In this manuscript, we review the data that suggests that selective impairment of renal somatic afferent and sympathetic efferent nerves in patients with resistant hypertension both reduces markers of central sympathetic drive and favorably impacts diseases linked through central sympathetics—insulin resistance, heart failure, congestion, diuretic resistance, and cardiorenal disorders.
Diminished capacity within the right frontal region may be expressed in poor regulatory control over anger and hostility and over sympathetic drive.
We proposed that anger regulation and concurrent regulatory control over sympathetic drive suffer in hostile, violent-prone men due to diminished capacity within right frontal systems.
Finally, we were aware of the potential influence of antihypertensive medication (calcium blocking agents, beta blocking agents) that may alter sympathetic drive and thereby uptake of 123I mIBG.
Greater sympathetic drive has been established in the early stages of essential hypertension, suggesting that neurohormonal dysregulation may be key to its aetiology and progression.
As there is evidence in hypertension that target organ damage is associated with increased sympathetic drive, this study was designed to test the hypothesis that the magnitude of sympathetic hyperactivity in PE is greater than that in PIH.
However, increases in sAA activity have been found previously in both cervical- and thoracic-level athletes with SCI and non-spinal injured controls following strenuous exercise, which further questions sAA as a true indicator of central sympathetic drive [22].
The hypothesis that this response may be owed to an increase in sympathetic drive raises the intriguing question as to whether swearing results in an improvement in strength and power.
It has been theorized that diminished sympathetic drive may explain other findings in CH such as lower melatonin [73, 74, 111], lower testosterone [112 114], increased cortisol [115] (reviewed in [27]) and why manipulation of this axis with prednisone is effective in CH but not in other primary headache disorders [116].
Further, hypertensive patients exhibiting chronic inhibition of the sympathetic drive have increased circulating adiponectin [36].
Adults born with VLBW have a higher heart rate suggesting an elevated cardiac sympathetic drive [11], whereas other studies suggest a lower muscle sympathetic nerve activity [36].
