Actions of angiotensin on adrenergic nerve endings.
In the perfused vascular bed, vasoconstrictor responses to adrenergic nerve stimulation are augmented to a greater degree by angiotensin II than are the responses to injected norepinephrine. Overflow of adrenergic transmitter is also greater during nerve stimulation in the presence of angiotensin than in its absence. The evidence indicates that facilitation of adrenergic transmitter release rather than uptake blockade accounts for these results. In addition, an increased responsiveness of isolated arterial strips to norepinephrine as well as other agonists appears to contribute to the adrenergic potentiating effect of angiotensin II as well as angiotensin III. This action, which appears to be a cell membrane effect, seems to participate in adrenergic potentiation mainly in the arterial segment of the intact vascular bed. Both of these effects of angiotensin, i.e., facilitation of release and increased smooth muscle responsiveness, appear to be mediated by angiotensin receptors.
Actions of angiotensin on adrenergic nerve endings. In the perfused vascular bed, vasoconstrictor responses to adrenergic nerve stimulation are augmented to a greater degree by angiotensin II than are the responses to injected norepinephrine. Overflow of adrenergic transmitter is also greater during nerve stimulation in the presence of angiotensin than in its absence. The evidence indicates that facilitation of adrenergic transmitter release rather than uptake blockade accounts for these results. In addition, an increased responsiveness of isolated arterial strips to norepinephrine as well as other agonists appears to contribute to the adrenergic potentiating effect of angiotensin II as well as angiotensin III. This action, which appears to be a cell membrane effect, seems to participate in adrenergic potentiation mainly in the arterial segment of the intact vascular bed. Both of these effects of angiotensin, i.e., facilitation of release and increased smooth muscle responsiveness, appear to be mediated by angiotensin receptors.