which is eliminated by combined prostaglandin and nitric oxide (NO) synthesis inhibition and suggest that increased intrarenal activity of NO may be contributing to the renal alterations of liver cirrhosis.
Acetylcholine↗
Vascular reactivity to vasoconstrictors in aorta and renal vasculature of hyperthyroid and hypothyroid rats.
Vascular reactivity to vasoconstrictors in relation to altered thyroid function was studied in two preparations: aortic strips and the isolated perfused kidney. To assess whether the possible alterations in vascular reactivity were restricted to a specific agonist or whether they involved the contractile system, receptor-mediated and nonspecific smooth muscle stimulants were used. Male Wistar rats were divided into three groups: control, hyperthyroid and hypothyroid rats. Aortic strips from hypothyroid rats were less sensitive to phenylephrine and KCl when the data were expressed in absolute values or as percentages of the maximum responses. Sensitivity and reactivity in strips from hyperthyroid rats were similar to those observed in control strips. Renal vasculature obtained from hypothyroid rats also showed a markedly reduced sensitivity to phenylephrine, with normal maximal responses. The response to vasopressin at 3-10(-11) mol/l was also decreased, as was the reactivity to barium chloride. In contrast, renal vasculature of hyperthyroid rats showed markedly enhanced reactivity to all agonists: the concentration-response curves were characterized by a similar threshold and a greater maximal response. These results demonstrate that hypothyroidism is accompanied by a marked decrease in sensitivity to vasoconstrictors in large arteries as well as in resistance vessels. This decrease may be secondary to a generalized alteration in the contractile system of vascular smooth muscle cells and may play a role in the decreased blood pressure in these animals. In contrast, isolated perfused kidneys of hyperthyroid rats showed increased vascular reactivity to vasoconstrictors, which may play a role in the maintenance of elevated blood pressure in these animals.
Animals↗
Chronic insulin treatment in rats: evidence against a role for insulin as a pressor agent.
1. The present study was undertaken to test whether insulin acts as a pressor agent and causes hypertension in rats. 2. Insulin at doses of 10 or 100 units day-1 kg-1 was administered daily by subcutaneous injection to normal rats for 6 weeks. As it has been suggested that sodium retention plays a major role in the putative hypertensive activity of this hormone, insulin was also administered to saline- (1% NaCl) drinking rats according to the same protocol. Water- and saline-drinking rats served as controls. 3. After 6 weeks of insulin treatment, the mean arterial blood pressure did not increase in any of the insulin-treated or the insulin-salt-treated groups. However, in both insulin-salt-treated groups, absolute and relative ventricular and renal hypertrophy with increased ventricular water content as well as increased urine output with reduced osmolality were observed. 4. All insulin-treated groups showed increased plasma levels of glucose, insulin and antidiuretic hormone when compared with their respective controls. 5. These results demonstrate that chronic insulin treatment did not increase blood pressure in rats, even when drinking water was supplemented with NaCl, and suggest that a polyuria-polydipsia syndrome was present in both insulin-salt-treated groups. Moreover, increased plasma levels of antidiuretic hormone were observed in all insulin-treated groups.
Animals↗
Application of flow cytometry to the study of antiphagocytic properties of Klebsiella pneumoniae capsular polysaccharide.
We used flow cytometry to compare the effects of whole cells and capsular polysaccharides of Klebsiella pneumoniae on the phagocytic ability ot polymorphonuclear leukocytes. Our results showed a light decrease in phagocytic activity in the presence of capsular polysaccharides, but a marked decrease with whole cells. Our findings suggest that the resistance to phagocytosis in these microorganisms is not due exclusively to their capsule, as claimed by other authors.
Flow Cytometry↗
Renal beta-adrenoceptors in thyroxine-treated rats.
The number of beta-adrenoceptors was measured in cardiac and renal cortex membranes from controls and thyroxine-treated rats. Two methods of membrane preparation (sucrose- and KCl-extraction) were compared. KCl-extraction yielded a higher number of beta-adrenoceptors, accompanied by increased activity of the plasma membrane enzyme marker 5'-nucleotidase. Thyroxine increased the number of beta-adrenoceptors in both cardiac and renal cortex membranes prepared with both methods. These results suggest that: i) Enrichment of the membrane fraction may explain the higher number of beta-adrenoceptors found with KCl, ii) Thyroid hormone plays a role in the regulation of beta-adrenoceptors in the renal cortex.
5'-Nucleotidase↗
Effects on renal function and digoxin-like immunoreactivity produced by methimazole in low-renal mass hypertension.
This study evaluates the effects of methimazole, an antithyroid drug, on blood pressure, digoxin-like immunoreactive factor (DLIF) production and other variables related to salt and water metabolism in low-renal mass (LRM) hypertension. Drinking administration of methimazole (0.025%) from replacement of water by the 1% NaCl solution maintained the blood pressure of low-renal mass rats at normal levels during four weeks after hypertension induction. Serum and urinary excretion of DLIF were significantly increased in LRM rats with respect to controls; in all tests, the highest values of DLIF were found in LRM-methimazole treated (LRM-M) rats. Urinary excretion of DLIF showed positive correlations with diuresis and natriuresis in all three groups (control, LRM and LRM-M rats). However, the correlation between DLIF and sodium disappeared when both factors were expressed as a function of their concentrations. These results indicate that methimazole prevents LRM hypertension and suggest that DLIF might not represent the putative natriuretic hormone. Other findings were that methimazole-treatment reduced renal compensatory hypertrophy subsequent to subtotal nephrectomy, and did not modify the characteristic polyuria-polydypsia in this type of hypertension.
Animals↗