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A Cases Amenós

Publications and source records attributed to A Cases Amenós.

5 recordsLinked to original sources

Vasoactive hormones in uraemic patients with chronic hypotension.

BACKGROUND: We evaluated the possible role of an imbalance between vasoconstrictor and vasodilator hormones in the pathophysiology of chronic hypotension in uraemia. METHODS: Fourteen hypotensive haemodialysed patients, 14 normotensive haemodialysed patients, and 17 control subjects were included in this study. Plasma renin activity (PRA) and plasma levels of catecholamines, angiotensin II (AII), atrial natriuretic peptide (ANP), and arginine vasopressin (AVP) were measured. RESULTS: The mean time on haemodialysis (HD) was longer in hypotensive patients than in normotensive patients (P < 0.01). Catecholamine levels were higher in the whole group of HD patients than in controls (P < 0.01). Catecholamine levels were higher in hypotensive patients than in normotensive patients, but the differences reached significance only for adrenaline (P < 0.05). PRA and plasma AII levels were higher in hypotensive patients than in the other two groups (P < 0.05), while no differences were observed between normotensive patients and controls. Plasma ANP and AVP levels were higher in HD patients than in controls (P < 0.01), but there were no differences between hypotensive and normotensive patients. In HD patients, mean blood pressure inversely correlated with PRA (r = -0.59, P < 0.01) and plasma AII levels (r = -0.80, P < 0.01). CONCLUSIONS: Our results indicate that in HD patients with chronic hypotension there is an activation of the sympathetic and the renin-angiotensin systems. This activation is probably secondary in an attempt to compensate the vascular resistance to pressor stimuli reported in these patients.

Adult↗

Autonomic nervous system and adrenergic receptors in chronic hypotensive haemodialysis patients.

BACKGROUND: The pathophysiology of chronic hypotension (CH) in uraemia is not elucidated. The possible role of autonomic nervous system dysfunction and adrenoceptor alterations in the pathophysiology of CH in uraemia was evaluated in this study. METHODS: Seventeen hypotensive haemodialysis (HD) patients, 17 normotensive HD patients, and 17 control subjects were studied. We evaluated the integrity of the baroreflex arc (Valsalva manoeuvre), the parasympathetic efferent pathway ('deep-breathing test') and the sympathetic efferent pathway ('hand-grip test'). We also evaluated platelet alpha 2-adrenoceptor and lymphocyte beta 2-adrenoceptor densities (radioligand binding assay), and beta 2-adrenoceptor response (intracellular cAMP generation after isoproterenol stimulation in lymphocytes). RESULTS: Responses to the Valsalva manoeuvre and the deep-breathing test were altered in all HD patients (P < 0.05). Valvalva ratio was lower in hypotensive patients than in normotensive patients (P < 0.01), whereas the pressor response to the hand-grip test was reduced only in hypotensive HD patients (P < 0.01). In haemodialysed patients, basal mean blood pressure (MBP) correlated with MBP increases during the hand-grip exercise (r = 0.59, P < 0.01). Plasma catecholamine levels were elevated in both groups of patients (P < 0.025). Plasma adrenaline levels were higher in hypotensive HD patients than in normotensive patients (P < 0.05). alpha 2- and beta 2-adrenoceptor densities and beta 2-adrenoceptor response were reduced in hypotensive patients (P < 0.05 vs normotensive patients). MBP correlated with alpha 2-adrenoceptor (r = 0.46, P < 0.01) and beta 2-adrenoceptor (r = 0.43, P < 0.025) densities in HD patients. CONCLUSIONS: Normotensive haemodialysed patients have increased plasma catecholamine levels with preserved alpha 2- and beta 2-adrenoceptor numbers, as well as beta 2-adrenoceptor responses. In hypotensive patients, plasma adrenaline levels were even higher; the increased plasma catecholamine levels induced an alpha 2- and beta 2-adrenoceptor downregulation. This downregulation may play a role in the reduced cardiovascular responses to adrenergic stimuli reported in hypotensive HD patients.

Adult↗

[Autonomic dysfunction in chronic hypotension associated with uremia].

BACKGROUND: Chronic hypotension is a not uncommon complication among hemodialyzed patients which is responsible of an important morbidity. The autonomic nervous system (ANS) dysfunction seems to play a key role in the pathogenesis of chronic hypotension. METHODS: In order to study whether ANS dysfunction is responsible for chronic hypotension in hemodialyzed patients, the authors evaluated the integrity of the whole baroreflex arc by the Valsalva's manoeuver, of parasympathetic efferent pathway by the deep-breathing test and of sympathetic efferent pathway by the hand-grip test in 16 hemodialyzed patients with chronic hypotension, 17 normotensive hemodialyzed patients and 17 normal control subjects. Plasma catecholamine levels were also measured in these patients. RESULTS: In normotensive patients, Valsalva's manoeuver response (p < 0.005) and deep-breathing test response (p < 0.05) were lowered, while hand-grip test response was preserved. In chronic hypotensive patients, in addition to an impaired deep-breathing test (p < 0.05), a further reduced Valsalva's manoeuver response and a lower pressor response to hand-grip test were observed (p < 0.001). Catecholamine levels were higher in both groups of patients (p < 0.01) with respect to control subjects, specially in chronic hypotensive patients. CONCLUSIONS: In hemodialyzed patients (both normotensive and hypotensive) the whole baroreflex function and parasympathetic response are impaired. The lower pressor response to hand-grip test observed in hypotensive patients, in spite of the higher catecholamine levels, suggest that in these patients the cardiovascular dysfunction cannot be ascribed to a reduced sympathetic "outflow" but to a resistance of the target organs (heart and vessels) to the sympathetic stimulation.

Adult↗

[Vascular hyperreactivity to vasopressin in mild essential arterial hypertension].

The aim of the present study was to evaluate the hemodynamic effects of arginine vasopressin (AVP) infusion in essential hypertension. To this end, 9 hypertensive patients and 10 normotensive controls were evaluated. After one hour rest, AVP was infused at a dosage of 0.5 and 2 ng/(kg/min), in 20 minutes periods. After AVP infusion, mean arterial pressure increased only in hypertensive patients (from 125.8 +/- 7 to 131.8 +/- 7, p less than 0.01 and to 135.6 +/- 6 mmHg, p less than 0.01). Peripheral vascular resistance was significantly increased in both groups during AVP infusion, although the percent increase was higher in hypertensive patients during the last period of infusion (18.3 +/- 10 versus 4.6 +/- 4, p less than 0.05). Cardiac index decreased in both groups during infusion, although this reduction was significantly higher in hypertensive patients than in healthy controls in the last period of infusion (-8.16 +/- 6 versus -1.8 +/- 4%, p less than 0.05). These results confirm that in essential hypertension there is an exaggerated pressor response to AVP infusion, suggesting that it is due to an increased vascular response to this hormone. The compensatory reduction of cardiac output and the inhibition of sympathetic nervous activity mediated through baroreceptor reflexes do not apparently play a role in this pressor response.

Adult↗