To determine whether there may be an abnormality in sympathetic nerve activity in response to physical and psychological stressors, we microneurologically recorded muscle sympathetic nerve activity in 11 normotensive and 9 borderline hypertensive, age-matched men. Supine blood pressure, plasma levels of epinephrine and norepinephrine and muscle sympathetic nerve activity were measured before and during a cold pressor test or a mental arithmetic test. The resting basal values of muscle sympathetic nerve activity, blood pressure and plasma epinephrine were significantly higher in the borderline hypertensives than in the normotensives (P less than 0.05). Plasma norepinephrine levels tended to be higher in the borderline hypertensives than in the normotensives but not to a significant extent (P less than 0.10). The cold test produced significantly exaggerated pressor and muscle sympathetic nerve responses (P less than 0.05) with a trend towards an increase in plasma norepinephrine (P less than 0.10) in the borderline hypertensives as compared with normotensives. The mental arithmetic test produced significantly enhanced pressor and plasma epinephrine responses in the borderline hypertensives as compared with the normotensives (P less than 0.05). During the mental arithmetic test the muscle sympathetic nerve activity decreased significantly in the normotensives (P less than 0.05) but not in the borderline hypertensives. These findings indicate that in people with borderline hypertension an abnormality exists in sympathetic nerve activity at rest and in response to stressors.

The effect of angiotensin II (ANG II) on the sympathetic outflow was examined in normal humans. The mean arterial pressure and muscle sympathetic nerve activity (MSNA) were measured before and during intravenous infusions of phenylephrine (0.5 and 1.0 micrograms.kg-1.min-1) or ANG II (5, 10, and 20 ng.kg-1.min-1) for 15 min at 30-min intervals. The baroreflex slope for the relationship between the increases in mean arterial pressure and the reductions in MSNA was significantly less acute during the infusions of ANG II than during the infusions of phenylephrine. When nitroprusside was infused simultaneously to maintain central venous pressure at the basal level, MSNA significantly increased during the infusions of ANG II (5 ng.kg-1.min-1 for 15 min) but not during the infusions of phenylephrine (1.0 micrograms.kg-1.min-1 for 15 min), with accompanying attenuation of the elevation in arterial pressure induced by these pressor agents. These findings suggest that ANG II stimulates the sympathetic outflow without mediating baroreceptor reflexes in humans.

Abstract-Angiotensin-(1-7) has been suggested to be a novel vasodilating peptide. We investigated the direct vascular effect of angiotensin-(1-7) in human forearm resistant vessels, particularly with regard to the interaction with angiotensin II, in healthy normotensive men by strain-gauge venous occlusion plethysmography with intra-arterial infusions of peptides. Intra-arterial infusion of angiotensin-(1-7) at 0.1 to 2000 pmol/min did not cause vasodilatation but rather reduced forearm blood flow by Ϸ10% at the highest dose. A placebo-controlled study showed that angiotensin-(1-7) at 0.5 to 40 nmol/min caused weak but significant vasoconstriction (Pϭ0.0016 by ANOVA). Angiotensin-(1-7) at 100 pmol/min, but not at 10 pmol/min, significantly shifted the angiotensin II dose-response curve toward the right (meanϮSD of percent changes in forearm blood flow: Ϫ19Ϯ17%, Ϫ33Ϯ22%, Ϫ55Ϯ12%, Ϫ63Ϯ10%, and Ϫ68Ϯ5% at 5, 10, 25, 50, and 100 pmol/min of angiotensin II, respectively, with saline; 5Ϯ13%, 0.9Ϯ18%, Ϫ40Ϯ16%, Ϫ54Ϯ9%, and Ϫ61Ϯ6% with angiotensin-(1-7), Pϭ0.0021 by ANOVA). Angiotensin-(1-7) did not affect the dose-response curve of noradrenaline [3Ϯ12%, 5Ϯ16%, Ϫ20Ϯ22%, Ϫ31Ϯ18%, and Ϫ40Ϯ12% at 25, 50, 100, 300, and 600 pmol/min of noradrenaline, respectively, with saline; Ϫ4Ϯ15%, Ϫ2Ϯ23%, Ϫ29Ϯ22%, Ϫ34Ϯ16%, and Ϫ42Ϯ9% with angiotensin-(

Sympathetic activity is increased in patients with mitral stenosis. Mitral valvuloplasty in such patients results in early and long-lasting normalization of sympathetic nerve activity, possibly because of an improvement in arterial baroreflex sensitivity.

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