HORMONES AS LONG-TERM ERROR SIGNALS FOR THE SYMPATHETIC NERVOUS-SYSTEM - IMPORTANCE OF A NEW PERSPECTIVE

Authors
Citation
Jw. Osborn, HORMONES AS LONG-TERM ERROR SIGNALS FOR THE SYMPATHETIC NERVOUS-SYSTEM - IMPORTANCE OF A NEW PERSPECTIVE, Clinical and experimental pharmacology and physiology, 24(1), 1997, pp. 109-115
Citations number
38
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
03051870
Volume
24
Issue
1
Year of publication
1997
Pages
109 - 115
Database
ISI
SICI code
0305-1870(1997)24:1<109:HALESF>2.0.ZU;2-6
Abstract
1. A hormonal-sympathetic reflex model for long-term control of arteri al pressure is presented. It is hypothesized that the hormonal-sympath etic reflex regulates arterial pressure during chronic dietary salt lo ading by decreasing sympathetic tone. This sympathetic response is med iated by an increase in plasma vasopressin (AVP) and a decrease in pla sma angiotensin (AngII). 2. Three new models of neurogenic salt-depend ent hypertension are presented. All models are theoretically based on an impaired hormonal-sympathetic reflex. 3. In the first model, sympat hetic responsiveness is 'clamped' by long-term alpha-adrenergic blocka de with prazosin. Prazosin treated rats exhibit marked salt-dependent hypertension despite normal suppression of the renin-angiotensin syste m. 4. In the second model, the ability of the central nervous system t o respond to salt-induced changes in AVP and AngII concentrations was prevented by long-term administration of antagonists selective for the AVP-V-1 and AT(1). This 'clamp' of the afferent hormonal signal resul ted in salt-dependent hypertension identical in magnitude to that obse rved in prazosin treated rats. 5. In the third model, the long-term ar terial pressure responses to increasing dietary salt were examined in sino-aortic denervated (SAD) rats. SAD rats exhibited salt-dependent h ypertension, of lesser magnitude than that observed with 'clamped' aff erent and efferent pathways of the hormonal-sympathetic reflex.6. A pr imary role for hormonal 'error signals' is presented and the impact th is perspective has on past and future investigations of central mechan isms of long-term arterial pressure regulation is discussed.