The activity of single vasoconstrictor nerve units in hypertension.

Abstract

It has long been established from controlled experiments in anaesthetized animals that it is more accurate to quantify the mean frequency of efferent sympathetic nerve activity from single unit than from multi-unit bursts recordings. More recently, sympathetic nerve hyperactivity has been reported in patients with essential hypertension (EHT) when using microneurographic recordings from peripheral efferent nerves. This review will focus on the mean frequency of single unit of muscle sympathetic nerve activity (s-MSNA) in relation to that of multi-unit bursts (MSNA) as obtained by microneurography in EHT. We have shown that the resting levels of s-MSNA and MSNA were increased in uncomplicated EHT, white coat hypertension and in EHT complicated by left ventricular hypertrophy. There was a relatively greater increase in s-MSNA than in MSNA in mild hypertension and in complicated EHT. We also found that both s-MSNA and MSNA were increased to a similar extent in conditions known to affect reflexes emanating from the heart and influencing sympathetic output, such as acute myocardial infarction. In other preliminary studies, the increase of s-MSNA in response to the discomfort of cold pressor test was greater than that of MSNA and this difference was abolished by the centrally sympatholytic agent moxonidine. These results are consistent with the hypothesis that an increase in the mean frequency of central sympathetic discharge to the periphery (greater s-MSNA than MSNA) is involved in the pathogenesis and complications of EHT. Target organ damage may in turn lead to an increase in overall sympathetic output (excessive MSNA increase) through the operation of peripheral reflex mechanisms.