Recurrent depression: infectious-autoimmune etiology?
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Adolescent↗
Biomedical subjects
A Fernández-Rivas
Publications and source records attributed to A Fernández-Rivas.
Abnormal renal vascular reactivity to acetylcholine and nitroprusside in aging rats.
1. The actions of acetylcholine (ACh), CaCl2 and nitroprusside (NP) were studied in aortic strips and in the perfused kidneys from adult (4-6 months old) and aging (23-24 months old) rats. 2. ACh and CaCl2 produced a dose-related relaxation in aortic strips from adult and old rats; maximal responses to both vasodilators were significantly reduced (ACh: adult = 66.4 +/- 6.1%, Old = 27.1 +/- 5.7%, P < 0.001; CaCl2: adult = 75.6 +/- 3.9%, Old = 54.1 +/- 4.1%, P < 0.01) in aortas from old rats. NP-evoked relaxation was not significantly different between the two groups. 3. In kidneys from adult rats, ACh produced dose-related decreases in renal perfusion pressure (RPP), whereas, in kidneys from old rats, ACh produced a dose-related decrease at low doses, and biphasic responses (vasodilatation followed by vasoconstriction) at medium to high doses, with a reduced vasodilator component. Vasodilator response to ACh to the highest dose; ACh; adult = 78.7 +/- 2.8%, Old = 40.6 +/- 2.6%, P < 0.001). In kidneys from adult rats, NP produced a dose-related decrease in RPP. However, in kidneys from old rats, NP produced vasoconstriction at low doses, biphasic responses at medium doses (vasoconstriction followed by vasodilation), and vasodilation at the highest dose. 4. The results of the present study demonstrated that: (a) The isolated perfused kidney from aging rats had a dual response (with an important vasoconstrictor component) to ACh and NP, which may be due to the release of a nonprostanoid vasoconstrictor or to abnormalities in the renal vascular smooth muscle. In contrast, in aortic-strips from old and adult rats, these agents only caused relaxation; (b) aging is accompanied by reduced endothelium-dependent relaxation both in large arteries and in resistance vessels; and (c) large arteries from aging rats require a higher concentration of extracellular calcium to stabilize the membrane of smooth muscle cells.
Acetylcholine↗
Vascular reactivity and flow-pressure curve in isolated kidneys from rats with N-nitro-L-arginine methyl ester-induced hypertension.
OBJECTIVES: The purpose of this study was to determine the contribution of the functional changes in resistance vessels to the hypertension induced by chronic nitric oxide synthase inhibition in rats. Another goal of this study was to evaluate whether this model of hypertension is accompanied by changes in the activity of endothelium-derived hyperpolarizing factor (EDHF). METHODS: Hypertension was induced by long-term (6 weeks) oral administration of N-nitro-L-arginine methyl ester (L-NAME; 75 mg/100 ml in the drinking fluid). Vascular reactivity to vasoconstrictors (phenylephrine and barium chloride) and vasodilators (acetylcholine and nitroprusside) and the flow-pressure curve were examined in isolated perfused kidneys preparations. Vascular reactivity to vasoconstrictors and the flow-pressure curve were studied under basal conditions or after the infusion of L-arginine (100 mumol/l). The activity of EDHF was evaluated by comparing the dose-response curves for acetylcholine obtained in potassium chloride- and phenylephrine-preconstricted preparations. RESULTS: Kidneys from L-NAME-induced hypertensive rats showed increased sensitivity to vasoconstrictors with a greater duration of the pressor responses at high doses and markedly up-shifted flow-pressure curve in comparison with that obtained in control kidneys. These differences disappeared when the kidneys from control and L-NAME-treated rats were infused with L-arginine. The kidneys from L-NAME-treated rats also showed a decreased responsiveness to acetylcholine with an augmented reactivity to nitroprusside. The acetylcholine dose-response curve was reduced in control preparations and greatly attenuated in L-NAME-treated preparations when the renal vasculature was preconstricted with potassium chloride. CONCLUSIONS: The changes in vascular reactivity observed in L-NAME-induced hypertensive rats may play an important role in the pathogenesis of this type of hypertension. Moreover, it is also suggested that long-term nitric oxide inhibition may be associated with increased activity of EDHF.
Acetylcholine↗
Endothelium-dependent and endothelium-independent vasodilation in hyperthyroid and hypothyroid rats.
The effects of hyper- and hypothyroidism on the vasorelaxing responses to acetylcholine (ACh), sodium nitroprusside (NP), and CaCl2 were investigated in aortic strips and isolated perfused kidneys. The renal vascular reactivity to ACh and NP was increased in hyperthyroid rats, whereas the concentration-response curve to ACh in hypothyroid rats was flattened. In the renal vasculature from hypothyroid rats, NP produced a dual response: vasoconstriction at low doses and vasodilation at medium to high doses. Aortic strips from hyperthyroid rats showed an increased response to ACh without significant differences between hypothyroid and control groups. Aortic strips from all three experimental groups showed a similar relaxing response to CaCl2. These results indicate that: (1) the raised arterial pressure of hyperthyroid rats is not associated with a reduced endothelium-dependent and calcium-induced vasodilation, and (2) the changes in responsiveness to vasodilators in resistance vessels from hyper- and hypothyroid rats may play a role in the increased and decreased peripheral vascular resistances, respectively, previously reported in such animals.
Animals↗
Effects of chronic increased salt intake on nitric oxide synthesis inhibition-induced hypertension.
OBJECTIVE AND METHOD: Experimental evidence suggests that endogenous nitric oxide plays an important role in the homeostatic response to an increase in sodium intake. In the present study we evaluated the influence of a high sodium intake (1% NaCl as drinking water) on arterial hypertension induced by long-term (6-7 weeks) inhibition of nitric oxide synthesis [NG-nitro-L-arginine methyl ester (L-NAME), 75 mg/100 ml in the drinking fluid] in rats. RESULTS: Treatment with L-NAME induced progressive elevations in tail-cuff systolic blood pressure, but there were no differences between rats drinking tap water and rats drinking 1% NaCl. Direct measurement of blood pressure at the end of the treatment confirmed the hypertension and the lack of differences between the two groups treated with L-NAME. Metabolic studies performed at the end of L-NAME treatment showed a reduced glomerular filtration rate and elevated urinary excretion of immunoreactive endothelin in the two hypertensive groups treated with L-NAME. Drinking intake, diuresis and natriuresis were significantly higher only in the L-NAME group drinking 1% NaCl. Both groups treated with L-NAME showed an accelerated and increased diuretic and natriuretic response to an isotonic 0.9% NaCl load (2.5 ml/100 g body weight, intraperitoneally). At the end of the study ventricular hypertrophy was observed in both L-NAME groups. CONCLUSION: The present results indicate that the time-dependent elevation in blood pressure produced by long-term inhibition of nitric oxide production is not affected by an increased sodium intake. However, salt supplementation induced the development of a polyuria and polydipsia syndrome in rats treated with L-NAME. The elevated excretion of endothelin in both groups treated with L-NAME suggests the possible participation of endothelin in the development of L-NAME hypertension.
Animals↗