Gender differences in sympathetic nervous system regulation

C Hinojosa‐Laborde, I Chapa, D Lange… - Clinical and …, 1999 - Wiley Online Library
C Hinojosa‐Laborde, I Chapa, D Lange, JR Haywood
Clinical and Experimental Pharmacology and Physiology, 1999Wiley Online Library
1. Females are protected against the development of hypertension. The purpose of the
current review is to present the evidence for gender differences in the regulation of the
sympatho‐adrenal nervous system and to determine if these differences support the
hypothesis that, in females, the regulation of the sympathetic nervous system (SNS) is
altered such that sympatho‐adrenal activation is attenuated or sympatho‐adrenal inhibition
is augmented. 2. The central control of sympatho‐adrenal function is different in females and …
1. Females are protected against the development of hypertension. The purpose of the current review is to present the evidence for gender differences in the regulation of the sympatho‐adrenal nervous system and to determine if these differences support the hypothesis that, in females, the regulation of the sympathetic nervous system (SNS) is altered such that sympatho‐adrenal 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 regulating the SNS appear to be less sensitive to excitatory stimuli and more sensitive to inhibitory stimuli in females compared with males.
3. Gender differences in arterial baroreflex sensitivity suggest that females may have a greater baroreflex sensitivity, such that alterations in blood pressure are more efficiently controlled than in males. Cardiopulmonary reflex inhibition of sympathetic nerve activity is greater in females, possibly resulting in a greater renal excretory function.
4. An attenuated sensitivity to adrenergic nerve stimulation, but not to noradrenaline (NA), suggests that gender differences in noradrenergic neurotransmission may protect females against sympathetic hyperactivity. Gender differences in the regulation of NA release via presynaptic α2‐adrenoceptors, 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 differences in adrenal medullary catecholamine content, release and degradation.
6. We conclude that there is strong evidence that supports the hypothesis that, in females, the regulation of the SNS is altered such that sympatho‐adrenal activation is attenuated or sympatho‐adrenal inhibition is augmented.
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