Key result
Subcontractile concentrations of angiotensin nonspecifically potentiated human vascular smooth muscle contraction induced by norepinephrine and other agonists.
Why the study?
Does angiotensin potentiate vascular smooth muscle contraction induced by other agonists in human vascular preparations?
Does angiotensin potentiate vascular smooth muscle contraction induced by other agonists in human vascular preparations?
Angiotensin exerts a nonspecific potentiating effect on human vascular smooth muscle contraction at concentrations similar to those occurring in vivo, which may be of clinical importance.
May enhance vascular reactivity at physiological levels; hypothesis-generating and requires in vivo human confirmation before clinical consideration.
One of the possible sites of interaction between angiotensin and the sympathetic nervous system in man is at the level of vascular smooth muscle contraction. This study has used human vascular preparations to explore the potentiating effect of subcontractile concentrations of angiotensin on the contractile effects of other agonists, particularly norepinephrine. Angiotensin potentiated the effects of norepinephrine such that in the presence of angiotensin, approximately half the concentration of norepinephrine was required to produce the same contractile effect as in its absence. This potentiating effect occurred at concentrations of angiotensin approximately one-tenth of those that of themselves produced a contractile effect. Angiotensin, but not norepinephrine, also potentiated the contractile effects of 5-hydroxytryptamine, potassium chloride, and barium chloride. Barium chloride potentiated the contractile effects of norepinephrine to an extent similar to angiotensin, and 5-hydroxytryptamine and potassium chloride potentiated the effect of norepinephrine to a significantly lesser degree. Angiotensin potentiation occurred in the absence of external calcium ions. It is concluded firstly that angiotensin has a nonspecific potentiating effect on human vascular smooth muscle contraction, and secondly that it occurs at concentrations similar to those occurring in vivo and thus may be of clinical importance.
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Moulds et al. (1980) studied this question. Angiotensin vs. Absence of angiotensin was evaluated on Vascular smooth muscle contraction. Subcontractile concentrations of angiotensin nonspecifically potentiated human vascular smooth muscle contraction induced by norepinephrine and other agonists.
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