Hormones as long-term error signals for the sympathetic nervous system: importance of a new perspective.
1. A hormonal-sympathetic reflex model for long-term control of arterial pressure is presented. It is hypothesized that the hormonal-sympathetic reflex regulates arterial pressure during chronic dietary salt loading by decreasing sympathetic tone. This sympathetic response is mediated by an increase in plasma vasopressin (AVP) and a decrease in plasma angiotensin (AngII). 2. Three new models of neurogenic salt-dependent hypertension are presented. All models are theoretically based on an impaired hormonal-sympathetic reflex. 3. In the first model, sympathetic responsiveness is 'clamped' by long-term alpha-adrenergic blockade with prazosin. Prazosin treated rats exhibit marked salt-dependent hypertension despite normal suppression of the renin-angiotensin system. 4. In the second model, the ability of the central nervous system to respond to salt-induced changes in AVP and AngII concentrations was prevented by long-term administration of antagonists selective for the AVP-V1 and AT1. This 'clamp' of the afferent hormonal signal resulted in salt-dependent hypertension identical in magnitude to that observed in prazosin treated rats. 5. In the third model, the long-term arterial pressure responses to increasing dietary salt were examined in sino-aortic denervated (SAD) rats. SAD rats exhibited salt-dependent hypertension, of lesser magnitude than that observed with 'clamped' afferent and efferent pathways of the hormonal-sympathetic reflex. 6. A primary role for hormonal 'error signals' is presented and the impact this perspective has on past and future investigations of central mechanisms of long-term arterial pressure regulation is discussed.
Osborn
J W
JW
Department of Animal Science, University of Minnesota, St Paul 55108, USA.
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D004195:Disease Models, Animal; D006728:Hormones / Q000378:metabolism / Q000502:physiology*; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology; D011311:Pressoreceptors / Q000502:physiology; D011945:Receptors, Angiotensin / Q000378:metabolism; D012964:Sodium / Q000009:adverse effects / Q000502:physiology; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000502:physiology*; D013997:Time Factors; D014667:Vasopressins / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000502:physiology
D000317:Adrenergic alpha-Antagonists; D057911:Angiotensin Receptor Antagonists; D006728:Hormones; D011945:Receptors, Angiotensin; D014667:Vasopressins; D012964:Sodium