Neurohumoral stimulation

Abstract

The temporal relationship between the development of heart failure and activation of the neurohumoral systems involved in chronic heart failure (CHF) has not been precisely defined. When a compensatory mechanism switches to a deleterious contributing factor in the progression of the disease is unclear. This article addresses these issues through evaluating the contribution of various cardiovascular reflexes and cellular mechanisms to the sympathoexcitation in CHF. It also sheds light on some of the important central mechanisms that contribute to the increase in sympathetic nerve activity in CHF.

Figure 1

Muscle sympathetic nerve activity (MSNA) recorded from the peroneal nerve of patients with increasing levels of cardiac dysfunction. Reprinted with permission from reference 13.

Figure 2

Renal Sympathetic nerve activity in conscious rabbits during the progression of pacing-induced CHF (upper panel). There was a signfiicant increase in RSNA after 3 weeks of pacing (*p<0.05 compared to control; n=5). The lower panel shows plasma Angiotensin II concentration fo groups of rabbits examined before (black bars) and after each week of cardiac pacing. (* p<0.05 compared to pre pace; n= 5)

Figure 3

Relationship between the change in Renal Sympathetic Nerve Discharge (RSND) and change in Central Venous Pressure (CVP) in anesthetized sham operated control rats and coronary artery ligated rats with heart failure during acute volume expansion with iostonic saline. There was a signfiicantly blunted renal symptho-inhibition in rats with heart failure (P< 0.05).

Figure 4

The effects of normoxic and hypoxic states on renal sympathetic nerve activity (RSNA) and carotid body (CB) chemoreceptor discharge in sham, chronic heart failure (CHF) and chronic carotid occlusion (CAO) rabbits. A. Representative recording of RSNA; B. RSNA response to hypoxia (n=12); C. Representative recording of CB chemoreceptor afferent discharge; D. CB chemoafferent response to hypoxia (n=6); DF, discharge frequency; AP, action potential. PaO₂, arterial oxygen partial pressure. CAO: bilateral carotid artery flow was decreased chronically (3 wk) to the same extent as that observed in CHF rabbits. Data are mean ± SEM. *P<0.05 CHF and CAO compared with sham group. Reprinted with permission from reference 112.