1. Females are protected against the development of hypertension. The purpo
se of the current review is to present the evidence for gender differences
in the regulation of the sympatho-adrenal nervous system and to determine i
f these differences support the hypothesis that, in females, the regulation
of the sympathetic nervous system (SNS) is altered such that sympatho-adre
nal activation is attenuated or sympatho-adrenal inhibition is augmented.
2. The central control of sympatho-adrenal function is different in females
and responses vary during the oestral and menstrual cycles. Pathways regul
ating the SNS appear to he less sensitive to excitatory stimuli and more se
nsitive to inhibitory stimuli in females compared with males.
3. Gender differences in arterial baroreflex sensitivity suggest that femal
es may have a greater baroreflex sensitivity, such that alterations in bloo
d pressure are more efficiently controlled than in males. Cardiopulmonary r
eflex inhibition of sympathetic nerve activity is greater in females, possi
bly resulting in a greater renal excretory function.
4. An attenuated sensitivity to adrenergic nerve stimulation, hut not to no
radrenaline (NA), suggests that gender differences in noradrenergic neurotr
ansmission may protect females against sympathetic hyperactivity. Gender di
fferences in the regulation of NA release via presynaptic alpha(2)-adrenoce
ptors, the vasoconstrictor response to the cotransmitter neuropeptide Y and
the clearance of catecholamines are consistent with this hypothesis.
5. Similarly, attenuated stress-induced increases in plasma catecholamines
in women suggest that females are less sensitive and/or less responsive to
adrenal medullary activation. This is supported by findings of gender diffe
rences in adrenal medullary catecholamine content, release and degradation.
6. We conclude that there is strong evidence that supports the hypothesis t
hat, in females, the regulation of the SNS is altered such that sympatho-ad
renal activation is attenuated or sympatho-adrenal inhibition is augmented.