Angiotensin II (Ang II) potentiates sympathetic neurotransmission by presynaptic facilitation of norepinephrine release. We investigated whether endogenous Ang II modulates peripheral sympathetic activity in sodium- depleted essential hypertensive patients. We evaluated the effect of intrabrachial infusion of saralasin, an Ang II antagonist (5 μg/100 mL forearm tissue per minute), and benazeprilat, an angiotensin-converting enzyme inhibitor (2 μg/100 mL forearm tissue per minute), on forearm vasoconstriction (measured by strain-gauge venous plethysmography) induced by the application of lower body negative pressure (-10 mm Hg for 5 minutes). Both saralasin and benazeprilat (n = 6 for each group) blunted the vasoconstrictor action of lower body negative pressure, suggesting that circulating Ang II modulates peripheral sympathetic activity. In addition, since β-adrenoceptor stimulation can activate the production of vascular Ang II, the effect of saralasin and benazeprilat on lower body negative pressure application was evaluated in the presence of isoproterenol (0.09 μg/100 mL forearm tissue per minute) and propranolol (10 μg/100 mL forearm tissue per minute). In two other groups of hypertensive patients, isoproterenol infusion increased the release of Aug II in the forearm vasculature (arteriovenous values measured by radioimmunoassay). Furthermore, isoproterenol potentiated lower body negative pressure-induced vasoconstriction. This facilitating effect was abolished by either saralasin or benazeprilat (n = 6 for each group). In contrast, in two further groups of patients (n = 6 for each group), in the presence of the β-blocker propranolol, saralasin and benazeprilat did not alter the vasoconstrictor action of the endogenous sympathetic stimulus. The present data suggest that in sodium-depleted essential hypertensive patients, endogenous Aug II, activated by the stimulation of β-adrenergic receptors, can potentiate peripheral sympathetic neurotransmission.

Angiotensin II and sympathetic activity in sodium-restricted essential hypertension.

TADDEI, STEFANO;VIRDIS, AGOSTINO;SALVETTI, ANTONIO
1995

Abstract

Angiotensin II (Ang II) potentiates sympathetic neurotransmission by presynaptic facilitation of norepinephrine release. We investigated whether endogenous Ang II modulates peripheral sympathetic activity in sodium- depleted essential hypertensive patients. We evaluated the effect of intrabrachial infusion of saralasin, an Ang II antagonist (5 μg/100 mL forearm tissue per minute), and benazeprilat, an angiotensin-converting enzyme inhibitor (2 μg/100 mL forearm tissue per minute), on forearm vasoconstriction (measured by strain-gauge venous plethysmography) induced by the application of lower body negative pressure (-10 mm Hg for 5 minutes). Both saralasin and benazeprilat (n = 6 for each group) blunted the vasoconstrictor action of lower body negative pressure, suggesting that circulating Ang II modulates peripheral sympathetic activity. In addition, since β-adrenoceptor stimulation can activate the production of vascular Ang II, the effect of saralasin and benazeprilat on lower body negative pressure application was evaluated in the presence of isoproterenol (0.09 μg/100 mL forearm tissue per minute) and propranolol (10 μg/100 mL forearm tissue per minute). In two other groups of hypertensive patients, isoproterenol infusion increased the release of Aug II in the forearm vasculature (arteriovenous values measured by radioimmunoassay). Furthermore, isoproterenol potentiated lower body negative pressure-induced vasoconstriction. This facilitating effect was abolished by either saralasin or benazeprilat (n = 6 for each group). In contrast, in two further groups of patients (n = 6 for each group), in the presence of the β-blocker propranolol, saralasin and benazeprilat did not alter the vasoconstrictor action of the endogenous sympathetic stimulus. The present data suggest that in sodium-depleted essential hypertensive patients, endogenous Aug II, activated by the stimulation of β-adrenergic receptors, can potentiate peripheral sympathetic neurotransmission.
Taddei, Stefano; Virdis, Agostino; Mattei, P; Favilla, S; Salvetti, Antonio
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11568/204052
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